bluuebunny/crossref_metadata_2025 huggingface dataset:
Erythrocyte Aldehyde Dehydrogenase Activity in Alcoholism
Authors: Lin Cheng‐Chung , Potter James J. , Mezey Esteban
Published: February 2008

Erythrocyte aldehyde dehydrogenase activity was determined in 44 chronic alcoholic patients within 18–36 hr after discontinuation of chronic alcohol intake and in 20 nonalcoholic controls. The enzyme activity was decreased to 4.98 ± 0.52 mlU/mg of protein in the alcoholics as compared with a value of 8.25 ± 1.29 mlU/mg of protein in the controls (p < 0.05). The level of the enzyme activity did not correlate significantly with the daily quantity of alcohol consumption or the degree of liver injury reflected in elevations of serum aspartate aminotransferase. Repeat determination in 23 of the alcoholics after 2 weeks of supervised abstinence in an inpatient unit resulted in an increase in the enzyme activity to control levels. These findings show that the decreased activity of erythrocyte aldehyde dehydrogenase which occurs in association with alcohol ingestion is not an inherent characteristic of alcoholism.
Formation of Schiff Base Adduct between Acetaldehyde and Rat Liver Microsomal Phosphatidylethanolamine
Authors: Kenney William C.
Published: February 2008

Recent studies have established the formation of acetaldehyde adducts of proteins even at low concentrations of acetaldehyde expected to occur In vivo under conditions of ethanol metabolism. Although formation of acetaldehyde adducts with phospholipids has been obtained at high pH values and at high concentrations of acetaldehyde, the occurrence of such adducts under more physiological conditions had yet to be demonstrated. Rat liver microsomes were incubated with 0.2 mm [14C]acetaldehyde at pH 7.4 and 37°C. After treatment with sodium borohydride to reduce any Schiff bases formed, the phospholipids were isolated. The major radioactive component within the phosphoslipid fraction had chromatographic properties identical to N‐ethylphosphatidylethanolamine. In addition, the nitrogenous base derived therefrom by acid hydrolysis was identical to N‐ethylethanolamine. These results indicate that a Schiff base adduct between acetaldehyde and microsomal phosphatidylethanolamine had been formed during incubation of low concentrations of acetaldehyde with rat liver microsomes.
The Effects of Dietary Zinc Deficiency on Voluntary Alcohol Drinking in Rats
Authors: Collipp P. J. , Kris V. K. , Castro‐Magana M. , Shih A. , Chen S. Y. , Antoszyk N. , Baltzell Jan , Noll Jamie , Trusty Cheryl
Published: February 2008

The effects of dietary zinc deficiency on voluntary alcohol drinking in rats were examined in three separate experiments. Zinc‐deficient rats showed a significantly greater voluntary alcohol intake as compared with the pair‐fed controls. In the first experiment there were 14 male Sprague‐Dawtey rats with 7 controls and 7 who were begun on a zinc‐deficient diet (below 2 pom) at body weight 58–81 g. In the second experiment with 11 male Sprague‐Dawley rats, the same diet was begun at 103–107 g. In the last experiment, 11 rats were begun at 120–199 g. Hair zinc measurements documented lower levels in the zinc‐deficient rats after 6 weeks on the diet The data indicate that a zinc‐deficient state did increase voluntary alcohol intake in rats. In each experiment, the per cent alcohol consumed declined when a normal diet was given after the 6th week, and the difference was significant in experiments 1 and 3.
Alcoholism in Vietnam and Korea Veterans: a Long Term Follow‐up
Authors: Branchey L. , Davis W. , Lieber C. S.
Published: February 2008

The prevalence of alcoholism was assessed in veterans of the Vietnam and Korean wars. In addition, the role played by exposure to combat in excessive alcohol consumption was evaluated. One‐third of patients attending clinics that were not devoted to the treatment of alcoholism had alcohol‐related problems. This is far in excess of general population prevalence estimates. A significant association was found between combat exposure and excessive alcohol use. Close to 60% of a group of veterans exposed to combat drank excessively at the time of our study versus only 25% of a group of veterans of the Vietnam and Korean eras. An association between alcoholism and war experiences had already been observed by others in the early postwar era. Our data show that the effects of combat exposure can persist for more than a decade after the stressful events.
Cultural Level Interventions in the Arena of Alcoholism
Authors: Pattison E. Mansell
Published: February 2008

Three traditions of alcoholism are reviewed: a moral model, a disease model, and a public health model. The public health model is emerging as a major paradigmatic shift, supported by substantial empirical data of the past decade. The arena of alcoholism has heretofore included only alcoholics, and excluded consideration of all other drinkers. The public health model reformulates alcoholism as a general population problem. The definition of alcoholism is disaggregated into discrete behavioral factors. In turn, this affords consideration of targeted interventions at different levels of cultural action to modify alcoholic factors in drinking behavior
Brain Membrane Sensitivity to Ethanol during Development of Functional Tolerance to Ethanol in Rats
Authors: Beaugé Franĉoise , Fleuret‐Balter Catherine , Nordmann Jo , Nordmann Roger
Published: February 2008

Adult male rats were rendered progressively tolerant to ethanol by daily intragastric administration of doses of 3–6 g/kg body weight. Functional tolerance assessed by the hypothermic effect after injection of a challenge dose of ethanol developed slowly and was demonstrable after 2 weeks of treatment

Intrinsic crude synaptosomal membrane fluidity, as assessed by fluorescence polarization of DPH, as well as (Na++ K+)ATPase activity, did not change significantly during the whole treatment. However, the extra addition of ethanol (0.175‐0.700 m) in vitro to the membranes of rats, having received ethanol over a period of at least 2 weeks, fluidized less and inhibited the (Na++ K+)ATPase activity less than in starch‐fed controls. The time‐course for the appearance of this membrane hyposensitivrty was found to be the same as the time course for the development of functional tolerance to ethanol

The correlation between the degree of functional tolerance and the (Na++ K+)ATPase sensitivity to ethanol appeared very significant, highlighting the sensitivity of membrane‐bound enzymes to detecting adaptive changes in complex biological membranes tolerance
Predicting Treatment Outcome after Ten Years among American Indian Alcoholics
Authors: Westermeyer Joseph , Neider John
Published: February 2008

Forty‐five American Indian alcoholics were intensively studied in 1970–1971. In addition to the usual demographic characteristics, research scales included Alcoholism History Scale, Alcohol Withdrawal Scale, Indian Culture Affiliation Scale, Social Competence Scale, Legal Problems Scale, Psychiatric Problems Scale, Liver Dysfunction Scale, Malnutrition Scale, and Abnormal Laboratory Screening Scale. These findings in 1970–1971 were then correlated with a four‐item outcome rating obtained in 1980–1981. Better outcome was associated with less parental loss, ever having been married, compliance with treatment recommendations, and having predominantly Indian rather than non‐Indian friends. Women alcoholics were unlikely to deteriorate and still survive, although this was the most frequent pattern among the men. Higher Indian Culture Affiliation and more severe Liver Dysfunction in 1970–1971 were correlated with better outcome in 1980–1981. Possible explanations for these findings are considered
Effect of Acute Ethanol Administration on Diamine Oxidase Activity in the Upper Gastrointestinal Tract of Rat
Authors: Sessa Angela , Desiderio M. Alfonsina , Perin Antonio
Published: February 2008

The effect of a single dose (2 g/kg, body weight) of ethanol on diamine oxidase activity of the upper gastrointestinal tract was studied in fasted rats. Ethanol given by gastric intubation as a 10%, 20%, or 40% solution caused an early and transient increase in diamine oxidase activity in gastroduodenal fluid that was concentration‐dependent. The 20% ethanol solution caused, at 3 and 6 hr, a diminution of enzyme activity in the wall of the stomach and duodenum, but not in that of the jejunum. Diamine oxidase activity in the gastroduodenal tract returned to control values at 12 hr, when ethanol had disappeared from the blood. The plasma enzyme activity diminished, starting from the first hour. The same dose of ethanol administered intravenously caused diminutions in diamine oxidase activity in the stomach and duodenum similar to those observed after gastric intubation. The enzyme decrease in the stomach and duodenum was not correlated with the gastroduodenal or blood ethanol levels. Pretreatment with pyrazole, an inhibitor of ethanol metabolism, prevented the ethanol‐induced decrease in gastroduodenal enzyme activity, thus suggesting that this diminution was principally a consequence of ethanol oxidation. These results indicate that ethanol modifies in the gastroduodenal tract the activity of diamine oxidase the enzyme which regulates the physiologic activity of histamine in gastric secretion and oxidizes the toxic diamines of dietary and bacterial origin.
Estimated Lethal Ethanol Concentrations in Relation to Age, Aspiration, and Drugs
Authors: Poikolainen Kari
Published: February 2008

In 98 deaths certified to be due to accidental alcohol poisoning, maximum antemortal blood ethanol concentrations were estimated as the sum of postmortal concentration and the product of blood ethanol elimination rate (0.258 g/liter/hr) and the time interval between the discontinuation of drinking and death. The estimated mean maximum concentration (g/liter) was 4.63 for uncomplicated cases, 4.26 for cases with heart disease, 3.98 for cases in which aspiration of stomach contents had contributed to death, 3.59 for ethanol‐barbiturate poisonings, and 3.11 for combinations of ethanol and other psychotropic drugs. The mean for this last group was significantly lower than that for the first or the second group (p < 001). The mean concentration for ethanol‐barbiturate poisonings was significantly lower than the mean for the uncomplicated cases (p = .01). In the two first groups combined, the higher the age, the lower the ethanol concentration (r = ‐.27; p = .02). Likewise, the postmortal blood ethanol concentration correlated negatively with age (r = ‐.26; p = .02), after controlling for the time interval. The lethal ethanol concentration for the aged seems to be lower than that for young people. A possible explanation for this phenomenon is the loss of ethanol tolerance.
Effects of Chronic Ethanol Treatment on Lipid Composition and Prostaglandins in Rats Fed Essential Fatty Acid Deficient Diets
Authors: Ailing Christer , Becker Wulf , Jones A. W. , Änggärd Erik
Published: February 2008

Rats of the third generation fed on a diet with 0.3 energy‐% (low‐essential fatty acids (EFA) or 3 energy‐% (normal‐EFA) essential fatty acids wens given once‐daily intraperitoneal injections of ethanol 3 g/kg or isocakmc glucose for 23 days. At the end of the experiment, organs were removed and their weight and lipid composition were determined. The postmortem accumulation of the prostaglandins PGE2, PGF2, and 6‐keto‐PGF 1α, was used to assess prostaglandin (PG) precursor availability in the organs.

Ethanol was found to amplify the biochemical indicators of EFA‐deficiency. The fatty acids 20:3 n‐9 in brain phosphatidylethanolamine and phosphatidylinositol and 22:5 n‐6 in brain phosphatidytethan‐oiamine and phosphatidylserine were significantly higher in the ethanol group compared to the control group. In the kidney, the 20:3 n‐9/20:4 n‐6 ratio in phosphatidylinositol and phosphatidylserine was significantly higher in the ethanol group compared to the control group. The low‐EFA animals had a lower output of urinary PGF2α. than the normal EFA animals. Chronic ethanol treatment gave a pronounced increase of urinary PGF2α in both groups. Kidney levels of PGs were lower in the low EFA‐animals. Chronic ethanol treatment gave a further decrease in kidney PGs. PG levels were the same in brains from low‐EFA and normal‐EFA animals with no effects of ethanol.

The data are consistent with an increased utilization of EFA during chronic ethanol intoxication leading to a depletion of PG precursor stores in some but not all organs.
Book Review
Authors: Rohrs Charles
Published: February 2008

Smart, Reginald G., Glaser, Frederick B., Israel, Yedy, Kalant, Harold, Pophan, Robert E., and Schmidt, Wolfgang, (eds): Research Advances in Alcohol and Drug Problems, Volume 7. New York, Plenum Press, 1983.
Exaggerated Acetaldehyde Response after Ethanol Administration during Pregnancy and Lactation in Rats
Authors: Gordon Barbara H. J. , Baraona Enrique , Miyakawa Happei , Finkelman Frances , Lieber Charles S.
Published: February 2008

The exaggerated blood acetaldehyde response that has been reported after ethanol administration to pregnant rats was found to be the beginning of a much larger alteration occurring during lactation. Indeed, at the end of pregnancy, we confirmed a 4‐fold increase in the acetaldehyde values above nonpregnant values after an intragastric dose of 3 g/kg ethanol. During gestational days 1 to 17, the levels did not differ. After delivery, the exaggerated acetaldehyde response to ethanol was increased, producing acetaldehyde concentrations 15‐fold greater than in nonlactating controls. This response returned to nonpregnant levels with weaning and could be abolished by removing the pups at birth. The intensified response was associated with both an enhanced rate of ethanol oxidation and a decreased low Km aldehyde dehydrogenase activity in Jtver mitochondria. At the end of pregnancy, measurable concentrations of acetaldehyde were found in umbilical venous Wood and fetal blood. However, they amounted to only one‐quarter of maternal values whereas ethanol levels were similar. Thus, during late pregnancy and lactation, there is a marked increase in maternal blood acetal‐ j dehyde after ethanol intake. In the presence of a normal placenta, [ however, an acetaldehyde concentration gradient exists between ] the mother and the fetus.
Effects of Ethanol and Maternal Nutritional Status on Fetal Development
Authors: Weinberg Joanne
Published: February 2008

This study investigated the Interactive effects of alcohol and nutritional status of the pregnant female on fetal growth and development Three liquid diets were formulated ranging in protein content from suboptimal to supraoptimal: diet I provided 18% kcal as protein and 1.0 kcal/ml; diets II and III provided 25 and 32% kcal, respectively, as protein and 1.2 kcal/ml. In all cases, alcohol provided 36% of total calories. Both pair‐fed and ad libitum fed control groups were included. We found that blood alcohol levels were consistently high in all three diet regimens throughout gestation. Alcohol intake suppressed weight gains and increased adrenal weights and placenta weights in pregnant females. Both body weights and brain weights were reduced in alcohol‐exposed fetuses. However, relative brain weights were found to be increased in alcohol fetuses, indicating “brain sparing.” Maternal nutritional status had no major effect on developmental outcome. Thus, with alcohol administered as a high proportion of total dairy calories, increasing dietary protein levels did not attenuate the major adverse effects of alcohol on fetal development.
Alcohol Withdrawal Syndromes: Clinical Management with Lofexidine
Authors: Cushman P. , Forbes R. , Lemer W. , Stewart M.
Published: February 2008

Sixty‐three mainly male alcoholics were randomly assigned to placebo or lofexidine treatment for 48 hr shortly after admission to the hospital. Their starting points were similar regarding their semiquantitative estimates of alcohol withdrawal symptoms (AWS). Their demographics, histories of past alcohol use, physical findings, and laboratory abnormalities usually associated with alcoholism were similar. Starting 3 hr after 0.4 mg of oral lofexidine, which was given every 6 hr as eight doses, the AWS scores were significantly lower than those of the placebo group. Hypotension was the strongest finding. Six placebo recipients had to be prematurely interrupted due to increasing or intolerable alcohol withdrawal symptoms and switched to a benzodiazepine. Only one lofexidine recipient was prematurely interrupted, due to transient hallucinations. The study has a large placebo effect both groups of patients rated the treatment process very highly. Lofexidine, an α2‐adrenergic agonist, was superior to placebo in alcohol withdrawal. This drug, as with its analogue donidine, may represent a new and important pharmacological treatment for alcohol withdrawal symptoms.
Long Lasting Changes in Gerbil Brain after Chronic Ethanol Exposure: A Quantitative Study of the Glial Cell Marker S‐100 and DNA
Authors: Rosengren Lars E. , Wronski Andrzej , Briving Carin , Haglid Kenneth G.
Published: February 2008

Glial S‐100 protein, soluble protein, and DNA were quantitatively studied in brains of gerbils chronically exposed to ethanol in a nutritionally complete fluid diet Eight different brain areas were studied. After exposure to ethanol for 3 months followed by a 4‐month post‐treatment ethanol‐free period, increased amounts of S‐100 protein per wet weight were found in the frontal cerebral cortex, the sensory‐motor cerebral cortex, the posterior cerebellar vermis, and the brainstem. The increase of S‐100 in the posterior cerebellar vermis was paralleled by an increase in DNA per wet weight, which was also increased in the anterior cerebellar vermis. However, a decreased content of DNA was observed in the frontal cerebral cortex, despite the increase of S‐100 protein, suggesting a cell loss affecting cells other than astroglial in this area. In the cerebellar vermis, elevated concentrations of soluble proteins per wet weight were found, whereas a decreased amount was found in the anterior cerebellar hemispheres. It is suggested that the S‐100 protein acts as a marker for astroglial cell volume and that a concomitant increase of S‐100 protein and DNA might indicate an increase in the number of astroglial cells. Thus, our results obtained after ethanol exposure and subsequent ethanol abstinence are compatible with changes consisting of astroglial hypertrophy in the cortex areas and brainstem, as well as astroglial hypertrophy and/or proliferation in the posterior cerebellar vermis, a dear sign of the preceding noxae.
Lack of Recovery in Male Alcoholics' Neuropsychological Performance One Year after Treatment
Authors: Yohman J. Robert , Parsons Oscar A. , Leber William R.
Published: February 2008

Thirty‐seven middte‐aged alcoholics and 20 nonalcoholic control equated for age and education were examined on measures of verbal, learning/memory, abstractmg/probiem‐solving, and percep‐tuat‐motor abttties 7 weeks after beginning detoxification and 13 months later. At 7 weeks, the alcoholics were significantly different from the controls on the verbal, abstrectmg/pcobtom‐sotving, and perceptual‐motor dusters and tended to differ on the learning/ memory tests. At 13 months, the same pattern of differences was found except the groups no longer differed on the verbal tests. Alcoholics who resumed drinking during the 13 months differed from the controls to a greater extent than did abstainers on both the initial and final testings. These results have implications for treatment programs and recidivism.
The Disulfiram‐Alcohol Reaction: Factors Determining and Potential Tests Predicting Severity
Authors: Beyeter Christine , Fisch Hans‐Ulrich , Preisig Rudotf
Published: February 2008

13 ambulatory alcoholics (3 woman, 10 men) who consented to alcohol‐avorsive treatment with dtsuffiram were sutojectad to detailed investigations before, during, and after the disumram‐alcohol reaction (DAR). The studies included quantitative estimation of aver function (aminopyrine breath test, ABT; galactose elimination capacity, GEC) prior to the DAR, measurement of alcohol and ecetaMehyde plasma levels together with pulse rate and blood pressure during the DAR, and the effects of disulfiram on erythrocyte acetaMehyde‐oxidizing capacity (AOC). As expected, the severity of the DAR showed considerable interindividuai variation. However, the maximal fan in diastolic blood pressure was closely (r= 0.83; p < 0.001; n = 13) related to peak acetaidehyde plasma level (AAPL). The decrease m systolic blood pressure was age dependent, individuals >40 years exhibiting a larger drop for a given AAPL. The dependence of acetaidehyde formation on liver function was suggested by a significant correlation (r = 0.88; p < 0.01; n = 8) between ABT and AAPL; this relationship was influenced by the prior intake of enzyme‐inducing drugs. Measurements of AOC indicated that a disulfiram‐induced maximal suppression is achieved already after 6 days of treatment reaching levels of 0.7 ± 0.6 nmol/ml/min (so) (compared to pretreatment values of 4.1 ±0.9). Mean values in untreated alcoholics and in subjects with alcoholic or nonalcoholic liver disease were not significantly different from controls. It is concluded that AAPL appears to be the single, most important factor determining severity of the cardiovascular response in the DAR, and that the ABT (following disulfiram pretreatment) may be a suitable test for predicting changes in AAPL. Finally, AOC measurements dearly define subjects under treatment with disulfiram.
Pharmacokinetics of Ethanol in the Ferret
Authors: McLain Daniel E. , Babish John G. , Roe Daphne A.
Published: February 2008

Select doses of ethanol (25%, w/v) were administered to female ferrets (Mustefa putorkn) by gastric intubation to determine dosage corresponding to peak Wood alcohol levels (BAL) greater than 100 mg/100 ml of blood (mg%) for an extended duration. Low doses (6 ml/kg) resulted in peak BAL of 202 mg% in 1.5 hr and 50 mg% after 12 hr. Intermediate doses (8 ml/kg) resulted in peak BAL of 253 mg% in 1.4 hr and 89 mg% after 12 hr. High doses (12 ml/kg) did not increase peak BAL proportionately, resulted in BAL of 128 mg% after 12 hr, and increased the volume of distribution significantly. A computer‐based estimate of kinetic parameters led to the conclusion that metabolism in this range of BAL was not a first order process. Moreover, a decreasing enzyme velocity with increasing substrate concentration precluded calculation of Mtchaetis‐Menten parameters and suggested possible substrate inhibition effects.
Alcohol and Aldehyde Dehydrogenase Isoenzymes in North American Indians
Authors: Rex Douglas K. , Bosron William F. , Smialek John E. , Li Ting‐Kai
Published: February 2008

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) isoenzyme phenotypes were determined in autopsy liver samples from 50 North American Indians from New Mexico. Forty‐six of the 50 livers had sufficient ADH activity to allow phenotyping at the ADH, and ADH, loci. All 46 livers possessed the “typical” ADH,1–1 phenotype. The frequency of the ADH allele was 0.59 and is the highest thus far reported in any racial population. All 50 livers possessed the ALDH I isoenzyme which exhibits the greatest anodic mobility on starch gel electrophoresis at pH 7.6. The results show that ADH and ALDH phenotypes among American Indians living in New Mexico are very similar to those of Caucasian populations and quite different from those of Orientals.
Comparison of Ethanol Metabolism in Isolated Periportal or Perivenous Hepatocytes: Effects of Chronic Ethanol Treatment
Authors: Väänänen Hannu , Lindros Kai O.
Published: February 2008

Ethanol metabolism in rat hepatocytes isolated either from the periportal (pp) or the perivenous (pv) area by collagenase gradient perfusion was compared to reveal metabolic factors that could be associated with the development of perivenous alcoholic liver damage. Cells were also isolated from rats given ethanol (E) chronically by addition to the drinking fluid. One group (EM) received in addition the alcohol dehydrogenase inhibitor 4‐methylpyrazoie, which potentiated the ethanol treatment by causing sustained elevated diurnal blood ethanol levels. Fatty degeneration ensued in only one‐third of the E rats but in all of the EM rats. The periportal/perivenous activity distributions of alanine aminotransferase (ALAT) and glutamate dehydrogenase (GLDH) were 2.2 and 0.75, respectively. Both ethanol treatments significantly decreased the ALAT and increased the GLDH activities, but did not change their pp/pv distributions. Ethanol treatment also increased ethanol and acetaldehyde oxidation, but to the same extent in pp and pv cells. The increase was more marked in cells from EM rats despite their more severe liver fatty degeneration. Ethanol incubation also increased the lactate/pyruvate ratio to the same extent in pp and pv cells both from control or ethanoi‐treated rats. Our results indicate that periportal and perivenous hepatocytes convert ethanol via acetaldehyde to acetate equally well and with similar effects even after chronic ethanol treatment Consequently, preferential damage of the perivenous area after chronic ethanol intake is not caused by inherent or acquired differences in ethanol metabolism between perivenous and periportal hepatocytes. Rather, sinusoidal gradients only established in the intact liver may exaggerate the metabolic imbalance by ethanol in the perivenous area, thus explaining its greater vulnerability to damage by alcohol abuse.
Abnormal Fluidity and Surface Carbohydrate Content of the Erythrocyte Membrane in Alcoholic Patients
Authors: Beaugé Françoise , Stibter Helena , Borg Stefan
Published: February 2008

Erythrocyte membranes from 11 healthy individuals and 11 alcoholic patients, examined within 24 hr of withdrawal, were studied for membrane fluidity as assessed by fluorescence polarization of 1,6‐diphenyl‐1,3,5‐hexatriene and for the concentrations of sialic acid and galactose in the membrane surface. Basal fluorescence polarization was significantly higher in the alcoholics and the membranes were dearly more resistant to the flutdizing effect of ethanol added in vitro. The concentrations of sialic acid as well as galactose were significantly reduced in the patients. The increased resistance to the fluidizmg effect of ethanol added in vitro appeared to be functionally related to reduced concentrations of terminal sialic acid and terminal and sialic acid‐bound β‐galactose in the membrane surface. The increased basal rigidity is probably due to concomitant changes in the lipid Mayer of the membrane. The results also showed, for the first time, that similar perturbations of membrane fluidity occur in human alcoholics as have been found previously in chronically ethanol‐treated animals.
Premature Aging in Male Alcoholics: “Accelerated Aging” or “Increased Vulnerability”?
Authors: Noonberg Aaron , Goldstein GeraW , Page Horace A.
Published: February 2008

This study involved an evaluation of two versions of the “premature aging” theory of chronic alcoholism: the accelerated aging and increased vumerabHty versions. The major dependent measures used were the tests included in Reitan's brain age quotient (BAO), a series of neuropsychological tests known to be sensitive to the effects of alcoholism and aging. Subjects were 40 chronic alcoholic inpatients and 40 matched controls, divided into age groups by; decade, ranging from the 30s to the 60s. It was proposed that an j interaction between age and presence or absence of alcoholism, with BAO test differences between alcoholics and controls widening as age increases, would support the increased vulnerability version, while the absence of such aw interaction would support the accel‐] erated aging version. The results dearty favored the accelerated aging version, with merited BAO test differences between alcoholics, and controls appearing even in the 30‐year‐old groups. It was concluded that chronic ateohoftcs tend to perform at levels found for nonalconoiics 10 years their senior, but the discrepancy between, alcoholics and nonalcohoics does not increase with age.
γ‐Linolenic Acid Fails to Prevent the Effects of Prenatal Ethanol Exposure on Brain and Behavioral Development in B6D2F2 Mice
Authors: Wainwright Patricia , Ward Glenn R. , Molnar John D.
Published: February 2008

The purpose of this study was to obtain a quantitative assessment of the behavioral retardation caused by prenatal ethanol exposure in mice and to test the hypothesis that ‐γ‐Nnolenic acid (GLA) supplementation would prevent such effects. Pregnant B6D2F, mice were fed liquid diets containing 25% ethanol‐derrved calories from days7–17 of gestation. The experimental groups were given GLA via subcutaneous injection; the control was administered vehicle only. All groups were pair fed to this ethanol control, including a second control group which received sucrose substituted isocalorically for ethanol. Additional control groups included one fed lab chow ad libitum and two further ethanol groups, one treated with coconut oil, the other with arachidonic acid (AA). Behavioral development of the pups was measured on day 32 postconception and open field behavior was measured on day 50. Body and brain weight were also measured. The results indicated that reproductive outcome, as measured by animals which produced live pups, was worse in the GLA‐ and AA‐treated groups. Ethanol produced significant behavioral retardation of the order of 1.7 days. Body and brain weight were lower in etna not‐treated pups. Covariance analysis indicated that the effect on brain weight was independent of the effect on body weight Open field scores suggested that ethanol‐treated males were more active then sucrose controls. The data did not support the hypothesis that GLA would prevent the deleterious effects of prenatal ethanol exposure; in no instance was a GLA‐treated group different from the ethanol control.
Alcoholism and Psoriasis
Authors: Morse Robert M. , Perry Harold O. , Hurt Richard D.
Published: February 2008

Using criteria for the diagnosis of alcoholism established by the National Council of Alcoholism and by scores on the Self‐Administered Alcoholism Screening Test, we compared the prevalence of alcoholism in a group of 99 patients hospitalized for the treatment of psoriasis with that in an age‐ and sex‐matched control group hospitafaed for the treatment of other dermatologic disorders. Alcoholism was diagnosed in 11 psoriatic patients and 3 control patients (0.05 < p < 0.10); 10 of the 11 psoriatic patients were men, and 1 of the 3 control patients was a man (p < 0.05). These differences, not noted in certain eariier studies, may reflect a basic association between the two diseases in males or indicate that alcohotem contributes to the morbidity of psoriasis.
Inhibition of Benzodiazepine Receptor Binding by Urinary Extracts: Effect of Ethanol
Authors: Volicer L , Ullman M. D.
Published: February 2008

Two fractions which inhibit benzodiazepine receptor binding were isolated from both rat and human urine. The method used involved alkaline methanorysis followed by chloroform extraction and silicic acid chromatography. This method precludes artrfactual formation of esters of β‐carboline carboxylic acid (BCC) during the extraction procedure. One of the fractions (fraction E) behaved similarly to methyl ester of BCC on thin‐layer chromatography and also had a similar fluorescent spectra. Administration of ethanol to male Sprague‐Dawley rats decreased the concentration and the total excretion of both inhibitory fractions in a dose‐dependent manner. In a clinical study on males with different family histories of alcoholism, ethanol decreased excretion of fraction E. The excretion was not affected by placebo, and it was similar in family history‐positive and family history‐negative subjects. These results suggest that ethanol affects the ‐γ‐aminobutyric acid‐benzodiazepine receptor complex by changing release, metabolism, and/or excretion of an endogenous benzodiazepine ligand.
Hormonal Changes in Rats Consuming Alcohol prior to and during Gestation
Authors: Lee Melvin , Wakabayashi Katsumi
Published: February 2008

Although the fetuses of rats given alcohol prior to and during gestation are small, the placentas are large compared to those of untreated rats. It has been suggested that placental enlargement may be a consequence of a reduction in progesterone production. To investigate this, rats were given 20% ethanol in water prior to pregnancy and 30% ethanol in water throughout gestation, with rat chow ad libitum (alcohol group) or water with an equicaloric diet in which com starch was substituted for alcohol (pair‐fed group), or rat chow and water ad libitum (ad libitum control group). Serum progesterone and testosterone were measured on day 17 of gestation and plasma and pituitary luteinizing hormone (LH) and follicle‐stimulating hormone (FSH) on day 21 of gestation. Progesterone was significantly reduced in the alcohol but not the pair‐fed group. Testosterone levels were not different among the three groups. Plasma LH was significantly reduced in both the alcohol and the pair‐fed groups, but plasma FSH and pituitary LH and FSH did not differ among the three groups. These data are consistent with a possible role for progesterone in the placental enlargement seen in alcohol‐fed rats.
Interaction of Pyrazole and 4‐Methylpyrazole with Hepatic Microsomes: Effect on Cytochrome P‐450 Content, Microsomal Oxidation of Alcohols, and Binding Spectra
Authors: Feierman Dennis E. , Cederbaum Arthur I.
Published: February 2008

Microsomes isolated from rats treated with either pyrazole or 4 methylpyrazoie, potent inhibitors of alcohol dehydrogenase, cata lyzed the oxidation of ethanol and 2‐butanoJ at rates 2–3‐fold highe than saline controls. Time course experiments and dose‐response experiments indicated that an increase in the microsomal oxidatioi of alcohols could be observed 24 hr after a single treatment with 200 mg/kg body weight of either pyrazole or 4‐methylpyrazole, and after 2 or 3 days of treatment with 50 mg/kg of either of these compounds. The pyrazole treatment did not change the activity of NADPH‐cytochrome P‐450 reductase, the content of cytochrome P‐450, or the oxidation of aminopyrine. Hence, microsomal oxidatior of alcohols was increased by the pyrazole treatment whether results were expressed “per mg of protein” or “per nmol of P‐450.” Microsomes from the pyrazole‐treated rats displayed an increase in binding spectrum with ethanol as the substrate as compared to controls as well as type 2 binding spectrum with dimethyl sulfoxide and 2‐butanol. These results suggest the possibility that pyrazole ma) induce an alcohol‐preferring P‐450 isozyme. By contrast, the 4‐methylpyrazoie treatment, besides increasing the oxidation of alcohols, also increased the oxidation of aminopyrine and the content of cytochrome P‐450. The increase in the oxidation of alcohols arte aminopyrine was primarily due to the increase in content of P‐45C produced by the 4‐methylpyrazole treatment Binding spectra wrtti dimethyl sulfoxide and 2‐butanol were also observed after 4‐methylpyrazole treatment; however, the 2‐butanol‐binding spectrum was a modified type I spectrum, not type 2. Taken as a whole, these results indicate that pyrazole and 4‐methylpyrazole treatment can affect the microsomal mixed function oxidase system and the oxidation of alcohols by microsomes, and that there are differences in the interaction of these compounds with microsomes.
Alcohol‐Related Birth Defects: Syndromal Anomalies, Intrauterine Growth Retardation, and Neonatal Behavioral Assessment
Authors: Ernhart Claire B. , Wotf Abraham W. , Linn Patricia L , Sokol Robert J. , Kennard Mary J. , Filipovich Howard F.
Published: February 2008

Fetal alcohol effects in 359 infants born to disadvantaged women identified as having a history of alcohol abuse or as controls and who provided reports of alcohol use in pregnancy are being studied in a prospective design. Alcohol abuse was assessed with the Michigan Alcoholism Screening Test (MAST). Alcohol use (AA/day) was based on short‐term recall covering 2‐week periods prior to each antenatal visit A tally of anomalies associated with fetal alcohol syndrome was obtained in a blinded examination of each infant This tally was significantly related to the MAST classification and, for the MAST+ subjects, the tally was related to first trimester AA/day. Birth weight, length, and head circumference were negatively correlated with AA/day (entire pregnancy); however, the effect was attenuated and not statistically significant in models with covariate control. It is possible that these measures were near the threshold of effect Scale scores of the Brazetton Neonatal Behavioral Assessment Scale and three scale scores of the Graham/Rosenblith Behavioral Examination of the Neonate were unrelated to the MAST classification and to AA/day.
Liquid/Air Partition Coefficients of Acetaldehyde: Values and Limitations in Estimating Blood Concentrations from Analysis of Breath
Authors: Jones A. W. , Sato Akio , Forsander Otof A.
Published: February 2008

We report liquid/air partition coefficients for dilute solutions of acetaldehyde in water, saline (0.9% wt/vol NaCI), human plasma, and com oil. Equilibrium was studied at 34°C and 37°C with various concentrations of acetaldehyde in the liquid phases. At 37°C, the liquid/air partition ratios for water, saline, plasma, and oil were 143 ± 7.1,132 ± 6.6,183 ± 3.6, and 64 ± 9.9 (means ± SE), respectively. At 34°C, all the values were higher and the temperature coefficients of solubility were 3.7%, 3.3%, and 4.0% per 1°C for water, saline, and plasma solutions of acetaldehyde, respectively. The partition coefficients were independent of the concentration of acetaldehyde in the liquids, and the solubility was higher in water than in oil. The results are discussed with emphasis on the usefulness of expired breath as a biological specimen for the quantitative determination of acetaldehyde.
Cyclic Fluctuation in Alcohol Consumption among Female Social Drinkers
Authors: Harvey S. Marie , Beckman Linda J.
Published: February 2008

The main objective of this study was to investigate the relationship between menstrual cycle phase and alcohol use in female social drinkers. Sixty‐nine normally menstruating women monitored alcohol consumption and basal body temperature daily over three consecutive menstrual cycles. Temperature charts were used to ascertain five cycle phases (menstrual, postmenstrual, ovulatory, luteal, and premenstrual) and data were analyzed using single‐group repeated measures analysis of variance. Whereas frequency of alcohol use did not vary among the five cycle phases, quantity of alcohol consumed significantly fluctuated and peaked in the luteal phase. These data suggest that female drinking patterns may be influenced by hormonal fluctuations associated with the menstrual cycle.
Kinetic Characterization of Two Classes of Dog Liver Alcohol Dehydrogenase Isoenzymes
Authors: Bosron William F. , Gaither James W. , Magnes Leslie J.
Published: February 2008

In order to relate the catalytic properties of alcohol dehydrogenase (ADH), the rate‐limiting enzyme for alcohol metabolism, with the pharmacokinetics of ethanol elimination in vivo, the multiple molecular forms of dog Hver ADH were purified and their steady state kinetics investigated. Two different classes of ADH forms were identified by starch gel electrophoresis: the class I isoenzymes migrate to the cathode and the class II forms migrate to the anode. Three different patterns of the cathodic class I isoenzymes were identified in different liver specimens. Three molecular forms were observed for patterns A and C, and five for B. The two classes of isoenzymes were separated by affinity chromatography and purified by column chromatography. The three predominant class I isoenzymes, A1, B2, and C1, in type A, B, and C livers, respectively, were isolated by high performance cation‐exchange chromatography. The steady state kinetic constants of the A1, B2, and C1 isoenzymes are similar, but differ substantially from those of the class II enzyme. The class II enzyme is much less sensitive to pyrazole inhibition, Ki= 2 nw, than the class I forms, Ki= 0.6 μM. Methanol is not a substrate for the class II enzyme, whereas it is oxidized by the class I isoenzymes. The class I isoenzymes exhibit a lower K., and substrate inhibition K, for ethanol, 0.4 and 160 nw, respectively, than values for the class II enzyme, 10 and 610 mi, respectively. The properties of class I and II dog liver ADH are similar to those of the respective isoenzymes purified from human and monkey liver. Based on kinetic data for the two classes of dog liver alcohol dehydrogenase, we suggest that the pharmacokinetics of ethanol elimination should obey a two term Michaeiis‐Menten model with substrate inhibition at high alcohol concentration.
Relapse by Alcohol Abusers
Authors: Pickens Roy W. , Hatsukami Dorothy K. , Spicer Jerry W. , Svikis Dace S.
Published: February 2008

During the first year after treatment, 44% of a sample of alcohol abusers reported relapse to alcohol use. Relapse rate Increased to a peak at 6 months after treatment and then decined. Depressed or anxious mood was the reason most frequently given (31%) for relapse. Of subjects who relapsed, almost half (42%) reported a subsequent return to abstinence which was then maintained for the remainder of the foNowup period. Of these subjects, half (51%) reported the duration of the drinking period to be less than 2 weeks. Of subjects showing a daily drinking pattern prior to treatment, 20% showed a dairy drinking pattern after relapse, 46% showed bouts of drinking and abstinence, and 33% showed abstinence with no further drinking. Of subjects snowing bouts of drinking prior to treatment, none showed a deify drinking pattern after relapse, 44% showed bouts of drinking and abstinence, and 56% showed abstinence with no further drinking. There was no significant effect of sex or age on relapse rate, time to relapse, or reasons for relapse.
Analysis of Human Alcohol‐ and Aldehyde‐Metabolizing Isozymes by Electrophoresis and Isoelectric Focusing
Authors: Duley John A. , Harris Owen , Holmes Roger S.
Published: February 2008

Isoelectric focusing and electrophoresis were used to identify the various isozymes of alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), aldehyde oxidase (AOX), and xanthine oxidase (XOX). ADH types I, II, and III were located primarily in the cytosol fraction of liver, but some activity was found also in the small granule fraction. The ALDH‐I and ‐IV isozymes were found in the large granule fraction, while ALDH‐II and ‐III were present in the cytosol and ALDH‐V in the small granule fraction. AOX and XOX each appeared as a single cytosolic form with some small granule activity. The tissue distribution of these isozymes is presented and the physiological role of each enzyme is discussed.
Seasonal, Monthly, and Day‐of‐Week Trends in Homicide as Affected by Alcohol and Race
Authors: Abel Ernest L. , Strasburger Erich L. , Zeidenberg Phillip
Published: February 2008

Monthly, seasonal, and day‐of‐week patterns in criminal homicide were studied specifically with respect to the victim's alcohol consumption, race, or both. There were no overall significant monthly or seasonal patterns although day‐of‐the‐week was a significant factor affecting homicide. Alcohol did not affect monthly seasonal fluctuations for whites but did affect such fluctuations for blacks. The interaction between day‐of‐the‐week and alcohol was not significant, failing to support the possibility that high weekend rates for homicide are related to higher alcohol consumption.
Effect of temperature on the morbidity and recovery of the Pacific Coast wireworm, Limonius canus, following contact with tefluthrin‐treated wheat seeds
Authors: Van Herk W. G. , Vernon R. S.
Published: February 2008

Late instars of the Pacific Coast wireworm, Limonius canus (LeConte) (Coleoptera: Elateridae), were exposed to wheat seeds treated with tefluthrin at 10 g active ingredient/100 kg wheat seed, for 2 min, at 10, 15, 20, and 25 °C. All wireworms were moribund within 20 min of first exposure and recovered fully within 7 h. Morbidity induction time (i) decreased considerably as the temperature (t) was increased from 10 to 15 °C, but did not decrease further when the temperature was increased from 15 to 25 °C. For each temperature, induction time decreased as wireworm weight (w) increased, so that . A strong negative temperature coefficient was observed in wireworm recovery, the time required for recovery (r) after exposure decreasing as both temperature (t) and wireworm weight (w) increased, so that r = 1102.47(w)−0.1848 * e−0.1012t. The temperature at which wireworms contact insecticides in the field may significantly affect the induction and duration of morbidity, and determine whether wireworms will become moribund before they are repelled by tefluthrin. The ability of wireworms to recover from tefluthrin‐induced morbidity may seriously limit the efficacy of this insecticide in reducing wireworm populations in the field.
Olfactory coding in the insect brain: molecular receptive ranges, spatial and temporal coding
Authors: Galizia C. Giovanni , Szyszka Paul
Published: February 2008

Odor information is coded in the insect brain in a sequence of steps, ranging from the receptor cells, via the neural network in the antennal lobe, to higher order brain centers, among which the mushroom bodies and the lateral horn are the most prominent. Across all of these processing steps, coding logic is combinatorial, in the sense that information is represented as patterns of activity across a population of neurons, rather than in individual neurons. Because different neurons are located in different places, such a coding logic is often termed spatial, and can be visualized with optical imaging techniques. We employ in vivo calcium imaging in order to record odor‐evoked activity patterns in olfactory receptor neurons, different populations of local neurons in the antennal lobes, projection neurons linking antennal lobes to the mushroom bodies, and the intrinsic cells of the mushroom bodies themselves, the Kenyon cells. These studies confirm the combinatorial nature of coding at all of these stages. However, the transmission of odor‐evoked activity patterns from projection neuron dendrites via their axon terminals onto Kenyon cells is accompanied by a progressive sparsening of the population code. Activity patterns also show characteristic temporal properties. While a part of the temporal response properties reflect the physical sequence of odor filaments, another part is generated by local neuron networks. In honeybees, γ‐aminobutyric acid (GABA)‐ergic and histaminergic neurons both contribute inhibitory networks to the antennal lobe. Interestingly, temporal properties differ markedly in different brain areas. In particular, in the antennal lobe odor‐evoked activity develops over slow time courses, while responses in Kenyon cells are phasic and transient. The termination of an odor stimulus is reflected by a decrease in activity within most glomeruli of the antennal lobe and an off‐response in some glomeruli, while in the mushroom bodies about half of the odor‐activated Kenyon cells also exhibit off‐responses.