bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of paraquat on the mutagenicity of benzo(a)pyrene
Authors: Wei C. I. , Allen K. , Misra H. P. 
Published: October 2006

AbstractElevated activities of superoxide dismutase (SOD) were detected in histidine‐requiring strains of Salmonella typhimurium after the bacteria were preincubated for 1 h at 37°C with S‐9 mix and paraquat (methylviologen, PQ2+) at 10−4M. A fivefold increase in SOD level was found for strains TA 98 and TA 100. These elevated levels of SOD activity were correlated with a significant reduction of the mutagenicity of metabolically activated benzo(a)pyrene (B(a)P) in these tester bacteria when evaluated in a preincubation assay system. A 69.0–92.5% and 23.5–66.9% reduction was noticed when 0.5–4.0 μg per plate of B(a)P was used in TA 98 and TA 100, respectively. However, exogenous superoxide dismutase at 10–100 μg ml−1 added to top agar had no significant effect on the number of revertants produced by activated B(a)P. These data indicate a major role of intracellular superoxide anion in promoting mutagenicity of B(a)P.
Toxicity study of uracil in dogs
Authors: Spicer E. J. F. , Richter W. R. , Morita K. 
Published: October 2006

AbstractUracil was administered to male and female dogs for 3 months and to male dogs for 12 months at dose levels of 0, 210, 420, 840 and 1680 mg uracil per kg body weight per day by gavage. While there were minor differences seen in food consumption, water consumption and erythroid parameters between the 3‐month and the 12‐month studies, it was concluded that there were no adverse effects seen on these parameters nor on body weight, EKG, clinical laboratory studies and organ weights. Pathological observations did not show treatment‐related effects.
Oxidation state analysis of mercury: Evidence of the formation of mercurous ion in the oxidation of mercury by peracetic acid
Authors: Wigfield Donald C. , Perkins Sherry L. 
Published: October 2006

AbstractBoth elemental mercury and the mercurous ion give rise to a signal in Cold‐Vapor Atomic Absorption Analysis under non‐reducing conditions. Distinction between these species based on the greater solubility of the mercurous ion in water is possible, and the potential of this analytical distinction is illustrated with the finding that oxidation of mercury by peracetic acid involves the mercurous state.
The effect of chronic exposure to 3.5 ppm NO2 on hormone levels and organ weights in rats
Authors: Vyskočil Adolf , Tušl Miloslav , Zaydlar Karel 
Published: October 2006

AbstractMale Wistar rats were exposed continuously for 1 or 2 months to 3.5 ppm NO2. Levels of histamine and serotonin in lung, noradrenaline in hypothalamus, corticosterone and thyroxine in serum and catecholamines in the adrenals were estimated. No significant changes were observed in lung histamine and serotonin, serum corticosterone, or adrenal catecholamine levels; or in the weights of lung, spleen, adrenal glands, hypothalamus, liver and the whole body. The only significant change was a decrease in the concentration of hypothalamic noradrenaline after 2 months of exposure. The results suggest that prolonged exposure to 3.5 ppm NO2 does not result in changes in hormone levels, organ and body weights, and therefore does not precipitate pulmonary defensive reactions or non‐specific stress response.
Biogenic amines and some metals in brain of cadmium‐exposed diabetic rats
Authors: Chandra Satya V. , Kalia Kiran , Hussain Tahir 
Published: October 2006

AbstractDiabetic rats (alloxan diabetes) were exposed to cadmium (2 mg kg−1 i.p.) daily for 21 days to investigate the levels of blood glucose, biogenic amines and iron, copper, zinc and cadmium in the brain. Cadmium exposure to diabetic rats produced a significant exacerbation in the hyperglycemic effect and accumulation of cadmium in the blood compared with that observed after diabetes or cadmium exposure alone. The elevation in the levels of brain dopamine and 5‐hydroxytryptamine were also more pronounced in cadmiumexposed diabetic rats compared with either cadmium exposure or diabetes alone. Cadmium exposure to diabetic rats also produced significant changes in the concentrations of copper in the blood. These results indicated enhanced cadmium toxicity in diabetic rats.
Effects of intravenous infusion of doxorubicin on blood chemistry, blood pressure and heart rate in rabbits
Authors: Robison Timothy W. , Giri Shri N. , Schiedt Mary , Parker Harold R. , Ishizaki Goro , Curry Donald L. 
Published: October 2006

AbstractThe effects of a 1h continuous infusion of doxorubicin (12.5 mg kg−1, 200 mg M−2) on blood chemistry was examined in rabbits over a 6‐h period. Plasma glucose levels remained unchanged while insulin levels were significantly decreased to 39, 45 and 61% of the zero time value (12.8 ± 2.9 ng ml−1) at 30, 60 and 120 min, respectively, after starting the drug infusion. Plasma cortisol levels were increased to 141, 140 and 131% of the initial zero time value (12.3 ± 2.2 ng ml−1) at 120, 240 and 360 min, respectively. Doxorubicin had no effect on plasma electrolytes, osmolality and urea nitrogen but significantly increased plasma creatinine over the corresponding control value (2.2 ± 0.8 μg ml−1 to 4.9 ± 0.7 μg ml−1) at 120 min and the level remained elevated for the remaining period of the study. Systolic and diastolic pressure, and heart rate were also depressed at 240 and 360 min. The data collected in the present study indicate that the doxorubicin infusion might have a direct effect on beta cells in the pancreas as well as muscle tissue. Changes in cortisol, blood pressure and heart rate appear to be secondary to other effects produced by doxorubicin.
The inhibitory effect of alcide®, an antimicrobial drug, on protein synthesis in Escherichia coli
Authors: Scatina Joann , Abdel‐Rahman Mohamed S. , Goldman Emanuel 
Published: October 2006

AbstractAlcide®, a broad‐spectrum antimicrobial drug, has been shown to kill a wide range of common pathogenic bacteria as well as fungi, in vitro. This agent consists of Part A and Part B which contain sodium chlorite and lactic acid as the active ingredients, respectively. The mixing of these two parts immediately prior to use results in the formation of chlorine dioxide (ClO2), a potent germicidal compound.Exposure of exponentially growing E. coli cells to Alcide® resulted in a rapid inhibition of growth as well as loss of viability. Alcide® inhibited DNA, RNA, and protein synthesis; however, RNA and protein synthesis were affected at much lower concentrations. The accumulation of the amino acid analog aminoisobutyric acid into growing cultures of E. coli was only partially impaired by Alcide®. Cell‐free protein synthesis using an RNA directed system was inhibited by Alcide® and this effect was lessened in the presence of mercaptoethanol. Higher concentrations of Alcide® (1 mM) oxidized 25% of the methionine to methionine sulfoxide. Aminoacylation of E. coli bulk tRNA was decreased in vitro and the amino‐acylation of tRNAfMet was particularly sensitive to Alcide®.
Cimetidine enhances and phenobarbital decreases parathion toxicity
Authors: Mourelle Marisabel , Girón E. , Amezcua J. L. , Martinez‐Tabche L. 
Published: October 2006

AbstractParathion toxicity has been attributed to its metabolic product paraoxon which is formed in the mammal liver through the multiple oxidase enzymes. These are induced by barbiturates and inhibited by SKF 525 A and cimetidine. We assessed the effects of these drugs on the acute toxicity of parathion in rats by measuring the rate of survival at 24 h after the administration of the oral LD50 of parathion to four groups of rats: control and pretreated with the aforementioned drugs. Additional rats of these groups were used to measure the capability of liver isolated microsomes to transform p‐nitroanisole to p‐nitrophenol. In the control and cimetidine groups we also measured the transformation of parathion to paraoxon and p‐nitrophenol by the liver microsomes. Phenobarbital increased the survival 100% whereas cimetidine and SKF 525 A dramatically potentiated parathion toxicity. Phenobarbital increased the formation of p‐nitrophenol but cimetidine and SKF‐525 A produced the opposite effect. Paraoxon and p‐nitrophenol from parathion were decreased by cimetidine. Our results strongly suggest that parathion itself is largely responsible of its toxicity and the inhibition of its metabolism is harmful rather than beneficial.
Imipramine prevention of carbon tetrachloride‐induced liver necrosis at late states of the intoxication process
Authors: Fernández G. , Villarruel M. C. , de Ferreyra E. C. , de Fenos O. M. , Castro J. A. 
Published: October 2006

AbstractImpiramine administration (50 mg kg−1, i.p.) to Sprague–Dawley male rats (240–290 g) 6 or 10 h after CCl4 (1 ml kg−1, i.p.) partially prevents liver necrosis induced by the hepatotoxin. When imipramine is given 30 min before CCl4, it inhibits in part the CCl4‐inhibits in part the CCl4‐induced lipid peroxidation and the covalent interactions of reactive metabolites with microsomal lipids or proteins and partially prevents CCl4‐induced cytochrome P‐450 destruction, but not glucose 6 phosphatase activity depression.Impiramine administration prior to CCl4 does not modify levels of the hepatotoxin reaching the liver or the body temperature of CCl4 treated animals. Early preventive effects of imipramine on cytochrome P‐450, might be attributed to inhibition of covalent interactions of reactive metabolites.The hypothesis that imipramine exerted late preventive effects by interfering with calcium deleterious effects or by modulation of protein and phospholipid synthesis or degradation is analyzed.
Evidence of differential hematopoietic compensation to lead intoxication in blood, liver and kidney
Authors: Hollebone B. R. , Johnson P. M. , Chakrabarti C. L. , Karwowska R. 
Published: October 2006

AbstractThe dependence of fluorescent porphyrin levels on the concentration of lead in blood, liver and kidney has been examined as functions of both the level and duration of dosing. Individually housed male Wistar COBS rats of 200 g were randomly selected for 3, 7, 21 and 35 day dosing periods in groups of: control, 50, 100 and 1000 ppm dosing in drinking water. The plot of all data points for porphyrin concentration against measured lead burden covers the same range of levels and closely resembles the scatter of data observed in humans. However, subsets of this plot defined by individual dose levels and durations yield well‐defined linear relationships. At all dose levels at 7 days the correlation of porphyrin concentration to lead tissue burden is negative in all tissues, showing a direct inhibition of hemopoiesis with lead burden. Depending on the tissue the slope becomes less negative, or, as in blood, positive at 21 and 35 days at all doses. This compensation is most rapid in blood, then liver and is least evident in kidney. The time at which compensation is observed is the same for all doses in each tissue and seems therefore, to depend on the rate of protein turnover in different tissue types.These results suggest that a direct correlation of porphyrin concentration to lead burden is not valid without knowledge of the dosing history. As well, evidence of compensation in one tissue does not imply successful compensation in other affected tissues where regeneration rates are slower. However, these observations do suggest that a correlation could be made between the extent of compensation in blood and that implicit for less accessible systems. Since blood compensation is most rapid, caution will be necessary in establishing tolerable lead levels for tissues at higher risk.
The effect of cadmium on chemical‐ and viral‐induced tumor production in mice
Authors: Blakley Barry R. 
Published: October 2006

AbstractFemale Swiss mice were exposed to cadmium in the drinking water at concentrations ranging from 0 to 50 ppm for 105 or 280 day time periods. In the 105 day study, the effect of cadmium on urethan‐induced pulmonary adenoma formation was evaluated. Urethan‐induced sleeping times observed following i.p. injection of urethan after 3 weeks of cadmium exposure were not affected by cadmium indicating that chronic cadmium exposure did not alter the eliminaton of urethan. Pulmonary adenoma formation which was evaluated 84 days later was not affected by cadmium. The size and number of tumors remained unchanged. This suggests that the immunosuppressive actions of cadmium do not influence urethan‐induced adenoma formation. In the 280‐day study, the effects of cadmium on the incidence of spontaneous murine lymphocytic leukemia was evaluated. Mortality from the leukemia virus was greater in the cadmium‐exposed mice. Mice exposed to 10 or 50 ppm cadmium experienced 33% more deaths from the virus. The average time till death was unaffected. It appears that the immunosuppressive effects of cadmium impair immunosurveillance mechanisms that control expression of the murine lymphocytic leukemia virus.
Effects of some monocyclic aromatic solvents and their metabolites on brain dopamine in rabbits
Authors: Romanelli Alessandro , Fatzol Maurizio , Mutti Anomio , Bergamaschi Enrico , Franchini Innocente 
Published: October 2006

AbstractAdult male rabbits were exposed to high concentrations (750 ppm, 12 hours daily for 7 days) of toluene, xylenes, styrene, ethylbenzene, vinyltoluene (3‐methylstyrene), and 7‐methyl‐styrene vapours or were dosed with 4 mM/kg/day i.p. of hippuric, methylhippuric, mandelic, phenylglyoxylic, and 7‐methyl‐mandelic acids. Styrene, vinyltoluene and ethylbenzene caused a marked depletion of striatal and tuberoinfundibular dopamine. Such an effect was also caused by treatment with phenylglyoxylic and mandelic acids. Dopamine depletion was associated with an increase in homovanillic acid concentration in the same regions. These results indicate that dopamine metabolism is a target for the neurotoxic effects of some monocyclic aromatic hydrocarbons and their metabolites, a lateral vinyl‐ or ethyl‐chain being crucial for the structure/activity relationship of such compounds.
The effect of carbon monoxide on hormone levels and organ weights in rats
Authors: Vyskočil Adolf , Tušl Miloslav , Zaydlar Karel 
Published: October 2006

AbstractMale Wistar rats were exposed continuously for 1 or 2 months to 25 or 100 ppm CO. The concentrations of noradrenaline in the hypothalamus, corticosterone and thyroxine in serum and of adrenal catecholamines were estimated. After exposure to 25 ppm CO no significant changes were observed in the serum corticosterone and thyroxine, hypothalamic noradrenaline, adrenal catecholamines levels, or in the weights of lung, spleen adrenal glands, liver and the whole body. Exposure to 100 ppm CO induced a decrease in hypothalamic noradrenaline and serum thyroxine and an increase in adrenal catecholamines and serum corticosterone. Whole‐body and organ weights were unchanged except for a slight decrease in liver weight. The results suggest a non‐specific stress response in the rat to 100 ppm CO whilst concentration of 25 ppm CO was without any stress effect.
Pyrethroid inhibition of basal and calmodulin stimulated Ca2+ ATPase and adenylate cyclase in rat brain
Authors: Kabeer Sahib I. Ahammad , Rao K. S. Prasada , Desaiah D. 
Published: October 2006

AbstractEffects of two classes of pyrethroids, permethrin and resmethrin (type I), cypermethrin and deltamethrin (type II), on basal (calmodulin‐deficient) and calmodulin stimulated activities of Ca2+ ATPase and adenylate cyclase from rat brain were studied in vitro. None of the pyrethroids inhibited synaptosomal basal Ca2+ ATPase, but permethrin and deltamethrin inhibited basal adenylate cyclase in the nuclear fraction of a brain homogenate. Both groups of pyrethroids decreased the calmodulin activated Ca2+ ATPase and adenylate cyclase from brain synaptosomes and nuclear fraction. The results indicate that calmodulin‐stimulated Ca2+ ATPase is more sensitive to type II pyrethroids and pyrethroids are more effective on calmodulin stimulated enzymes than basal enzyme activities. Since calmodulin, adenylate cyclase and Ca2+ ATPase are known to participate in various brain processes, it is possible that pyrethroids alter neural transmission, however, additional in vivo work would be needed to confirm this possibility.
Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts
Authors: Singh Shivendra V. , Rahman Q. 
Published: October 2006

AbstractSilicic acid and silicate dusts (slate dust and chrysotile asbestos) cause hemolysis of erythrocytes in vitro. The peroxidation of polyunsaturated fatty acids (PUFA) of erythrocyte membrane lipids is also enhanced by incubating the erythrocytes with silicic acid and silicate dusts in in vitro. Hemolysis of erythrocytes elicited by silicic acid and silicate dusts is inhibited significantly by polyvinyl‐pyrrolidone and dipalmitoyl lecithin (DPL). These agents, however, have no effect on silicic acid and silicate dust induced peroxidation of erythrocyte membrane lipids. On the other hand, peroxidation of erythrocyte membrane lipids, induced by silicic acid and silicate dusts, is inhibited almost completely by adding superoxide dismutase and catalase to the incubation system, whilst the hemolysis of erythrocytes induced by silicic acid and silicate dusts is unaffected by these agents. Similarly the lysis of erythrocytes, induced by silicic acid and silicate dusts, proceeds at a much faster rate than silicic acid and silicate dust induced lipid peroxidation. These results indicate that silicic acid and silicate dust induced hemolysis and lipid peroxidation represent two independent processes.
Halothane hepatotoxicity in glutathione depleted rats
Authors: Wilhelm Klaus‐Peter , Younes Maged , Sellin Dieter , Siegers Claus‐Peter 
Published: October 2006

AbstractExperimental models for halothane hepatotoxicity require microsomal enzyme induction by phenobarbital or triiodo‐thyronine pretreatment and hypoxic conditions. The role of GSH in the metabolism of halothane, however, is still unclear. We therefore pretreated male rats with phorone to deplete hepatic GSH, phenobarbital as a microsomal enzyme inducer and exposed them to halothane 1 % for 4 h under hypoxia (10% O2). Increases in serum enzyme activities of alanine aminotransferase (GPT) and sorbitol dehydrogenase (SDH) were observed 24 and 48 h later. Histomorphological examinations showed centrilobular hepatic necrosis. In GSH‐depleted rats the increments of serum enzyme activities and histomrphological alterations were significantly aggravated as compared with controls.In this model (+)‐catechin protected against halothane‐induced hepatotoxicity as evidenced by reduced serum enzyme elevations and morphological alterations whereas diethyldithiocarbamate faiied to exert any protective effects. Free fluoride concentrations in plasma was used as an index of the non‐oxidative defluorination of halothane. Increased plasma fluoride levels were observed under conditions which evoked hepatotoxicity but did not correlate with the protective effect of (+)‐catechin. Our experimental data indicate that glutathione might be involved in the non‐oxidative metabolic pathways of halothane. Furthermore, (+)‐catechin seems capable of protecting against the direct toxic effect of halothane metabolites resulting from the reductive pathways.
Studies of the in vitro effect of methylmercury chloride on rat brain neurotransmitter enzymes
Authors: Kung Mei‐Ping , Kostyniak Paul , Olson James , Malone Maureen , Roth Jerome A. 
Published: October 2006

AbstractThe in vitro effect of methylmercury (MM) on the enzymatic activities of brain cell specific marker enzymes, choline acetyltransferase (CAT), glutamic acid decarboxylase (GAD), 2′, 3′‐cyclic nucleotide phosphohydrolase (CNP), glutamine synthetase (GS) and enolase was examined. The results demonstrate that at 100 μM MM, GS activity was not affected whereas a small decrease in the activity of both GAD (20%) and enolase (10%) was observed. CNP and CAT activity appeared to be more sensitive toward MM with 100 μM MM producing inhibition of 50% and 30%, respectively. The addition of sulfhydryl protecting reagents such as DTT or sodium thioglycolate can restore the enzyme activities to normal control levels despite prior exposure of the enzymes to MM.
Mechanisms of toxicity of 2‐ and 5‐hydroxy‐1,4‐naphthoquinone; absence of a role for redox cycling in the toxicity of 2‐hydroxy‐1,4‐naphthoquinone to isolated hepatocytes
Authors: Doherty Mary D'Arcy , Rodgers Adrian , Cohen Gerald M. 
Published: October 2006

AbstractThe mechanisms of toxicity to isolated rat hepatocytes of two structurally related naphthoquinones have been studied. Both 5‐OH‐1,4‐naphthoquinone (5‐OH‐1,4‐NQ; juglone) and 2‐OH‐1,4‐naphthoquinone (2‐OH‐1,4‐NQ; lawsone) caused a concentration‐dependent cytotoxicity to hepatocytes which was preceded by a depletion of intracellular glutathione. 5‐OH‐1,4‐NQ caused a depletion of intracellular glutathione when incubated either at 4°C or 37°C whereas 2‐OH‐1,4‐NQ caused a depletion of intracellular glutathione when the hepatocytes were incubated at 37°C but not at 4°C. 5‐OH‐1,4‐NQ but not 2‐OH‐1,4‐NQ reacted with glutathione in buffered solution. These results suggested that the depletion of intracellular glutathione by 2‐OH‐1,4‐NQ is enzyme mediated whereas in the case of 5‐OH‐1,4‐NQ the direct chemical reaction with glutathione may be largely responsible for the depletion. A critical role for depletion of protein thiols in menadione‐induced cytotoxicity has been proposed. In agreement with earlier work, menadione caused a decrease in protein sulphydryls prior to cell death, however, at cytotoxic concentrations of both 2‐OH‐1,4‐NQ and 5‐OH‐1,4‐NQ this decrease only accompanied rather than preceeded cell death.The mechanism of toxicity of 5‐OH‐1,4‐NQ is similar to that of other naphthoquinones and involves formation of its corresponding naphthosemiquinone, active oxygen species and redox cycling as it stimulated a disproportionate increase in both microsomal NADPH oxidation and oxygen consumption. No evidence for redox cycling of 2‐OH‐1,4‐NQ was obtained either with microsomes or hepatocytes and thus its cytotoxicity must involve a different mechanism to that currently proposed for other naphthoquinones. This inability of 2‐OH‐1,4‐NQ to redox cycle may be due to its very low one‐electron reduction potential (E1/7‐415 mV). Thus, it is a very poor substrate for reduction to a semiquinone by cellular reductases.