bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparative study on the changes in AChE and ATPase activities in neonate and adult rat brains under thiobencarb stress
Authors: Pentyala Srinivas N. , Chetty C. S. 
Published: October 2006

AbstractThiobencarb (S‐(4‐chlorobenzyl)‐N,N‐diethyl thiol carbamate), a dithiocarbamate herbicide, was found to cause neuronal dysfunction in adult and neonate albino rats. In general, organocarbamates exert their action by inhibiting acetylcholinesterase (AChE) activity. Thiobencarb inhibited both acetylcholinesterase and adenosine triphosphatase (ATPase) activities in rat brain. Withdrawal of thiobencarb treatment resulted in the recovery of AChE activity to a normal level, whereas there was no recovery of Na+–K+‐ATPase activity in either neonate or adult rat brains. The results suggest that neuronal dysfunction caused by thiobencarb is mainly due to the inhibition of ATPase activity rather than to the inhibition of AChE activity.
The renal handling of calcium and phosphorus in environmental cadmium‐exposed subjects with renal dysfunction
Authors: Kido Teruhiko , Nogawa Koji , Hochi Yasushi , Hayano Masashi , Honda Ryumon , Tsuritani Ikiko , Ishizaki Masao 
Published: October 2006

AbstractClearance methods were used to clarify the renal handling of calcium (Ca) and phosphorus (P) in a population with renal dysfunction induced by exposure to environmental cadmium (Cd). Seventy‐six Cd‐exposed subjects (32 men and 44 women) and 36 non‐exposed subjects (18 men and 18 womén) took part in this study.Fractional excretion of P was higher in the Cd‐exposed subjects than in the non‐exposed subjects, while that of Ca was equal to that of the non‐exposed subjects. The urinary excretion rates of Ca and P tended to be lower in the Cd‐exposed subjects than in the non‐exposed subjects. The urinary excretion rate of Ca was closely related to creatinine clearance, while that of P was related to creatinine clearance and the percentage tubular reabsorption of phosphorus. It is thought that in Cd‐induced renal dysfunction the urinary excretion of Ca depends on glomerular function, and no increased excretion of urinary Ca was observed by these clearance methods.It is also clarified that the parallelism in the urinary excretion of Ca and Na persists in Cd‐exposed subjects with renal dysfunction.
Acute and subacute toxicity of 7.5% hypertonic saline–6% dextran‐70 (HSD) in dogs 2. biochemical and behavioral responses
Authors: Dubick Michael A. , Zaucha Gary M. , Korte Don W. , Wade Charles E. 
Published: October 2006

Abstract7.5% Hypertonic saline–6% Dextran‐70 (HSD) is currently being evaluated in our laboratory as a resuscitation solution for the treatment of hypovolemia at a dose of 4 ml kg−1 body weight. A few reports of dextran toxicity, particularly of the kidney, have been cited in the literature, so the present study evaluated the acute and subacute toxicity of HSD administered i.v. to beagle dogs. In the acute toxicity studies animals were infused with a single dose of HSD, or its components of hypertonic saline (HS) or Dextran‐70 (D‐70), at the maximum tolerated dose (MTD: 20 ml kg−1). Controls received Ringers lactate (RL). In the HSD‐infused dogs, transient but significant increases in serum alanine (ala) aminotransferase (AT), aspartate (asp) AT and alkaline phosphatase (AP) were observed for the first 72 h. In most cases this increase was also observed in the HS group. In the subacute studies, dogs were infused daily with the MTD of the above test solutions. Serum ala AT activity was 2–3‐fold higher in the HSD than the RL group for the first 3 days. Again, a similar effect was observed in the HS group. Slight, transient increases in asp AT and AP activity were also observed in the HSD group. Higher lactate dehydrogenase (LDH) activity was only observed at Day 14 in dogs infused with the MTD of HSD or HS. In both studies, no adverse effects on blood urea nitrogen (BUN) or serum creatinine were observed and other transient changes in serum parameters were attributable to hemodilution induced by HSD. No gross or microscopic lesions were observed in any major organ. Considering that the proposed therapeutic dose of HSD is only 4 ml kg−1, it appears that its use should be associated with minimal or no adverse effects.
Effect of propane‐1,2‐diol ingestion on carbohydrate metabolism in female rat erythrocytes
Authors: Saini Mohini , Nagpaul J. P. , Amma M. K. P. 
Published: October 2006

AbstractThis study was undertaken to assess the effect of propane‐1,2‐diol(PD) ingestion on carbohydrate metabolism in female rat erythrocytes. For this purpose, two different groups of adult albino female rats were treated orally with PD at two different dose levels of 73 and 294 mg 100 g−1 body wt. The blood samples drawn from the retro‐orbital sinus prior to the treatment served as the controls, whereas the treated samples were collected at peak periods (1/2 and 2 h) 2 and 7 days after the treatment. A' single dose of PD was found to elevate levels of blood glucose, lactate, pyruvate and the lactate/pyruvate ratio at the peak periods (P < 0.001) and after 2 days (P < 0.001) in both the groups. A significant (P < 0.05) increase in the contents of erythrocyte 2,3‐diphosphoglycerate (2,3‐DPG) was observed only at the peak periods. All these parameters returned to their base level after 7 days of treatment. The activities of hexokinase (HK), 2,3‐diphosphoglycerate phosphatase (2,3‐DPG Pase), lactate dehydrogenase (LDH), glucose‐6‐phosphate dehydrogenase (G‐6‐PD), 6‐phosphogluconate dehydrogenase (6‐PGD) and aldehyde reductase II (AR II) declined markedly, whereas those of pyruvate kinase (PK) and aldose reductase increased as a result of PD ingestion. The changes in the activities of 2,3‐DPG Pase and LDH were persistant up to 8 days post‐treatment. The [14C]glucose flux through glycolysis and the hexose monophosphate shunt pathway in erythrocytes was found to be lowered (P < 0.001) in response to PD treatment. The present work revealed that a single oral dose of PD was capable of producing significant alterations in carbohydrate metabolism in female rat erythrocytes.
Effect of acute pretreatment of lead on picrotoxin‐induced convulsions in rats
Authors: Krishnamoorthy M. S. , Parthiban N. , Muthu P. , Paul V. , Balagopal G. , Kumaravel T. S. 
Published: October 2006

AbstractThe effect of acute exposure to lead acetate (LA)/lead nitrate (LN) on onset and severity of convulsions induced by a low dose of picrotoxin was examined in rats. Both LA and LN reduced the time of onset and exacerbated the severity of convulsions, with a resultant high lethality. On comparison, it was noted that in the LA‐pretreated group, convulsion scores and incidence of tonus and mortality were much higher; the appearance of tonus was more delayed than in the LN‐pretreated group. In lead‐pretreated animals, the potentiation of picrotoxin‐induced convulsions was accompanied by higher lead levels in blood (p<0.001). However, the whole‐brain lead levels were not significantly different in these animals compared to the controls. The difference in the degree of potentiation by the two forms of lead could possibly be attributed either to the role of a combination of anions and cations or to the variable cerebral uptake and regional distribution of lead or due partly to the extent of competitive interaction involving d‐aminolaevulinic acid—whose level is known to be elevated consequent to lead‐induced disruption of haem biosynthesis–at GABA receptors.
Soman‐induced morphological changes: An overview in the non‐human primate
Authors: Baze Wallace B. 
Published: October 2006

AbstractA review of the literature was conducted to provide an overview of organophosphorus (OP)‐induced morphological changes in the non‐human primate. Most studies have evaluated effects of the OP nerve agent soman (pinacolyl methylphosphonofluoridate), an irreversible inhibitor of acetylcholinesterase. Soman‐induced acute and chronic morphological changes have been examined. The effects of nerve agent therapy (i.e. pyridostigmine, praloxidime chloride and atropine), with and without an anticonvulsant (i.e. diazepam, midazolam), on soman‐induced lesions have also been studied. Acute changes in the central nervous system of rhesus and cynomolgus monkeys exposed to soman alone or soman and therapy, without an anticonvulsant, were characterized by neuronal degeneration and necrosis and neuropil edema. The lesions were usually present in the frontal cortex, entorhinal cortex, amygdaloid complex, caudate nucleus, thalamus and hippocampus. Morphologically, these lesions resemble lesions produced by hypoxic‐ischemic injury or by seizures and are similar to soman‐induced changes in other laboratory animals. Nerve agent therapy supplemented with an anticonvulsant reduced or prevented soman‐induced acute neural lesions. Acute changes in non‐neural tissues were limited to the heart (e.g. hemorrhage, myofiber necrosis, myocarditis) and skeletal muscle (e.g. myofiber necrosis). Heart lesions in the non‐human primate are similar to OP‐induced heart lesions in man. The pathogenesis of the acute lesions in both the central nervous system and heart is discussed. Consistent soman‐induced chronic morphological changes have not been produced in the rhesus monkey or baboon.
Maximum dosage level in testing low‐toxicity chemicals for carcinogenicity in rodents
Authors: Apostolou Alexander , Helton Edward D. 
Published: October 2006

AbstractOwing to the lack of sufficient theoretical and empirical information, the initial guidelines regarding animal carcinogenicity testing of chemicals adopted the most conservative approach possible. One of the recommendations was that non‐toxic chemicals be tested at a level as high as 5% of the diet. Since then, a wealth of information has been accumulated, which indicates that such highly exaggerated dosage levels are not only unnecessary but produce scientifically misleading and regulatorily detrimental results that impede the development and evaluation of useful chemicals, including human drugs. This paper presents the rationale supporting the necessity of revision of the outdated maximum level of dietary exposure from 5% to 1% or 1000 mg kg−1 day−1 when the test chemical is administered in drinking water or by gavage.
Relationship between physicochemical properties of prussian blue and its efficacy as antidote against thallium poisoning
Authors: Kravzov J. , Rios C. , Altagracia M. , Monroy‐Noyola A. , López F. 
Published: October 2006

AbstractIn the present work we established a relationship between some physicochemical properties of two different batches of Prussian blue (PB) and their in vivo efficacy as an antidote against thallium poisoning. They physicochemical properties studied were crystallite size and thallium‐adsorbing capacity. One of the batches was synthesized and the other was obtained from commercial sources. The synthesized PB batch with the smallest crystallite size had both the highest adsorption capacity and antidotal efficacy. Synthesized PB protected 100% of the animals against one LD50 thallium dose, whereas the commercial PB batch protected only 80%. Thallium content in blood and tissues (liver, kidney, brain) was also analysed after antidotal PB treatment in rats previously intoxicated with a sublethal dose of Tl+, Animals treated with synthesized PB showed significantly less thallium in blood and tissue contents than those values of commercial PB‐treated rats, indicating better antidotal properties of the synthesized PB. According to the present study we suggest an in vivo evaluation of the compound before distribution of the product to toxicological units, if X‐ray diffractometric analysis is not available, in order to identify and determine the crystallite size of the compound as it plays an important role in the efficacy of PB.
Developmental toxicity of OTTO fuel II in the rat and rabbit
Authors: Cooper James R. , Lee Lanfong H. , Macys David A. 
Published: October 2006

AbstractOTTO Fuel II (OFII) is a propellent used by the United States Navy in its Mk 46 and Mk 48 torpedoes. Owing to the possibility of human exposure during fueling and defueling operations, studies were initiated to determine if OFII was a developmental toxin. Phase I of the investigation involved dosing four groups of time‐mated Fischer‐344 rats with OFII. The fuel was administered dermally at the rate of 0, 400, 2000 and 4000 mg kg−1 day−1. A significant reduction in body weight was seen at necropsy in dams receiving 2000 and 4000 mg kg−1 day−1 of OFII. Fetuses from these dams also weighed significantly less than control fetuses.Phase II of the investigation involved dosing of artificially inseminated rabbits with OFII. The fuel was administered to the skin of the animal's back at the rate of 0, 100, 316 and 1000 mg kg−1 day−1. Maternal toxicity was evidenced by a significant reduction in body weight of the dams in the 1000 mg kg−1 day−1 dose group on days 20 and 25 of gestation. There were no significant differences observed in maternal weight or fetal weight at necropsy. Morphological examination of both rat and rabbit fetuses failed to reveal significant evidence of fetal malformations.
Mechanism of testicular atrophy induced by Di‐n‐butyl phthalate in rats. part 4. changes in the activity of succinate dehydrogenase and the levels of transferrin and ferritin in the sertoli and germ cells
Authors: Fukuoka Masamichi , Kobayashi Tetsu , Zhou Yu , Hayakawa Takao 
Published: October 2006

AbstractA single oral dose of di‐n‐butyl phthalate (DBP) to male rats caused a sloughing of the germ cells at 6 h both with a decrease in the activity of succinate dehydrogenase (SDH) in the Sertoli cells and in the Sertoli‐germ connection and with an increase in the activity of lactate dehydrogenase (LDH) in the germ cells. Increases in transferrin (Tf) concentrations were observed in the Sertoli cells, Sertoli‐germ connection, epididymis‐ductus deferens and liver of rats. Decreases in Tf and ferritin (Ft) levels were observed in the seminal vesicle and seminiferous lumen, respectively. An increase in favin adenine dinucleotide (FAD) level was found in the interstitial cells.
Lipid peroxidation and disintegration of the cell membrane structure in cultures of rat lung fibroblasts treated with asbestos
Authors: Iguchi Hiroshi , Kojo Shosuke , Ikeda Masayuki 
Published: October 2006

AbstractRat lung fibroblasts were cultured for 24 and 48 h with UICC standard reference asbestos samples of amosite, crocidolite or Canadian chrysotile at various concentrations, and thiobarbituric acid‐reactive substances (TBARS) in the media and the cells were measured. Tests by the trypan blue dye‐exclusion method showed that cell viability was 80 ± 5% (mean ± SD) and 71 ± 6% when cultured for 48 h in the presence of 500 μg ml−1 of amosite and crocidolite, respectively, but was not affected by chrysotile. In cultures for 24 and 48 h, both chrysotile and crocidolite at > 250 μg ml−1 significantly increased TBARS in the medium, whereas amosite did so at > 500 μg ml−1.TBARS in the cells was not increased significantly by chrysotile at any concentration in the cultures for 24 and 48 h, but crocidolite at > 250 μg ml−1 significantly increased TBARS in the cells when cultured for 24 or 48 h. Although amosite at all concentrations tested did not increase significantly TBARS in the cells of the 24‐h culture, it did increase TBARS significantly in the cells when cultured for 48 h at a concentration of 500 μg ml−1 amosite.The increases of TBARS in media of the cultures with asbestos were accompanied by increases of lactate dehydrogenase (LDH) activity in the media, indicating the leakage of the enzyme from the cell into the media. The activity of LDH and the amount of TBARS showed a good correlation with each other, with a significant correlation coefficient value of 0.655.Thus, the amount of TBARS produced during the culture seemed to change, depending on both the asbestos concentration and the inherent properties. The findings suggest that when certain types of asbestos are cultured with rat lung fibroblasts the cell membranes are peroxidized to cause disintegration of the membrane structure, followed by leakage of cellular LDH into the medium.
Phosphatase activities in pesticide‐treated growing and developing cells of Dictyostelium discoideum
Authors: Gayatri R. , Chatterjee S. 
Published: October 2006

AbstractThe effects of benzene hexachloride (BHC), an organochlorine pesticide, on cell growth and phosphatase activities were studied in the growing and developing stages of cells of the cellular slime mould Dictyostelium discoideum exposed to BHC (containing α‐, β‐, δ‐ and γ‐isomers) at concentrations of ≥ 60 μg ml−1. A significant increase in acid and alkaline phosphatase activities was recorded in both growing and differentiating Dictyostelium cells treated with different doses (≥ 60 μg/ml) of BHC. The cytotoxicity of BHC has been correlated with the stimulation of acid and alkaline phosphatase activities of this organism.
Gas chromatographic determination of vaporphase biomarkers formed from rats dosed with CCl4
Authors: Dennis K. J. , Ichinose T. , Miller M. , Shibamoto T. 
Published: October 2006

AbstractSprague‐Dawley rats dosed with CCl4 (3 ml kg−1) were placed in a glass chamber through which air was passed continuously at a rate of 60 ml min−1. Volatile aldehydes and ketones in expired air from rats were derivatized to thiazolidines by passing the effluent gas stream through an aqueous cysteamine solution. The thiazolidine derivatives were then extracted and analyzed by gas chromatography with a nitrogen‐phosphorus detector and gas chromatography/mass spectrometry. The compounds identified were formaldehyde, acetaidehyde, acetone and formyl chloride. There were no appreciable differences in levels of formaldehyde and acetaldehyde between CCl4‐dosed rats and control rats, whereas the levels of acetone in CCl4‐dosed rats showed an increase compared to those in control rats. Results suggest that acetone is the major volatile carbonyl compound produced following acute doses of CCl4. Results of thiobarbituric acid assay on the livers from a control rat and a CCl4‐dosed rat did not show any appreciable differences.
Decreasing 203Hg retention by intraperitoneal treatment with monoalkyl esters of meso‐2,3‐dimercaptosuccinic acid in rats
Authors: Kostial K. , Blanuša M. , Šimonović I. , Jones M. M. , Singh P. K. 
Published: October 2006

AbstractThe effect of nine monoalkyl esters of meso‐2,3‐dimercaptosuccinic acid (DMSA) on 203Hg retention after a single i.p. dose was evaluated in 6–7 week‐old female albino rats. The monoesters were the monomethyl (MMDMS), monoethyl (MEDMS), mono‐n‐propyl (Mn‐PDMS), monoisopropyl (Mi‐PDMS), mono‐n‐butyl (Mn‐BDMS), monoisobutyl (Mi‐BDMS), mono‐n‐amyl (Mn‐ADMS), monoisoamyl (Mi‐ADMS) and mono‐n‐hexyl (Mn‐HDMS). Dimercaptosuccinic acid or one of the monoesters were administered at a dose of 0.25 mmol kg−1 body wt. twice, i.e. 30 min and 24 h after 203Hg administration. The whole body (WB) radioactivity was determined on the 2nd, 4th and 6th days. The radioactivity in the carcass (C) whole body without the gastrointestinal tract), liver (L), both kidneys (K) and brain (B) was determined 6 days after 203Hg administration. All treated animals had a significantly lower body burden of mercury than the controls. The reduction of 203Hg retention in WB and other body compartments was higher in animals treated with monoesters than in rats treated with DMSA. The relative effectiveness of the monoesters was dependent on the nature of the alkyl groups, the efficiency being higher in higher analogues. Maximum activity was attained with the C5 (Mn‐ADMS, Mi‐ADMS) and C6 (Mn‐HDMS) esters. These chelators reduced WB, C, L, K and B mercury retention by 90, 89, 76, 93 and 80%, respectively. Iso derivatives were more efficient than the normal isomers (Mi‐PDMS > Mn‐PDMS; Mi‐BDMS > Mn‐BDMS; Mi‐ADMS > Mn‐ADMS). The effect of all monoesters was higher in reducing kidney than liver mercury retention.
Studies on the delayed neuropathic and anticholinesterase potential of quinalphos (diethyl 2‐quinoxalyl phosphorothionate) in hens
Authors: Jokanović Milan 
Published: October 2006

AbstractIncidence of numerous human poisonings by quinalphos (Ekalux®, Bayrusil®) in agricultural areas near Belgrade initiated this study on the ability of the compound to inhibit hen brain neuropathy target esterase, acetylcholinesterase and plasma butyrylcholinesterase in vivo. Hens were treated with a single oral dose ranging from 25 to 600 mg kg−1 quinalphos (LD50 = 72 mg kg−1) or 500 mg kg−1 triorthocresyl phosphate (positive control), sacrificed 24–96 h later for enzyme assays and monitored for 25 days for evaluation of walking impairments. High inhibition (> 80%) of both cholinesterases was obtained with 25 and 50 mg kg−1 quinalphos. Doses of 200 and 600 mg kg−1 of the agent inhibited up to 23 and 28% of hen brain neuropathy target esterase activity, respectively. Clinical signs of neuropathy were not seen. Quinalphos was slowly absorbed from the gastrointestinal tract, as indicated by the severity of the cholinergic symptoms and the inhibiton of neuropathy target esterase, which reached its maximum 72 and 96 h after poisoning. The results suggest that quinalphos, at doses tested, has no ability to cause delayed neuropathy in hens without showing signs of severe cholinergic intoxication.
The toxicity of seed extracts and their fractions from Lupinus angustifolius L. and Lupinus albus L.
Authors: Stobiecki M. , Blaszczyk B. , Kowalczyk‐Bronisz S. H. , Gulewicz K. 
Published: October 2006

AbstractSeed extracts obtained from Lupinus albus and Lupinus angustifolius by treatment with 48% ethanol contained ca. 10% alkaloids (on a dry weight basis) and were non‐toxic. Their acute toxicity (LD50) in the mouse is > 4000 mgkg−1 body wt.After fractionation, the extract from L. angustifolius seeds afforded several fractions with differing toxicities (LD50 750–4000 mg kg−1 body wt.).None of the fractions tested in vitro were toxic. The results obtained showed that, in spite of the alkaloids, other low‐molecular‐weight constituents present significantly modified the toxicity of the lupin extracts.
In Vitro Cytotoxicities of 1,4‐Naphthoquinone and Hydroxylated 1,4‐Naphthoquinones to Replicating Cells
Authors: Babich H. , Stern A. 
Published: October 2006

AbstractUsing the human hepatoma cell line, HepG2, and the BALB/c mouse fibroblast cell line, 3T3, as the bioindicators in the neutral red cytotoxicity assay, the effect of hydroxyl substitution on the toxicity of 1,4‐naphthoquinone was studied. The sequence of potency for the quinones was 5,8‐dihydroxy‐1,4‐naphthoquinone > 5‐hydroxy‐1,4‐naphthoquinone > 1,4‐naphthoquinone > 2‐hydroxy‐1,4‐naphthoquinone. Pretreatment of the cells with dicoumarol, an inhibitor of DT‐diaphorase, enhanced the cytotoxicity of 1,4‐naphthoquinone but not of the hydroxylated naphthoquinones. Pretreatment of the BALB/c cells with buthionine sulfoximine, an inhibitor of glutathione synthesis, enhanced the sensitivity of the cells to all the hydroxylated naphthoquinones but not to 1,4‐naphthoquinone. A similar pretreatment of the HepG2 cells with buthionine sulfoximine enhanced the toxicity of the 2‐hydroxy‐ and 5,8‐dihydroxy‐1,4‐naphthoquinones but not of 5‐hydroxy‐1,4‐naphthoquinone or of 1,4‐naphthoquinone.Some differences were noted in the responses to the hydroxylated 1,4‐naphthoquinones between buthionine sulfoximine‐treated replicating cells and buthionine sulfoximine‐treated isolated rat hepatocytes, a non‐replicating cell in culture. The use of a replicating cell system in studying the mechanisms of the cytotoxicity of quinones may be an important adjunct to studies using the isolated rat hepatocytes, which is the standard model system.