bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of aflatoxin on the immune system of the chick
Authors: Virdi J. S. , Tiwari R. P. , Saxena M. , Khanna V. , Singh G. , Saini S. S. , Vadehra D. V. 
Published: October 2006

AbstractA decreased antibody response to injected sheep red blood cells and weight losses to the extent of 25–38% were observed in the bursa Fabricii and thymus in chicks fed an aflatoxin diet (10% w/w) for 3 weeks. The immune organs did not show any significant histopathological changes. The antibody titre decreased from day 6 of treatment onward until the 15th day, when the antibody titre had disappeared completely in the test chicks. The body weight gain was also less in test chicks (9.7–37.3%) given test feed or test feed along with Salmonella pullorum in water (108cfu ml−1) in comparison to chicks given toxin‐free diet and water after 3 weeks of feeding trials. The disappearing component in the test chicks' liver homogenate was found to be antigenic by immunoelectrophoretic studies.
Predicting toxicokinetic parameters in humans from toxicokinetic data acquired from three small mammalian species
Authors: Bachmann Kenneth 
Published: October 2006

AbstractValues for the indepedent kinetic variables, clearance (CL) and volume of distribution (V), for six xenobioticsantipyrine, ethosuximide, phencyclidine, theophylline, valproic acid and warfarin—were culled from the literature for each of three small subhuman species and for humans, and then allometrically scaled. Scaling was performed in two ways. First, using kinetic data acquired for three small subhuman species and for man, scaled parameters were observed for goodness of fit to a standard allometrie expression. Second, scaled parameters were averaged for three subhuman species. Mean scaled kinetic parameters from only three species were used to predict half‐life values of the xenobiotics in humans. Finally, predicted percentages of the xenobiotic burdens remainig in humans at the end of four allometrically‐predicted half‐lives were compared with the expected percentages of remainig xenobiotic based upon four actual half‐lives in humans. The results suggest that it may be feasible to estimate, using three small subhuman specie, allometrically‐derived toxicokinetic parameters of some substances in man with sufficient accuracy to be of practical value.
Lipid peroxidation in acrylonitrile‐treated rats, evidenced by elevated ethane production
Authors: Ivanov V. , Rahier J. , Lauwerys R. 
Published: October 2006

AbstractThe intraperitoneal administration of acrylonitrile (> 25 mg kg−1) to rats is associated with an increased production of ethane and a rise of the serum activity of the cytosolic enzyme, sorbitol dehydrogenase. These effects are prevented by pretreatment with vitamin E and the microsomal enzyme inhibitor SKF 525A, but are exacerbated by pretreatment with the microsomal enzyme inducer, phenobarbital.Repeated intraperitoneal administration of acrylonitrile (40 mg kg−1) for four weeks also increases ethane production and serum SDH activity, and produces various morphological changes in liver parenchymal cells (necrosis, increased mitotic activity, increased nucleolar size and myelinic figures in mitochondria) and inhibits the growth of the animals. All these effects are prevented by the administration of vitamin E (190 mg kg−1 i.p., daily) during the last two weeks of treatment.A dose of sodium cyanide (2.5 mg kg−1 i.p.) which leads to a urinary excretion of thiocyanate similar to that found after the intraperitoneal administration of 25 mg kg−1 acrylonitrile, does not stimulate ethane production.This study suggests that the hepatoxicity of acrylonitrile may, at least partly, result from a lipoperoxidation process and is linked with its microsomal oxidative biotransformation.
Effects of intrauterine exposure to parathion on the activity of renal ATPases in offspring
Authors: Jaramillo‐Juárez Fernando , Del Rio Francisco A. Posadas , Reyes José L. , Rodríguez Maria Luisa , Irene Sánchez Elsa , Cuellar Luis Humberto 
Published: October 2006

AbstractThe effects of ethyl parathion on the activities of various renal enzymes were studied in the offspring from dams treated with this insecticide during pregnancy. The enzymes tested were the (Na+‐K+)‐ and the Mg2+‐dependent ATPases, the glutathione S‐transferases and carboxylesterases. The postnatal effects of parathion on kidney ATPases from undernourished rats were also assessed. The organophosphate was administered per os to pregnant rats at a dose of 1 mg kg−1 body weight per day throughout gestation, and suspended after delivery. The offspring were divided in groups of normally‐fed and undernourished rats. In the undernourished group, food restriction produced a decrease of 43% in body weight as compared to the normally‐fed group. Offspring were sacrificed 6 weeks after birth and the enzymatic activities were determined in kidney homogenates. We found a decrease in the enzymatic activity of total ATPases, at the expense of the Mg2+‐dependent ATPase. However, the activities of the (Na+‐K+)‐dependent ATPase, the glutathione S‐transferases and the carboxylesterases did not show significant changes. On the other hand, undernutrition did not potentiate the effects of parathion on the ATPases. Thus, this organophosphate administered during pregnancy produced a selective inhibition on the renal Mg2+ ‐dependent ATPase from offspring, which was not potentiated by our undernutritional model.
Effects of short‐term and long‐term administration of amiodarone on hepatobiliary function in male rats
Authors: Young Robert A. , Mehendale Harihara M. 
Published: October 2006

AbstractFunctional, biochemical and histological parameters of hepatotoxicity were assessed in male Sprague‐Dawley rats receiving amiodarone (Am) short‐term by gavage (5, 50, 150 and 500 mg Am kg−1day−1, 10 days) or dietary exposure (50 ppm, 1500 ppm, 4‐week duration), or by long‐term dietary exposure (50 ppm, 8‐month duration). Serum enzyme (ALT, AST, ICD) levels and histopathological examination indicated no observable evidence of toxicity among rats of any of the treatment groups. Reduced food intake and reduction in weight gain was observed for rats exposed short‐term to 1500 ppm dietary Am. Assessment of hepatobiliary function in treated rats indicated that short‐term and long‐term dietary exposure to Am resulted in a compromised excretion of readily excretable phenolphthalein glucuronide (PG), although inanition may account for this effect in the 1500 ppm group. Rats receiving Am by gavage exhibited a reduction in biliary excretion of PG, which was not dose‐dependent. Distribution of Am and its major metabolite, desethylamiodarone, was similar to previous reports wherein both compounds accumulated in adipose, lung and liver tissue. These data suggest that minor alterations of hepatobiliary function occur in the absence of histological alterations and may preceed biochemical changes, as assessed in this study.
Structure–activity relationships for osteolathyrism. III. Substituted thiosemicarbazides
Authors: Dawson Douglas A. , Schuitz T. Wayne , Baker Leslie L. , Mannar Anuradha 
Published: October 2006

AbstractEight substituted thiosemicarbazides were assayed for their toxicity and teratogenicity using early embryos of Xenopus laevis. Results of the 96‐h static tests on seven 4‐position alkyl substituents were used for quantitative structure–activity relationship (QSAR) analyses, with thiosemicarbazide as the parent compound. The compounds induced malformations via the connective tissue defect osteolathyrism. Teratogenicity (log EC50) was negatively correlated with molar refractivity, suggesting that steric inhibitions were important in explaining the variations in biological activity due to changes in the 4‐position substituent. It appeared that there were two separate modes of lethal action, one associated with the ring‐containing substituents and the other with straight‐chain substituents. However, QSARs were not developed for embryolethality (log LC50) or for the mortality/malformation index (LC50/EC50) due to the limited number of chemicals eliciting each lethal mode of action.
Triiodothyronine (T3) increases cisplatin nephrotoxicity in young and adult rats
Authors: Appenroth Dorothea , Gambaryan Stephan , Bakhteeva Vera , Winnefeld Klaus , Schröter Heinz , Gerhardt Steffen , Bräunlich Helmut 
Published: October 2006

AbstractThe influence of pretreatment with triiodothyronine (T3) on cisplatin (CP)‐induced nephrotoxicity was investigated in 10‐ and 55‐day‐old rats. Triiodothyronine pretreatment enhanced CP proteinuria in young and adult rats, and increased blood urea nitrogen concentration in 55‐day‐old rats. As T3 decreased Pt concentrations in renal tisssue, the enhanced nephrotoxicity of CP by T3 must have another mechanism. Enhanced CP nephrotoxicity is discussed in connection with an increase of glutathione concentration obtained in renal tissue as a consequence of T3 pretreatment.
A teratological assessment of coal liquefaction products in the rat
Authors: Chu I. , Villeneuve D. C. , Valli V. E. , Black W. D. , Robinson K. , Beyrouty P. 
Published: October 2006

AbstractTeratogenicity of coal liquefaction products (CLP) was assessed in the pregnant rat. Three product streams of CLP (medium, hydrotreated medium and heavy fractions) were each administered dermally on Sprague‐Dawley rats at doses of 125, 250 or 500 mg kg−1day−1 from Day 6 through to Day 15 of gestation. Depressed maternal weight gain and reduced number of fetuses resulting from an increased resorption rate, decreased fetal weight and retarded ossification were observed in the group treated with the heavy fraction at a dose of 500 mg kg−1day−1. The heavy fraction at 500 mg kg−1 day−1 also caused anaemia and increased liver and spleen weights in dams. The dams exposed to the highest dose of three CLP fractions had mild and adaptative hepatic changes consisting of increased cytoplasmic eosinophilia and nuclear anisokaryosis. No treatment‐related histological changes were observed in fetuses. None of the fractions demonstrated any teratological effects.
Acute toxicity and mutagenicity of the copper complex of pyruvaldehyde‐bis (N‐4‐methylthiosemicarbazone), Cu‐PTSM
Authors: Kostyniak Paul J. , Nakeeb Shaheen M. , Schopp Ellen M. , Maccubbin Alexander E. , John Elizabeth K. , Green Mark A. , Kung Hank F. 
Published: October 2006

AbstractCu‐PTSM is a potential imaging agent for the heart and brain when labeled with either 64Cu or 62Cu. Unlabeled Cu‐PTSM was evaluated for its acute toxicity and mutagenicity. Cu‐PTSM had an i.v. LD50 of 26 mg kg−1 in the rat and 2 mg kg−1 in the rabbit. At necropsy, rats exhibited severely hemorrhagic lungs, histological findings of acute pulmonary congestion, hemorrhage and edema, and mild congestion in kidney, liver and brain. The rabbit displayed marked polymorphonuclear infiltration in alveoli, peribronchial and periarterial areas with marked macrophage hyperplasia, congestion and mild hemorrhage into alveolar spaces. No effects were found in kidney, liver, testes or brain. Administration of 2.16 μg kg−1 day−1 for 5 days per week for 2 weeks resulted in no changes in histopathology, hematology or clinical chemistry parameters. This daily dose is at least 300 times the diagnostic dose intended for use in man. Cu‐PTSM was not mutagenic when tested in the absence of S9 supernatant, but elicited a weakly mutagenic response in the presence of S9. Since acute effects in the lung occur at doses approaching 300000 times the diagnostic dose, it is highly unlikely that the clinical use of Cu‐PTSM would result in any acute adverse effects.
Plasma clearance of 51Cr‐EDTA as an estimator of glomerular filtration rate in conscious rats
Authors: Seefeldt Torben , Houghton Donald C. 
Published: October 2006

AbstractA method is described whereby the plasma clearance of 51Cr‐EDTA is used to estimate the glomerular filtration rate (GFR) in conscious rats. EDTA clearance rates were calculated based on one and two exponential disappearance curves and compared in groups of animals studied under conditions of normal, high and low GFR. Like previously described related methodologies, this technique obviates the need for urine collections and marker infusions for GFR estimates. An important added advantage is that it provides the opportunity to study animals free of the effects of anesthetic, supine position and surgical stress.
Proposal and application of an ecotoxicity biotest based on escherichia coli
Authors: Espigares M. , Roman I. , Alonso J. M. Gonzalez , de Luis B. , Yeste F. , Galvez R. 
Published: October 2006

AbstractThe authors propose the use of an ecotoxicity biotest based on Escherichia coli for the sanitary control of water. The sensitivity of the proposed model was evaluated using a group of representative toxicants, and its response (synergism, additive or antagonism) to toxicants was observed. Finally, the biotest was applied to 124 water samples from rivers, underground sources, drinking water and wastewater.The results of the biotest were compared with the sanitary classification of the waters.
Mechanisms of testicular atrophy induced by Di‐n‐butyl phthalate in rats. Part 3. Changes in the activity of some enzymes in the sertoli and germ cells, and in the levels of metal ions
Authors: Zhou Yu , Fukuoka Masamichi , Tanaka Akira 
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, with more severe sloughing at 24 and 48 h. DBP is metabolized to mono‐n‐butyl phthalate (MBP), which is transported through the blood‐tubular barrier into the seminiferous lumen. MBP is incorporated into the lumen at a maximum rate between 1 and 3 h after dosing with DBP. MBP caused decreases in the activities of succinate dehydrogenase in the Sertoli cells and sorbitol dehydrogenase in the germ cells, an increase in the activity of lactate dehydrogenase (LDH) in the germ cells and in the seminiferous lumen and a decrease in testicular iron levels.
Changes in lipid peroxidation levels and lipid composition in the lungs, livers, kidneys and brains of mice treated with paraquat
Authors: Sato Nobuyoshi , Fujii Kohyu , Yuge Osafumi , Morio Michio 
Published: October 2006

AbstractWe examined lipid peroxide levels and the lipid composition of homogenates prepared from the lungs, livers, kidneys and brains of 48 male ICR mice treated with 30 mg kg−1 paraquat (1,1′‐dimethyl‐4,4′‐bipyridylium dichloride). The mice were divided into eight groups, in which they were killed 0, 1.5, 3, 6, 12, 24, 48 and 120 h after the administration of paraquat. A significant increase in the lipid peroxide level was identified only in the liver. Change in lipid composition was identified in all the examined organs. However, the change was not a characteristic one in which there is a selective decrease of polyunsaturated fatty acids which become degraded in a lipid peroxidation reaction. It is possible that the mechanism of paraquat toxicity may differ in different organs.
ATP‐mgcl2increases cisplatin toxicity in the dog and rat
Authors: Hardie Elizabeth M. , Page Rodney L. , Hoopes P. Jack 
Published: October 2006

AbstractThe purpose of this study was to examine if ATP‐MgCl2, an agent that protects against acute cisplatin toxicityin vitro, protected against cisplatin toxicityin vivo. Baseline renal function measurements were obtained on dogs (n= 12) and rats (n= 20) on day –1. Dogs were given 90 mg m−2cisplatin (n= 5), 90 mg m−2cisplatin and 50 μmol kg−1ATP‐MgCl2(n= 5), or 90 mg m−2cisplatin and 150 μmol kg−1ATP‐MgCl2(n= 2), in a slow bolus i.v. injection on day 0, Rats were given 4 mg kg−1cispiatin i.p. (n= 6) and 25 μmol kg ATP‐MgCl2(n= 8) i.v. or 4 mg kg−1cisplatin i.p. and 25 μmol kg−1ATP‐MgCl2(n= 6) i.v. on day 0. Renal function was assessed on a routine basis for 14 days. All dogs had significantly decreased creatinine ciearance following cisplatin administration. There were no significant differences in renal function tests between groups of dogs. One dog given 50 μmol kg−1ATP‐MgCl2and both dogs given 150 μmol kg−1ATP‐MgCl2in addition to cisplatin developed acute anuric renal failure and were euthanatized prior to completion of the study. Rats given 4 mg kg−1cisplatin and 25 μmol kg−1ATP‐MgCl2had significantly increased blood urea nitrogen and serum creatinine after drug administration, compared to rats given cisplatin alone. The results indicated that ATP‐MgCl2worsenedin vivocisplatin renal toxicity in the dog and rat.
Mutagenicity evaluation of riot control agent o‐chlorobenzylidene malononitrile (cs) in the ames salmonella/microsome test
Authors: Meshram Ghansham P. , Malini R. Padma , Rao Kola M. 
Published: October 2006

Abstracto‐Chlorobenzylidene malononitrile (CS), a riot control agent, was evaluated for its possible mutagenic activity in the Ames Salmonella/mammalian microsome mutagenicity test. Five histidine‐deficient (His−) mutant tester strains of Salmonella typhimurium—TA97a, TA98, TA100, TA102 and TA104—were used. The liquid preincubation procedure was used with metabolic activation (presence of S9 mixture) and without metabolic activation (absence of S9 mixture). For the experiments with metabolic activation, three different concentrations of S9 fraction (supernatant of Aroclor 1254‐induced rat liver homogenate at 9000 g)—5%, 15% and 30% in S9 mixture—were used. Along with mutagenic activity, CS was also evaluated for cytotoxic activity in all the five tester strains of Salmonella typhimurium, both in the presence and absence of S9 mixture. The mutagenic and cytotoxic activities of CS were assessed by counting the His+ revertant colonies and by counting the microcolonies (His−, auxotrophs in the background lawn), respectively, and the respective mean values were compared with the relative negative (solvent) control. A dose range of 12.5–800 μg plate−1 for CS did not induce a mutagenic response either in the presence or absence of S9 mix. No change in the negative mutagenic response of CS has been observed even in the presence of an elevated level of S9 fraction in the S9 mix. A dose of 200 μg plate−1 for CS was found to be cytotoxic by decreasing the surviving cells as well as His+ revertant colonies; however, the effect was reduced in the presence of an elevated level of S9 fraction in the S9 mix.
Pulmonary reactivity to vanadium pentoxide following subchronic inhalation exposure in a non‐human primate animal model
Authors: Knecht Edwin A. , Moorman William J. , Clark John C. , Hull R. Delon , Biagini Raymond E. , Lynch Dennis W. , Boyle Terrence J. , Simon Stephen D. 
Published: October 2006

AbstractAn experimental study was conducted to evaluate changes in pulmonary reactivity resulting from repeated vanadium pentoxide (V2O5) dust inhalation. The study assessed pulmonary reactivity to V2O5 through the use of provocation challenges, and compared V2O5 reactivity before and after subchronic V2O5 exposure. A total of 24 adult, male cynomolgus monkeys (Macaca fascicularis) were exposed by inhalation for 6 h per day, 5 days per week, for 26 weeks. Two V2O5‐exposed groups (n=8 each) received equal weekly V2O5 exposures (concentration x time) with different exposure profiles. One V2O5‐exposed group received 0.1 mg V2O5 m−3 on Mondays, Wednesdays and Fridays, with a twice‐weekly peak exposure of 1.1 mg V2O5 m−3 on Tuesdays and Thursdays, and was included to investigate the influence of an exposure regimen with peaks on the development of pulmonary hyper‐reactivity. The other V2O5‐exposed group received a constant daily concentration of 0.5 mg V2O5 m−3. A control group (n‐8) received filtered, conditioned air. Pre‐exposure challenges with V2O5 produced a concentration‐dependent impairment in pulmonary function, characterized by airway obstructive changes (increased resistance and decreased flow). Analysis of respiratory cells recovered from the lung by bronchoalveolar lavage demonstrated that airway obstruction was accompanied by a significant influx of inflammatory cells into the lung. Subchronic V2O5 inhalation did not produce an increase in V2O5 reactivity in comparison to the control group, and cytological, immunological and skin test results indicate the absence of allergic sensitization. Instead, a trend toward decreased pulmonary reactivity was found following subchronic V2O5 inhalation. Pulmonary reactivity to V2O5 (both functional and cellular responses) was affected, as well as non‐specific reactivity to methacholine. This finding suggests that the absence of increased pulmonary reactivity to V2O5 following subchronic inhalation may be related to the induction of tolerance under the exposure conditions used in the study.
Silymarin protects against paracetamol‐induced lipid peroxidation and liver damage
Authors: Muriel Pablo , Garciapiña Tania , Perez‐Alvarez Victor , Mourelle Marisabel 
Published: October 2006

AbstractThe effect of silymarin on liver damage induced by acetaminophen (APAP) intoxication was studied. Wistar male rats pretreated (72 h) with 3‐methylcholantrene (3‐MC) (20 mg kg−1 body wt. i.p.) were divided into three groups: animals in group 1 were treated with acetaminophen (APAP) (500 mg kg−1 body wt. p.o.), group 2 consisted of animals that received APAP plus silymarin (200 mg kg−1 body wt. p.o.) 24 h before APAP, and rats in group 3 (control) received the equivalent amount of the vehicles. Animals were sacrificed at different times after APAP administration. Reduced glutathione (GSH), lipid peroxidation and glycogen were measured in liver and alkaline phosphatase (AP), gamma‐glutamyl transpeptidase (GGTP) and glutamic pyruvic transaminase (GPT) activities were measured in serum. After APAP intoxication, GSH and glycogen decreased very fast (1 h) and remained low for 6 h. Lipid peroxidation increased three times over the control 4 and 6 h after APAP treatment. Enzyme activities increased 18 h after intoxication. In the group receiving APAP plus silymarin, levels of lipid peroxidation and serum enzyme activities remained within the control values at any time studied. The fall in GSH was not prevented by silymarin, but glycogen was restored at 18 h. It was concluded that silymarin can protect against APAP intoxication through its antioxidant properties, possibly acting as a free‐radical scavenger.
Body distribution and endocrine toxicity of hexachlorobenzene (HCB) in the female rat
Authors: Foster Warren G. , Pentick Julie A. , McMahon Avril , Lecavalier Pierre R. 
Published: October 2006

AbstractHexachlorobenzene (HCB) residue levels in dosed rats (50.0 mg kg−1 body wt. day−1, n = 9) were significantly (P<0.05) greater in the periovarian fat compared to the thyroid gland. Hexachlorobenzene residue levels were significantly (P<0.05) greater in the thyroid versus the adrenal and ovary. Ovarian HCB residue levels were greater than those found in the thymus, liver and lung. Serum thyroxin (T4) and the free T4 index (FTI) were significantly (P<0.05) suppressed in HCB‐treated rats compared to the control group (n = 8). In contrast, no significant differences in serum concentrations of oestradiol (E2), progesterone (P4) or percentage triiodothyronine uptake (%T3) were observed, thus suggesting an HCB‐induced hypothyroid‐like state. In a second experiment, adult female Sprague Dawley rats (n = 16) were dosed as above and superovulated with pregnant mare serum gonadotrophin (PMSG, 10 IU s.c.) and human chorionic gonadotrophin (hCG, 20 IU s.c.). Circulating levels of P4 were significantly (P<0.05) elevated compared to the control group (n = 8). The %T3 uptake and serum T4 levels were significantly (P = 0.05) suppressed compared to controls. Hexachlorobenzene treatment had no effect on circulating levels of E2 or on the FTI. These results suggest that HCB‐induced changes found in the spontaneously cycling rat are augmented by ovulation induction strategies. We also conclude that HCB concentrates in the endocrine tissues in addition to the fat.