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Biomedical subjects

S M Charbonneau

Publications and source records attributed to S M Charbonneau.

At least 19 recordsLinked to original sources
PubMed1985

Long-term toxicity of hexachlorobenzene in the rat and the effect of dietary vitamin A.

The toxicological effects of analytical-grade hexachlorobenzene (HCB) were examined in two chronic studies. Study I was an in utero exposure carcinogenicity feeding experiment in which Sprague-Dawley rats, in groups of 40 males and 40 females except where noted, were fed from weaning on diets containing 0.0 (64 M/64 F), 0.32, 1.6, 8.0 or 40.0 (66 M/66 F) ppm HCB. After 3 months on test, the F0 rats were bred and 50 pups (F1) of each sex were randomly selected from every group. From weaning, when the F0 animals were killed, the F1 animals were fed their parents' diet for the rest of their life (130 wk). There were no treatment-related effects on growth, feed consumption, haematological parameters or survival in either generation. Increased heart and liver weights were found in the 8.0 and 40 ppm F0 males. HCB had no effect on fertility but pup viability was significantly reduced in the 40 ppm group. Histopathological changes in the F1 generation included significant linear trends in the incidence of parathyroid adenomas and phaeochromocytomas in both sexes, neoplastic liver nodules in females, centrilobular basophilic chromogenesis of the liver in both sexes, peliosis of the liver in females, peribiliary lymphocytosis of the liver in males and chronic nephrosis of the kidney in males. In Study II, the toxicological effects of HCB were examined as a consequence of varying the dietary levels of vitamin A. In this single generation lifetime (119 wk) feeding study, groups of 50 weanling Sprague-Dawley male rats were randomly assigned to each of the following dietary groups: control, control + 40 ppm HCB, 1/10 the vitamin A content of the control diet, 1/10 vitamin A + 40 ppm HCB, 10 times the vitamin A content of the control diet and 10 times vitamin A + 40 ppm HCB. After 25 and 49 wk on test, five animals from each group were killed and subjected to haematological and histological examinations. All other aspects of evaluation were similar to those for the F1 generation in Study I. No consistent differences were observed in the haematological parameters and there were no significant differences in the incidence of pathological lesions between the test groups. The animals in the 1/10 vitamin A groups, with or without HCB, had significantly lower body weights and poorer survival than did their corresponding control (normal vitamin A) groups.

Administration, Oral↗
PubMed1984

Mammary transfer and metabolism in the rat of halogenated fatty acids of halogenated olive oil.

To assess possible incorporation of halogenated fatty acids into the neonate via the milk, a 4-day study was carried out in which lactating Wistar rats were orally dosed with either brominated olive oil (BOO) (0.6 g/kg body wt/day) or chlorinated olive oil (COO) (0.4 g/kg body wt/day) for the first 4 days. On days 1-5 inclusive 2 pups per litter were sacrificed and the stomach curd and livers analyzed for halogenated fatty acids by gas liquid chromatography (GLC). On day 5 all dams also were sacrificed and their livers and adipose tissue similarly analyzed. With BOO, brominated fatty acids (bfa) accumulated in both the milk lipids and neonate liver lipids, and appeared to plateau on day 4 at levels of 2% and 5% respectively. In contrast to the BOO in which approximately 100% of the bfa was dibromostearic (DBS), the milk bfa comprised 79% (DBS), 9% dibromopalmitic (DBP) and 12% dibromomyristic (DBM) acids, suggesting maternal metabolism to the shorter chain brominated acids. In the neonate liver lipids the bfa composition was 47% (DBS), 12% (DBP) and 41% (DBM), suggesting either further metabolism in the neonate and/or preferential accumulation of the shorter chain brominated acids. The analysis of maternal tissue indicated very low bfa residues, contrary to previous studies in non-lactating rats. Similar results were obtained with COO.

Adipose Tissue↗
PubMed1980

Whole-body retention, excretion and metabolism of [74As]arsenic acid in the hamster.

In order to assess the whole-body retention, excretion and metabolism of inorganic arsenic, male and female hamsters were given either a single oral or i.v. dose of 74As (congruent to 33' microCi/hamster; 0.01 micrograms arsenic/hamster) as arsenic acid. 74As radioactivity was measured in the whole body, urine and feces for up to 35 days. 24-h samples of urine were analyzed for arsenic metabolites. For the i.v. dosed hamsters, the half-period of elimination for the first component (65% of the dose) was 0.40 days; the second component (35% of the dose) had a half-period of 4.5 days. For the orally dosed hamsters, the half-period of elimination for the first component (98% of the dose) was 0.29 days; the second component (2% of the dose) had a half-period of 3.8 days. Differences in the percent of dose excreted between oral and i.v. dosed hamsters appeared to be due to the increased fecal excretion of arsenic (70%) in the orally dosed hamsters as compared to the i.v.v dosed hamsters (6%). No statistically significant differences between the i.v. and oral treatments were found in the half-periods of elimination for either of the 2 components. Analysis of the urine for metabolites revealed arsenic was present as dimethylarsinic acid and inorganic arsenic.

Animals↗
PubMed1976

Chronic toxicity of methylmercury in the adult cat. Interim report.

Doses of 3, 8.4, 20, 46, 74 or 176 mug Hg/kg/day were fed to groups of 8--10 adult cats, either as methylmercuric chloride or as methylmercury-contaminated fish, 7 days/week for up to 2 years. Food consumption, body weight change, blood mercury levels, haematology, urine analysis, serum blood urea nitrogen (BUN) levels and neurological status were assessed regularly in all animals. Clinical signs of methylmercury toxicity -- consisting of ataxia, loss of balance and motor incorrdination -- occured in groups receiving 176 mug Hg/kg/day after 14 weeks of treatment. Pathological findings were confined to the nervous system and consisted of loss of nerve cells with replacement by reactive and fibrillary gloisis. Terminal blood and brain mercury levels were approx. 10 ppm. There were no differences in the time required to develop clinical signs of methylmercury toxicity, tissue mercury levels or pathology between the groups of cats receiving methylmercury as methylmercuric chloride or as methylmercury-contaminated fish, at either dose level. Blood mercury levels in the remaining doses groups appeared to plateau after 40 weeks of treatment. Groups receiving 46 mug Hg/kg/day began to show some neurological impairment after 60 weeks of treatment which did not progress in subsequent weeks. No treatment-related effects were present in groups receiving 20, 8.4 or 3 mug Hg/kg/day after 2 years.

Animals↗