Spontaneous hyperglycemia, glycosuria, hypoinsulinemia, and glucose intolerance were observed in some WBN/Kob rats, at about 9 months of age, and in all at the age of 17 months. Females did not present this pathology. Histopathologic examination of the pancreas revealed severe changes in male rats at the age of 3 months. Between 3 and 6 months of age a distinct infiltration of inflammatory cells was found around islets and among adjacent acinar cells. At the same time, marked fibrosis was seen around the pancreatic ducts and blood vessels. With advancing age the fibrous tissue gradually invaded extensive areas of the pancreas where also the islets became involved in fibrotic degeneration. At 17 months of age and later, an obvious decrease in islet number and size (less than 50 mu in diameter) was observed, even in relatively unaffected areas of the organ. Frequent bilateral cataracts began to appear at about 15 months of age. Opacities were first observed in the periphery of the lens, then increased rapidly in intensity and extended centripetally. Nineteen-month-old male rats were hypersensitive to exogenous insulin, but showed no significant decrease in blood glucose level when treated with oral tolbutamide. These results suggest that these rats suffered from a decreased insulinogenic response.
Toluene is a widely used solvent in industry which is the subject of abuse among the younger generation. A teratogenicity study of toluene by inhalation exposure was carried out in Sprague-Dawley rats and the effects on dams, fetuses and offspring were assessed. Pregnant females were exposed to 600 or 2000 ppm toluene for 6 h/day from day 7 to day 17 of pregnancy. The control group inhaled conditioned clean air under the same exposure conditions. Maternal exposure to 2000 ppm toluene caused significant toxic effects such as body weight suppression of dams and offspring, high fetal mortality and embryonic growth retardation, but no external, internal or skeletal anomalies were observed in the fetuses of any treated group. In addition, there were no differences in the results of pre- and postweaning behavioral tests of the offspring. However, no toxic or teratogenic changes which could be related to toluene exposure were apparent in the 600 ppm group. Further studies are warranted with toluene at higher concentrations applied during the period of organogenesis.
Four-week-old Wistar male rats were fed a vitamin E (VE) deficient (OE) or a VE-sufficient (10E) diet for 6 weeks and then intra peritoneally treated with buthionine sulfoximine (BSO) at 1mmol/kg body weight once a day for 3days. Glutathione (GSH) depletion by BSO treatment caused injuries especially in the kidneys of VE-deficient rats. The kidney weight increased in the VE-deficient rats after BSO treatment (OE-BSO). It was observed that the epithelial cells of the renal tubules in this group were strongly impaired and the injuries were necrosis and desquamation. No injury was observed in the kidneys of the BSO-untreated OE group and the 10E groups. The TBA value of the kidney of OE-BSO group was lower than that of the BSO-untreated 0E group, but the lipofuscin content of the kidney of the OE-BSO group was 10 times higher than that of the BSO-untreated OE group. These results suggest that the kidney injuries in rats may be caused by lipid peroxidation induced by vitamin E deficiency and glutathione depletion. Key Words kidney injury, lipid peroxide, vitamin E deficiency, GSH depletion, DL-buthionine sulfoximine Vitamin E (VE) is considered to function as an important cellular antioxidant. Alpha-tocopherol, a component of YE, inhibits in vitro lipid peroxidation in a variety of membrane systems (1-3). Several lines of evidence suggest that alpha tocopherol exerts its antioxidant activity by scavenging free radicals generated in lipid peroxidation (4).
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