Genetic and biochemical studies on hepatocytes of young and old heat-stressed rats

Heat stress was shown to cause impairments in hepatocytes and result in oxidative damage, which can lead to cytotoxicity; thus, we carried out this study to investigate the age tolerance to oxidative stress caused by heat stress in young and old female Wistar rats and whether this effect varied with different postexposure periods. Heat stress-induced injury in hepatic cells was evaluated in young [6 months] and old [24 months] female Wistar rats by exposing them at an ambient temperature of 42[degree sign]C for 1 h. Livers were harvested at several time points [6, 24, and 72 h] after application of the heat stress protocol. The level of DNA damage assessed using the comet assay, percentage of fragmented DNA, quantitative changes in nucleic acid and protein contents, activity of liver enzyme marker, level of superoxide dismutase, and lipid peroxidation were determined. The results showed that exposure to heat stress significantly increased the oxidative DNA damage, percentage of DNA fragmentation, and activities of liver enzyme marker and stimulated the process of lipid peroxidation in liver cells of young and old rats. Further, it decreased total nucleic acid and protein contents and superoxide dismutase activities. In addition, it was observed that the damage from heat stress was more serious in old animals than in young ones and they needed more time to return to control values. It was concluded that aging and heat exposure instigate oxidative stress, which can contribute to cellular dysfunction and age-related reductions in stress tolerance

Evaluation of the genotoxicity and pathological changes induced by the prolonged bromuconazole triazole fungicide exposure in rats

Bromuconazole, is a triazole fungicide used in enclosed commercial greenhouses was evaluated for its potential toxic effects in rat liver. Sprague-Dawley male rats were treated orally at daily doses of 36.5 and 18.25 mg/kg b. wt [1/10 and 1/20 LD[50], respectively] Bromuconazole for 3 months. Measurements include potential DNA fingerprinting using random amplified polymorphic DNA [RAPD-PCR] analysis, total nucleic acids content, total protein as well as histopathological alteration in the liver were performed. The results revealed that, Bromuconazole fungicide had genotoxic and toxicopathological effects in rat liver. The genotoxic effects were indicated by appearance of some changes in polymorphism band patterns including deletion of stable bands or insertion of new bands. The effects on the liver were also manifested by different histopathological lesions including severe necrobiotic and proliferative changes with the appearance of hepatoma at high dose. In addition, the liver tissue DNA, RNA and protein contents were significantly increased with increasing the dose of Bromuconazole. Using of Bromuconazole fungicide should be reconsidered due to its possible cytotoxic. clastogenic and mutagenic effects