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ORIGINAL ARTICLE
Year : 2012  |  Volume : 7  |  Issue : 2  |  Page : 78-85

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


Cell Biology Department, National Research Center, Giza, Egypt

Correspondence Address:
Sally S. Alam
Department, National Research Center, El Tahrir Street, 12622 Dokki, Giza
Egypt
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Source of Support: None, Conflict of Interest: None


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Background/aims 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. Materials and methods 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 421C 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. Results 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. Conclusion It was concluded that aging and heat exposure instigate oxidative stress, which can contribute to cellular dysfunction and age-related reductions in stress tolerance.


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