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- W2186851504 abstract "8 Abstract: Recent studies have reported that the incidences of diseases related to social instability and psychological stress are increasing, however hepatic histopathological changes under psychosocial stress conditions have not been well defined and also little is known about the role of psychosocial stress and food deprivation at the liver disorders. So in present study the effects of food deprivation, food intake inequality with or without unstable social status were evaluated and histopathological changes in hepatocytes and premature cell death process were investigated. Forty eight Newzeland white male rabbits were divided into six groups and different social situations were applied to some groups during eight weeks. After the period of the experiment, lipofuscin accumulation and apoptosis as main markers of premature death process were studied by long Ziehl Nelseen staining, the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL reaction) assay were used to reveal the rate of lipofuscin pigmentation and apoptosis in the hepatocytes, respectively. Serum cortisol level was also measured. The simultaneous application of the mentioned situations (i.e. food deprivation, social inequality and instability), caused significant change in lipofuscin accumulation in the hepatocytes in comparison with the control group (p<0.05). The results also showed a significant increase in ratio of apoptotic to normal cells both in isolated and unstable social status groups compared with control (p<0.05). These findings suggest that food deprivation, inequality in food intake and social instability enhance the susceptibility of hepatocytes in young animal to premature aging by upregulating the ratio of apoptosis and increasing lipofuscin accumulation." @default.
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- W2186851504 date "2012-01-01" @default.
- W2186851504 modified "2023-09-27" @default.
- W2186851504 title "Social Instability, Food Deprivation and Food Inequality Can Promote Accumulation of Lipofuscin and Induced Apoptosis in Hepatocytes" @default.
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