Arsenic, mitochondrial Sirt3 and diabetogenesis
محل انتشار: پانزدهمین همایش سراسری سم شناسی ایران
سال انتشار: 1398
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 422
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شناسه ملی سند علمی:
TOXICOLOGY15_009
تاریخ نمایه سازی: 15 بهمن 1398
چکیده مقاله:
Accumulation of oxidative damage made by mitochondriotropic toxicants has been linked to the development of chronic diseases including diabetes and cancer. Arsenic is a diabetogenic metalloid which by interacting with mitochondrial normal function leads to reactive oxygen species (ROS) overproduction and oxidative stress. Sirtuins are a family of regulating enzymes and mitochondrially localized Sirt3 contributes mainly to the fine tuning of complex I activity and hence, ROS production as its activity’s byproduct. So we here discussed about the impact of arsenic exposure at the diabetogenic concentration on the mitochondrial function and SirT3. Serum glucose and insulin levels were assessed in rats following the arsenic exposure and isolated hepatocytes and mitochondria were then further assessed to determine any deleterious effects. Impairment in the complex II activity, glucose homeostasis, glucose tolerance and insulin sensitivity were observed. Increased SirT3 level probably is a compensatory mechanism to deal with the toxic insult. The SirT3 dependent regulation of mitochondria-associated ROS production and glucose homeostasis in the liver may play a crucial role against the diabetogenic effect of arsenic.
نویسندگان
Mohsen Rezaei
Toxicology Department, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
Mohammad Javad Khodayar
Toxicology Department, Faculty of Pharmacy, Jundishapur University of Medical Sciences, Ahvaz, Iran
Elham Keshtzar
Toxicology Department, Faculty of Pharmacy, Jundishapur University of Medical Sciences, Ahvaz, Iran
Monsoreh Javadipour
Toxicology Department, Faculty of Pharmacy, Jundishapur University of Medical Sciences, Ahvaz, Iran