Metformin in contrast to berberine reversed arsenic-induced oxidative stress in mitochondria from rat pancreas probably via Sirt3-dependent pathway.
Mansoureh JavadipourMohsen RezaeiElham KeshtzarMohammad Javad KhodayarPublished in: Journal of biochemical and molecular toxicology (2019)
Exposure to arsenic has been linked to the development of type 2 diabetes though its mechanism of toxicity remains unresolved. In this study berberine (BBR) effects on arsenic-induced sirtuin 3 (Sirt3) modifications in isolated mitochondria from rat pancreas were evaluated and compared with metformin (MET). With arsenic, mitochondrial reactive oxygen species (ROS), oxidative stress, and insulin resistance were obtained higher than control. From our results and in the presence of arsenic trioxide, insulin resistance and Sirt3 levels were found to be predominantly elevated that could be the result of compensating mechanisms. Apparently, BBR and MET recruit both direct (as an antioxidant) and indirect mechanisms (Sirt3 content) to deal with arsenic trioxide toxicity. Metformin compared with BBR exhibited a less significant effect on ROS levels and since its direct antioxidant property is minor, depressed the ROS level mainly through the Sirt3 modification.
Keyphrases
- oxidative stress
- reactive oxygen species
- drinking water
- diabetic rats
- dna damage
- ischemia reperfusion injury
- insulin resistance
- heavy metals
- cell death
- induced apoptosis
- metabolic syndrome
- high fat diet
- polycystic ovary syndrome
- magnetic resonance
- risk assessment
- heat shock
- computed tomography
- nitric oxide
- high glucose
- drug induced
- african american