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Methylmercury induces pancreatic beta-cell apoptosis and dysfunction.
Ya Wen Chen1, Chun Fa Huang, Keh Sung Tsai
1Institute of Toxicology, Department of Laboratory Medicine, and Department of Orthopaedics, College of Medicine, National Taiwan University, Taipei, Taiwan.
Chemical Research in Toxicology
|August 22, 2006
Summary
Methylmercury (MeHg) exposure induces oxidative stress, leading to pancreatic beta-cell dysfunction and apoptosis. The antioxidant N-acetylcysteine demonstrated protective effects against MeHg toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Endocrinology
Background:
- Mercury is a toxic metal known to induce oxidative stress.
- Pancreatic beta-cells are susceptible to oxidative damage.
- The precise impact of mercury on pancreatic beta-cell function is not fully understood.
Purpose of the Study:
- To investigate the effects of methylmercury (MeHg)-induced oxidative stress on pancreatic beta-cell viability and function.
- To elucidate the mechanisms underlying MeHg toxicity in these cells.
Main Methods:
- HIT-T15 cells and isolated mouse pancreatic islets were exposed to varying concentrations of MeHg.
- Cell viability, reactive oxygen species (ROS) levels, insulin secretion, and apoptosis markers were assessed.
- Mitochondrial membrane potential, cytochrome c release, and caspase-3 activation were analyzed.
- The protective effects of N-acetylcysteine were evaluated.
Main Results:
- MeHg reduced beta-cell viability and insulin secretion in a dose-dependent manner.
- MeHg significantly increased ROS production and mercury accumulation in cells.
- Apoptosis was induced, evidenced by increased sub-G1 population and annexin-V binding.
- Mitochondrial dysfunction and caspase-3 activation were observed.
- N-acetylcysteine treatment reversed MeHg-induced cellular damage.
Conclusions:
- Methylmercury-induced oxidative stress leads to pancreatic beta-cell apoptosis and dysfunction.
- MeHg disrupts mitochondrial integrity and activates apoptotic pathways.
- N-acetylcysteine can protect against MeHg-induced beta-cell toxicity.