Harmonization of Mangiferin on methylmercury engendered mitochondrial dysfunction

Area of Science:

• Biochemistry
• Toxicology
• Cell Biology

Background:

• Methylmercury (MeHg) is a potent neurotoxin that induces mitochondrial damage and cytotoxicity in hepatic cells.
• Mangiferin (MGN), a natural polyphenol from mango plants, possesses antioxidant properties.
• Understanding MGN's protective mechanisms against MeHg-induced liver injury is crucial for public health.

Purpose of the Study:

• To investigate the potential of mangiferin (MGN) to ameliorate methylmercury (MeHg)-induced mitochondrial dysfunction and cytotoxicity in HepG2 cells.
• To elucidate the underlying mechanisms of MGN's hepatoprotective effects against MeHg intoxication.

Main Methods:

• Cell viability was assessed using the MTT assay.
• Mitochondrial function was evaluated by measuring mitochondrial membrane potential, calcium flux, and Mitotracker red fluorescence.
• Oxidative stress markers, antioxidant enzyme activities (GSH, GST, GPx, GR), liver enzymes (AST, ALT), and apoptotic markers were analyzed.

Main Results:

• MGN (50 µM) significantly protected HepG2 cells against MeHg-induced cytotoxicity.
• MGN treatment reduced oxidative stress, normalized calcium homeostasis, preserved mitochondrial membrane potential, and prevented mitochondrial fission.
• MGN enhanced antioxidant enzyme activities and reduced liver enzyme leakage, while inhibiting apoptosis.

Conclusions:

• Mangiferin (MGN) effectively ameliorates methylmercury (MeHg)-induced mitochondrial dysfunction and hepatotoxicity in vitro.
• MGN's protective effects are attributed to its potent antioxidant and free radical scavenging activities, maintaining cellular redox homeostasis.
• Dietary intake of MGN may offer a promising strategy for mitigating MeHg toxicity and promoting liver health.