Bisphenol A impairs mitochondrial function in the liver at doses below the no observed adverse effect level

Area of Science:

• Toxicology
• Hepatology
• Mitochondrial Biology

Background:

• Bisphenol A (BPA) is a widely used industrial chemical with known hepatic toxicity.
• Concerns exist regarding the effects of BPA exposure below established safe levels (NOAEL).

Purpose of the Study:

• To investigate if BPA, at doses below the NOAEL, induces liver damage and mitochondrial dysfunction.
• To explore the role of oxidative stress and inflammation in BPA-induced hepatic effects.

Main Methods:

• Mice were administered two doses of BPA (0.05 and 1.2 mg/kg/day) intraperitoneally for 5 days.
• Hepatic mitochondria structure, oxygen consumption, and respiratory complex expression were assessed.
• Levels of malondialdehyde (MDA), glutathione peroxidase 3 (GPx3), and proinflammatory cytokines (IL-6, TNF-α) were measured.
• HepG2 cells were treated with BPA (10 or 100 nM) to assess mitochondrial function.

Main Results:

• BPA treatment impaired hepatic mitochondria structure at both doses.
• Higher BPA dose reduced oxygen consumption rate and respiratory complex expression.
• Increased hepatic MDA and decreased GPx3 expression indicated oxidative stress.
• Elevated IL-6 and TNF-α levels suggested inflammation.
• BPA reduced oxygen consumption, ATP production, and mitochondrial membrane potential in HepG2 cells.

Conclusions:

• Doses of BPA below the NOAEL can induce liver mitochondrial dysfunction.
• This dysfunction is linked to increased oxidative stress and inflammation.
• BPA poses a risk to liver health even at low exposure levels.