Subchronic bisphenol S exposure affects liver function in mice involving oxidative damage

Area of Science:

• Toxicology
• Environmental Health

Background:

• Bisphenol S (BPS) is a common substitute for Bisphenol A (BPA) in manufacturing.
• In vitro studies suggest BPS may cause toxicity and oxidative stress.
• Limited in vivo data exists on BPS effects on the liver.

Purpose of the Study:

• To investigate the in vivo effects of Bisphenol S (BPS) on liver function in mice.
• To evaluate a wide range of doses and durations of BPS exposure.
• To determine if BPS is a safe alternative to BPA.

Main Methods:

• Oral administration of BPS to mice at doses ranging from 5 to 5000 μg/kg for 4 or 8 weeks.
• Assessment of liver injury markers (ALT, AST, total bilirubin).
• Evaluation of hepatic morphology, antioxidant enzyme activities, lipid peroxidation, and gene expression (HO-1, GADD45B).

Main Results:

• High-dose (5000 μg/kg) BPS exposure for 8 weeks induced liver injury, evidenced by elevated liver enzymes and altered hepatic morphology.
• BPS exposure at this dose and duration increased oxidative stress markers, including decreased antioxidant enzyme activity and increased lipid peroxidation.
• Lower doses (5-500 μg/kg) or shorter exposure (4 weeks) did not cause significant liver damage or oxidative stress.

Conclusions:

• Subchronic exposure to high-dose Bisphenol S (BPS) induces liver injury and oxidative stress in mice.
• BPS may not be a completely safe alternative to BPA, as indicated by its potential to cause liver damage.
• Further research is needed to understand the long-term health implications of BPS exposure.