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Updated: Apr 1, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Vitamin C Alleviates BPA Embryotoxicity by Attenuating Oxidative Stress and DNA Damage-Mediated Apoptosis via
Fei Ren1, Zhen Lu1, Xueping Cheng1
1College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang 453003, Henan, China.
Abstract:
Bisphenol A (BPA), an environmental contaminant that migrates from food packaging, poses significant risks to embryonic development. This study investigated the protective effects and mechanisms of vitamin C (l-ascorbic acid) against BPA-induced embryotoxicity using Xenopus laevis embryos and P19 stem cells under a simultaneous exposure design. A multiassay approach was applied, including developmental bioassays, histological analysis, single-cell gel electrophoresis, and molecular profiling. The results showed that vitamin C significantly alleviated BPA-induced mortality, malformations, growth retardation, neurodevelopmental impairments, and notochord damage. Mechanistically, vitamin C restored the expression of antioxidant genes (gpx4, sod, ppard, and cat.2), reduced reactive oxygen species generation and oxidative DNA damage, and suppressed apoptosis via modulation of the ATM/Chk2/p53 signaling pathway. These findings demonstrate that vitamin C mitigates BPA-induced embryotoxicity by limiting oxidative stress and DNA damage-mediated apoptosis under coexposure conditions, supporting further evaluation of antioxidant-based protection across different exposure regimens and in combination with other antioxidants.
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