Bisphenol A induces apoptosis, oxidative stress and inflammatory response in colon and liver of mice in a mitochondria-dependent manner

• Published in: Biomedicine & pharmacotherapy 2019-09, Vol.117, p.109182, Article 109182
• Main Authors: Wang, Kai, Zhao, Zhenguo, Ji, Wu
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - metabolism; Apoptosis; Apoptosis - drug effects; Benzhydryl Compounds - adverse effects; Bisphenol A; Catalase - metabolism; Colon - drug effects; Colon - metabolism; Glutathione Peroxidase - metabolism; Inflammation - chemically induced; Inflammation - metabolism; Inflammatory response; Liver - drug effects; Liver - metabolism; Male; Malondialdehyde - metabolism; Membrane Potential, Mitochondrial - drug effects; Mice; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondrial function; Oxidative stress; Oxidative Stress - drug effects; Phenols - adverse effects; Reactive Oxygen Species - metabolism; Superoxide Dismutase - metabolism
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2019.109182

[Display omitted] •Dietary BPA uptake induces oxidative stress in the colon and liver.•Dietary BPA uptake induces local inflammation in the colon and liver.•Dietary BPA uptake induces mitochondrial dysfunction in the colon and liver.•Dietary BPA uptake induces apoptosis in the colon and liver. Bisphenol A (BPA), a widely used industrial compound worldwide, was recently classified as an environmental toxicant. The intestines and liver are responsible for detoxification in humans and animals, and functional damage to these organs adversely affects the health of the body. However, the effect of BPA on intestinal and liver function remains unclear. In this study, we investigated the effects of dietary BPA uptake on oxidative stress, inflammatory response, apoptosis and mitochondrial function in the colons and livers of mice. Dietary BPA uptake significantly reduced the body weights of mice as well as their colon and liver weights. Dietary BPA uptake increased the levels of oxidative stress indicators such as reactive oxygen species, reactive nitrogen species, malondialdehyde and hydrogen peroxide in mouse serum, colon and liver tissues. Antioxidant indicators, such as superoxide dismutase, glutathione peroxidase, catalase and total antioxidant capacity, as well as proinflammatory cytokines (interleukin-1β, interleukin-6, interleukin-8 and tumor necrosis factor-α) were also significantly reduced in the serum, colon, and liver tissues in the BPA group. Moreover, mitochondria-encoded genes and mitochondrial copy numbers were significantly reduced in the colon and liver tissues of the BPA mice. Dietary BPA uptake also increased gene abundance and enzyme activity of caspase-3, -8, -9 and -10. Our study found that dietary BPA induced oxidative stress, inflammatory response, apoptosis and mitochondrial dysfunction in mouse colons and livers.