This study investigated oxidative stress and the consequent DNA damage induced by lipopolysaccharide (LPS) in bovine mammary epithelial cell line MAC-T cells. Cells were cultured for 48 h with different LPS levels (0, 0.1, 0.5, 2.5, 12.5, and 100 ng/mL). The results showed that cell viability was negatively correlated with LPS concentrations. The production of reactive oxygen species increased in a dose-depend manner. Cellular concentrations of oxidative damage markers were positively correlated with applied LPS concentrations. Total antioxidant capability and the activity of superoxide dismutase (SOD) increased with increasing LPS concentrations. Gene expression of antioxidants including SOD, NADPH-quinone oxidoreductase 1, and hemeoxygenase 1 were significantly increased at the LPS concentrations of 12.5 and 100 ng/mL. Both Fanconi Anemia complementation group D2 protein and Fanconi Anemia complementation group L had significantly higher gene expression at 100 ng/mL LPS level. The protein expression of phosphorylated histone 2AX showed a linear rise in the range of LPS levels from 0 to 12.5 ng/mL, then significantly declined at 100 ng/mL LPS level. Oxidative stress and oxidative damage to protein and DNA were induced by LPS treatments, although the antioxidative defense was not impaired under LPS treatments. Upregulation of the Fanconi Anemia pathway mediated genes for activating cellular DNA repair pathway alleviated DNA damage at high LPS levels.
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