Cr(VI) is a widely used chemical. Excessive Cr(VI) exposure not only causes inflammatory damage but also induces mitophagy. This study aimed to demonstrate the effect of Cr(VI) on inflammatory injury and mitophagy in chicken liver. A total of 120 Hyland Brown cockerels (1 day old) were randomly divided into four groups and orally treated with different Cr(VI) doses (10% median lethal dose, 6% median lethal dose, 2% median lethal dose, and 0% median lethal dose) daily for 45 days to explore the underlying mechanism. Results showed that excessive Cr(VI) increased tumor necrosis factor-α, interleukin-6, and heat shock protein but decreased interferon-γ expression and adenosine triphosphate content in chicken liver. Cr(VI) significantly increased reactive oxygen species production, induced mitochondrial membrane potential collapse, and promoted autophagosome formation. Cr(VI) treatment also caused an increase in LC3-II, stimulated Parkin translocation, and inhibited the expression of p62/SQSTM1 and translocase of outer mitochondrial membrane 20. Therefore, excessive Cr(VI) caused inflammatory damage and mitophagy in chicken liver.
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