Crotonaldehyde is a highly toxic pollutant, widely present in tobacco smoke and automobile exhaust. Exposure to crotonaldehyde can cause hepatotoxicity and induce liver tumors in rats; however, the underlying mechanism is unclear. Liver cells contain many mitochondria, which serve to maintain energy levels in the body. We hypothesized that the energy metabolism disorder caused by mitochondrial dysfunction is an important cause of liver injury in rats exposed to crotonaldehyde. To test this, we randomly divided 40 male Wistar rats into four groups, and provided crotonaldehyde at 0, 2.5, 4.5, and 8.5 mg/kg for 90 days by intragastric administration. The results showed that crotonaldehyde exposure caused damage to liver mitochondrial structure, reduced electron-transport chain activity and ATP levels, and interfered with mitochondrial DNA transcription. In response to increased crotonaldehyde exposure, rats exhibited increased reactive oxygen species levels, decreased superoxide dismutase and glutathione activity, and activation of the caspase-mediated apoptosis pathway, as well as elevated levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, and histopathological damage. Our findings, together with those of previous reports, should help elucidate the underlying mechanism of crotonaldehyde-induced mitochondrial dysfunction and energy metabolism disorder, and provide an important direction for the prevention and clinical intervention of liver diseases caused by crotonaldehyde and aldehydes with similar structures.
Keywords: Crotonaldehyde; energy metabolism; hepatotoxicity; mitochondria; oxidative stress.