Hexavalent Chromium Causes Apoptosis and Autophagy by Inducing Mitochondrial Dysfunction and Oxidative Stress in Broiler Cardiomyocytes.

Abstract

Hexavalent chromium (Cr(VI)) is a common environmental pollutant, which has a strong toxic effect on humans and animals. However, the cardiac toxicity of Cr(VI) in broilers remains to be explored. The development of heart disease is often linked to mitochondrial dysfunction especially exposure to toxic substances. In order to investigate the role of mitochondrial dysfunction in apoptosis and autophagy of broiler cardiomyocytes induced by hexavalent chromium, broiler cardiomyocytes were cultured in potassium dichromate of 0\xa0mM, 16\xa0mM, and 32\xa0mM medium for 24\xa0h. The results showed that, compared with the control group, reactive oxygen species (ROS) and apoptosis rate in the Cr(VI) treatment group increased in a dose-dependent manner, the mRNA levels of apoptosis-related genes Bax and p53 were significantly increased, and the mRNA level of Bcl-2 was significantly decreased. Compared with the control group, the mRNA level of autophagy-related genes (LC3-I, LC3-II, and Beclin1) in the Cr(VI) treatment group was significantly increased, the mRNA level of mTOR was significantly decreased, and the protein level of p62/SQSTM1 was significantly decreased. The protein level of Beclin1 and the ratio of LC3-II/LC3-I significantly increased. In addition, compared with the control group, mitochondrial membrane potential decreased in a dose-dependent manner, and mitochondrial dynamics-related genes SIRT1, SIRT3, and Mfn2 mRNA decreased significantly in the Cr(VI) treatment group. In this study, we concluded that Cr(VI) could cause broiler myocardial apoptosis and autophagy by inducing mitochondrial dysfunction and oxidative stress.