Cadmium exposure exacerbates hyperlipidemia in cholesterol-overloaded hepatocytes via autophagy dysregulation

Toxicology
Patricia Rosales-CruzVerónica Souza-Arroyo

Abstract

Metabolic factors are the major risk of non-alcoholic fatty liver disease, although other factors may contribute steatosis. Cadmium exposure produces histopathological and molecular changes in liver, which are consistent with steatosis. In the present study, we describe the effect of low cadmium acute treatment on hepatocytes obtained from mice fed with a high cholesterol diet. Our data suggest that hepatocytes with cholesterol overload promote an adaptive response against cadmium-induced acute toxicity by up-regulating anti-apoptotic proteins, managing ROS overproduction, increasing GSH synthesis and MT-II content to avoid protein oxidation. Cadmium treatment increases lipid content in cholesterol-fed mice hepatocytes because of an impaired autophagy process. Our data suggest an essential function of macroautophagy in the regulation of lipid storage induced by Cd on hepatocytes, that implies that alterations in this pathway may be a mechanism that aggravates hepatic steatosis.

Citations

Jul 28, 2019·International Journal of Environmental Research and Public Health·Hyejin Park, Kisok Kim
Sep 17, 2020·Biometals : an International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine·Haitao LiuHaifeng Shi
Aug 24, 2021·Journal of Toxicology·Suryakant NitureDeepak Kumar
May 7, 2019·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Xue-Lei ZhouChun-Guang Xie
Jan 1, 2022·Environmental Toxicology and Pharmacology·Giammichele GraziaMonti Carlo

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