Zinc Deficiency Induces Endoplasmic Reticulum Stress Leading To Hepatocyte Apoptosis in Mice

Abstract

Abstract Zinc (Zn) is a crucial trace element for the organism. We investigated Zn deficiency causing endoplasmic reticulum stress and apoptosis by establishing a mouse Zn deficiency model (34 mg/kg in CG group and 2 mg/kg in LG group) and hepatocyte Zn deficiency model (add 0 umol TPEN in CCG group, add 50 umol TPEN in C50 group, add 100 umol TPEN in C100 group). The Zn deficiency caused oxidative stress and produced a large amount of ROS, which had a greater effect on the endoplasmic reticulum and caused endoplasmic reticulum stress. HE staining, liver tissue showed more inflammatory cell infiltration, and TUNEL showed that more apoptotic cells appeared in the LG group compared with the CG group. In RT-PCR assay, we found that the expression of GRP78, IRE-1α, ATF6, PERK, and Chop gene increased in the Zn deficiency group, and caspase-12, caspase-9, caspase-3, caspase-7, PARP apoptotic gene expression were increased. In the apoptosis assay, AO/EB staining clearly showed an increase in apoptotic cells in the Zn-deficient group. Our study provides some basis for the effects of trace element Zn on the liver in terms of endoplasmic reticulum stress.