Effects of selenium deficiency and low protein intake on the apoptosis through a mitochondria-dependent pathway

Abstract

ObjectiveSelenium(Se)is an important trace element for human health. Studies have shown that selenium deficiency and low protein(Pr) intake are the primary risk factors for Keshan disease.The relationship between the cardiac malfunction induced by these two risk factors and the mitochondria-mediated apoptotic pathway is poorly understood.This study aimed to determine the effect of selenium deficiency and low protein intake on the mitochondria-mediated apoptotic pathway. MethodsIn the present study, 120 weaning Wistar rats were randomly fed one of six different diets. The myocardial tissue sections were deparaffinized in water and subjected to hematoxylin-eosin staining. Mitochondrial changes in the myocardial tissue were observed and photographed using an H-7650 Hitachi transmission electron microscope. Levels of whole blood Se were measured using hydride generation atomic fluorescence spectrometry. Whole blood glutathione peroxidase (GSH-Px) activity was measured using a glutathione peroxidase cellular activity assay kit. Malondialdehyde (MDA), total-anti-oxidizing-capability(T-AOC)and reactive oxygen species(ROS)levels in serum and myocardial tissue were measured using MDA, T-AOC and ROS kits. Apoptosis was detected by immunohistochemistry. ResultsExperimental results showed that the selenium-deficient diet decreased serum selenium levels and GSH-PX activity, which caused severe cardiac dysfunction. Importantly, the levels of MDA and ROS in serum and myocardial tissue defects were significantly increased, where as total-anti-oxidizing-capability(T-AOC) levels were dramatically decreased as a result of the combination of selenium deficiency and low protein intake (P<0.05).The levels of cleaved caspase-9 and cleaved caspase-3 were enhanced, but the expression of B-cell lymphoma-2 (Bcl-2) was reduced (P<0.05). ConclusionsOur results suggest that selenium deficiency and low protein intake can cause oxidative stress in the myocardium and induce cell apoptosis via the mitochondria-mediated pathway.