Effects of N-Acetyl Cysteine on Genes Expression of c-myc, and Ask-1, Histopathological, Oxidative Stress, Inflammation, and Apoptosis in the Liver of Male Rats Exposed to Cadmium.

Abstract

This study aimed to consider the oxidative damage induced by cadmium (Cd) and apoptosis and the role of N-acetylcysteine (NAC) in preserving hepatic cells against Cd toxicity. Male rats were randomly divided into seven groups including G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd +continuous dose of NAC), and G5 (continuous dose of Cd +continuous dose of NAC). Hepatic cells apoptosis was measured using TUNEL assay method. Levels of malondialdehyde (MDA), TNF-α, IL-10, and total antioxidant capacity (TAC) were measured by specific kits. Expression of c-myc and Ask-1 genes was considered using RT-PCR. NAC treatments significantly improved TAC and IL-10, but decreased MDA and TNF-α values in rats that were exposed to a single and continuous dose of Cd (p < 0.05). Exposure to a single and continuous dose of Cd caused a significant increase in c-myc expression by 3.76-fold (p < 0.001) and 8.17-fold (p < 0.0001), respectively. Single and continuous dose treatment of Cd led to a significant increase in Ask1 expression by 4.38-fold (p < 0.001) and 13.52-fold (p < 0.001), respectively. NAC treatments significantly decreased the expression of c-myc, and Ask-1 in rats exposed to single or continuous Cd. Cd exposure is strongly associated with oxidative stress, inflammation, antioxidant depletion, and liver cells apoptosis. NAC can protect liver tissue against Cd by elevating antioxidants capacity, mitigating oxidative stress and inflammation, as well as down-regulating of apoptotic genes.