Ameliorative Effects of N-acetylcysteine on the Expression of Oxidative Stress-Related Genes and Inflammatory Biomarkers in the Cardiac Tissues of Rats Exposed to Lead

Background: Lead, as the most important toxic heavy element, has several devastating effects on human health and influences most biochemical and physiological functions. It is widely accepted that lead can adversely affect the cardiovascular system since it can be quickly absorbed and recycled in the blood strain. Objectives: This survey scrutinized the effects of N-acetylcysteine (NAC) on the oxidative damage, inflammation, and expression of protein kinase C-alpha (PKC-alpha) and ankyrin repeat domain 1 (ANKRD1) genes in the heart tissue of rats exposed to lead (Pb). Methods: The rats were incidentally divided into five groups, including four study groups for the investigation of the effects of the single and continuous doses of lead were examined with and without NAC and a control group (G1). The levels of malondialdehyde (MDA), total antioxidant capacity (TAC), interleukin (IL)-10, and tumor necrosis factor alpha (TNF-alpha) were analyzed. A reverse transcription polymerase chain reaction was applied to investigate the expression of PKC-alpha and ANKRD1 genes. Results: Continuous exposure to Pb significantly decreased serum levels of TAC and IL-10; however, it increased MDA and TNF-alpha contents (P<0.001). The continuous dose of Pb also dramatically increased the expression of PKC-alpha and ANKRD1 genes in the cardiac tissue by 4.27-fold and 3.07-fold, respectively (P<0.001). N-acetylcysteine treatments not only improved morphological changes, oxidative stress, and inflammatory biomarkers but also compensated antioxidant capacity and the expression of PKC-alpha and ANKRD1 genes in cardiac tissues. Conclusion: Lead exposure is remarkably related to cardiotoxicity mainly by inducing oxidative stress, inflammation, and antioxidant discharge. N-acetylcysteine ameliorates Pb-induced cardiotoxicity by improving the antioxidants capacity, mitigating oxidative stress, and down expressing PKC-alpha and ANKRD1 genes.