N-Acetylcysteine as an anti-oxidant and anti-inflammatory agent in decreasing histopathological damages and oxidative stress after mercury exposure in lung tissue of rats

Mercury (Hg) is a naturally occurring heavy metal with high toxicitythat affects various organs. This study aimed to evaluate the protective effects of N-acetylcysteine (NAC) on the lung tissue of Wistar rats exposed to mercury. Rats were divided into five groups: H1 (control), H2 (single dose of Hg), H3 (continuous dose of Hg), H4 (single dose of Hg+ single dose of NAC), and H5 (continuous dose of Hg+ continuous dose of NAC). The expression levels of SOD1, NOS, TIMP1, Fibronectin1, HIF1, MPO, MMP2 and TIMP2 were analyzed using qRT-PCR. Mercury levels in the blood and lung tissues significantly increased in the H2 and H3 groups compared to the H4 and H5 groups, respectively. Hg exposure in H3 group significantly (P < 0.001) led to the upregulation of MPO (4.55-fold), HIF1(4.31-fold), MMP2 (4.20-fold), TIMP1(3.18-fold), TIMP2 (4.83-fold), NOS (3.52-fold), and FN1 (3.52-fold), along with the downregulation of SOD1 (0.51-fold) compare to control group (H1). In contrast, rats treated with NAC after Hg exposure in H5 group significantly (p < 0.01–0.001) showed downregulation of MPO (2.49-fold), HIF1(2.12-fold), MMP2 (1.94-fold), TIMP1(1.92-fold), TIMP2 (1.96-fold), NOS (2.00-fold), and FN1 (1.90-fold), and upregulation of SOD1 (0.76-fold) compare to H3 group. A significant reduction in mercury levels was also observed in the blood and lung tissue of rats treated with NAC compared to those exposed Hg alone. NAC exerts a protective effect against mercury-induced cytotoxicity and genotoxicity in rat lungs by scavenging mercury and modulating the expression of oxidative stress-related genes.