The effect of N-acetylcysteine and cadmium on histopathological properties of liver tissue and expression of some effective genes on cell proliferation

The toxic effects of cadmium exposure are mainly due to the production of oxygen free radicals, reduction of cellular antioxidants and oxidative stress, which can lead to cell component destruction, DNA damage, apoptosis and ultimately tissue damage. In this study, the protective effects of N-acetylcysteine, as a substance with antioxidant properties, in cadmium-exposed Wistar mice were investigated by liver histology and measuring the expression of effective genes in apoptosis and cell proliferation.

Mice weighing approximately 150-200 g were classified into three treatments including, G1) control treatment, G2) cadmium recipient treatment, and G3) concomitant cadmium and N-acetylcysteine treatment and for four weeks received the desired. Then liver tissue samples were taken for histopathological examination and expression of eif4e and mad1 genes.

The results of this study showed that cadmium exposure resulted in serious damage to rat liver tissue, including central artery hyperemia, increased number of inflammatory cells and inflammation in the liver parenchyma, while the use of N-acetylcysteine significantly reduced the mentioned injuries. Also, the use of N-acetylcysteine resulted in a significant reduction in the expression of eif4e and mad1 genes by 2.14 and 2.27 times, compared with mice that received only cadmium.

The results of this study suggest that N-acetylcysteine as an antioxidant can play an important role in preventing tissue damage due to oxidative stress and preventing the induction of cellular apoptosis.