Role of Autophagy in Rats Lung Injury Induced by Arsenic Exposure

Objectives To study the role of autophagy in the lung injury of rats induced by arsenic exposure.

Methods Twenty four specific pathogen free (SPF) healthy male SD rats were randomly divided into four groups, namely the control group, the low (10 μg/L), medium (100 μg/L) and high (1000 μg/L) arsenic exposure groups. Arsenic exposure groups were intoxicated by sodium arsenite (NaAsO₂) in drinking water for 28 days. The level of TNF-α, IL-6, IL-8 and IL-10 in bronchoalveolar lavage fluid (BALF) were determined by ELISA and the expression of NBR1, p62 and LC3Ⅱrelated to the autophagy in lung tissue were determined by Western Blot.

Results The expression of proinflammatory cytokines TNF-a, IL6 and IL8 in arsenic exposure groups were significantly higher than that in the control group (P < 0.05). The level of IL6 in the medium arsenic exposure group (100 μg/L) was the highest and the level of IL-10 in the high arsenic exposure group (1000 μg/L) was significantly lower than the control group (P < 0.05). Compared with the control group, the expression of p62 and NBR1 in the lung tissue of arsenic exposure groups was higher (P < 0.05), and there was a dose-response relationship. In contrast, compared with the control group, the expression of LC3Ⅱ in the lung tissue of arsenic exposure groups were lower (P < 0.05), and there was a dose-response relationship too.

Conclusions The exposure of rats to arsenic would increase the inflammation of lung tissue when the autophagy was inhibited. In particular, when the concentration of NaAsO₂reaching to 100 μg/L, the damage of lung tissue in rats was more severe.