Found programs:
Authors:Huang Damin; Zeng Weide; Luo Xueqing; Pang Yaqin; Guo Rui
Keywords:sodium fluoride;lung;oxidative damage;apoptosis
DOI:10.19405/j.cnki.issn1000-1492.2023.04.023
〔Abstract〕 Objective To study the relationship between different doses of subchronic sodium fluoride exposure and lung histopathological changes in rats, and to explore the effect and related mechanism of sodium fluoride induced lung tissue injury in rats. Methods Thirty-two Wistar male rats were randomly divided into control, low, medium and high dose groups, each group included 8 rats, intragastric administration of sodium fluoride toxin solution 0, 12, 24, and 48 mg/(kg·d). The experiment lasted for 16 weeks. The incidence of dental fluorosis and weight in each group of rats was recorded, the lung coefficient was calculated, the pathological changes of lung tissue was observed by HE staining, enzyme-linked immunosorbent assay(ELISA) was used to detect the content of superoxide dismutase(SOD) and malondialdehyde(MDA) levels in rats serum, apoptosis level of lung cells was assessed by TUNEL staining, and the Caspase-3 protein expression levels in lung tissues were determined by immunohistochemistry. Results At the end of exposure, the upper and lower incisors of rats in different dose groups showed different degrees of dental fluorosis. The increase in body weight of the rats in the high-dose group was lower than that in the other three groups(P<0.05). The coefficient of lung organs and the content of MDA in serum of the rats in the high-dose group were higher than those in the control group(P<0.05). The rats in the low, medium and high dose groups had different degrees of pulmonary interstitial inflammatory infiltration and alveolar morphological changes.Compared with the control group, the lung cell apoptosis rate and Caspase-3 protein expression of the rats in the low, middle and high groups significantly increased, and the differences were statistically significant(P<0.05). Conclusion Subchronic exposure to sodium fluoride can cause the lung tissue damage in rats, and the mechanism may be related to the apoptosis induced by oxidative stress.