Sodium butyrate attenuates oxidative stress, apoptosis, and excessive mitophagy in sodium fluoride-induced hepatotoxicity in rats

作者：Jing Xia, Xiaolin Zhang, Ling Xu, Nan Yan, Zhenxiang Sun, Xiaoxu Duan, Lu Meng, Rong Qi, Fu Ren, Zhengdong Wang · 发表于：Ecotoxicology and Environmental Safety · 年份：2025 · DOI：10.1016/j.ecoenv.2025.117821 · 被引用次数：11 · 研究领域：Fluoride Effects and Removal、Cassava research and cyanide、Arsenic contamination and mitigation

Long-term exposure to excess sodium fluoride (NaF) can cause chronic fluorosis. Liver, the most important detoxification organ, is the most vulnerable to the effects of fluoride. Sodium butyrate (NaB), a short-chain fatty acid produced in the intestinal tract, maintains normal mitochondrial function in vivo and reduces liver inflammation and oxidative stress. This study aims to investigate the protective effect and potential mechanism of NaB on liver injury in fluoride poisoned rats, particularly through the mitophagy pathway. Rats were randomly divided into four groups of 12 male rats each: control, NaF (100 mg/mL), NaB (1000 mg/kg), and NaF (100 mg/mL)+NaB (1000 mg/kg) group. Changes in the levels of liver enzymes (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and antioxidant enzymes (superoxide dismutase [SOD], catalase [CAT], and malondialdehyde [MDA]) confirmed NaF-induced liver injury. NaF also changed the levels of autophagy markers (Beclin-1, LC3α/β, P62), and increased the level of apoptosis. The combined use of NaB and NaF significantly ameliorated these indices. These findings indicate that NaB may provide effective protection against NaF-induced liver injury through its attenuates oxidative stress, apoptosis, and excessive mitophagy mechanisms. • After exposure to sodium fluoride, the level of oxidative stress, apoptosis, and mitophagy in rat liver tissue significantly increased. • Sodium butyrate can alleviate liver tissue damage caused by ...