Protective effect of lactic acid bacteria intervention on copper-induced liver injury

Purpose: Although copper (Cu) is an essential trace element, health damages caused by Cu overdose have occurred with the widespread use of Cu in industry and agriculture, among others. Excessive exposure to Cu can lead to liver accumulation and cytotoxicity. To address the growing risk of Cu exposure, a safe and effective method to remove Cu is needed. Recent studies have shown that lactic acid bacteria (LAB) are effective in binding and removing heavy metals from liquids. The aim of this study was to investigate the damaging effects of long-term low-dose Cu exposure on the liver and the protective effects of LAB intervention on the liver. Methods we exposed Wistar rats to different Cu concentrations and intervened with LAB. Results demonstrated that Cu exposure caused liver tissue damage and impaired liver function, which were partially alleviated by LAB intervention. Results Cu exposure increased liver inflammation and oxidative stress, evidenced by elevated IL-1β, IL-6, and IL-10 mRNA levels, and reduced SOD and MDA expression. LAB intervention mitigated these effects, reducing Nrf2 downstream gene expression (Keap-1, GCLC, HO-1, TrxR, NQO1), indicative of hepatocyte oxidative stress protection. Cu exposure altered upstream (PP65, PJNK) and downstream (Bax, Bcl-2) Nrf2 pathway genes, implicating oxidative stress and apoptosis. LAB intervention attenuated these effects, suggesting a protective role against Cu-induced liver damage via Nrf2 pathway modulation. Conclusion Our study demonstrates that Cu exposure impairs the structure and function of rat liver, whereas Nrf2 regulates Cu exposure-induced inflammation, oxidative stress and apoptosis. LAB intervention effectively protects the liver and mitigates Cu-induced damage.