Ameliorative effects of Bifidobacterium longum peptide-1 on benzo(α)pyrene induced oxidative damages via daf-16 in Caenorhabditis elegans

Oxidative stress is implicated in numerous diseases, with benzo(α)pyrene (BaP) known for causing substantial oxidative damage. Bifidobacterium longum ( B. longum ) is recognized as an antioxidant bacterium for certain hosts, yet its influence on oxidative damages instigated by BaP remains undetermined. In our study, we introduced various strains of Caenorhabditis elegans ( C. elegans ) to BaP to trigger oxidative stress, subsequently treating them with different forms of B. longum to evaluate its protective effects. Additionally, we explored the role of daf-16 in this context. Our findings indicated that in wild-type N2 C. elegans , B. longum —even in the form of inactivated bacteria or bacterial ultrasonic lysates (BULs)—significantly extended lifespan. BaP exposure notably decreased lifespan, superoxide dismutase (SOD) activity, and motility, while simultaneously down-regulating the expression of reactive oxygen species (ROS)-associated genes ( sod-3 , sek-1 , cat-1 ) and daf-16 downstream genes ( sod-3 , ctl-2 ). However, it significantly increased the ROS level, malondialdehyde (MDA) content, and lipofuscin accumulation and up-regulated another daf-16 downstream gene ( clk-1 ) ( P <0.05). Interestingly, when further treated with B. longum peptide-1 (BLP-1), opposite effects were observed, and all the aforementioned indices changed significantly. In the case of RNAi ( daf-16 ) C. elegans , BaP exposure significantly shortened the lifespan ( P <0.05), which was only slightly prolonged upon further treatment with BLP-1. Furthermore, the expression of daf-16 downstream genes showed minor alterations in RNAi C. elegans upon treatment with either BaP or BLP-1. In conclusion, our findings suggest that B. longum acts as a probiotic for C. elegans . BLP-1 was shown to safeguard C. elegans from numerous oxidative damages induced by BaP, but these protective effects were contingent upon the daf-16 gene.