Bacteria affect Caenorhabditis elegans responses to MeHg toxicity.

The organic form of mercurial complex, methylmercury (MeHg), is a neurotoxin that bioaccumulates in the food web. Studies in model organisms, such as Caenorhabditis elegans (C. elegans), provide powerful insights on the role of genetic factors in MeHg-induced toxicity. C. elegans is a free living worm that is commonly cultured in nematode growth medium (NGM) agar plates seeded with bacteria. The bacteria have broad impact on C. elegans biology, including development, reproduction and lifespan, as well as metabolism of experimental chemicals. We hypothesized that MeHg toxicity in C. elegans could be modified by the bacterial food. Using a C. elegans wild-type (WT) strain and transgenic reporter strains, we found that bacterial food reduced the chronic toxicity of MeHg in C. elegans in a dose- and live-status-dependent manner. The MeHg-induced death rate in C. elegans was highest in fasted worms, followed by dehydrated dead bacteria, dead bacteria and live bacteria fed worms. Among the different bacterial foods, dehydrated dead bacteria fed worms were most sensitive to the toxicity of MeHg. The distinct bacteria food (dehydrated dead bacteria food) attenuated oxidative stress and development delay in C. elegans exposed to MeHg. The FOXO transcriptional factor DAF16 was not changed by MeHg but modified by the distinct bacteria food. Independent of MeHg treatment, daf-16 expression in fed worms migrated from the intestine to muscle. We conclude that, in chronic exposure studies in C. elegans, the effects of bacteria on toxicological outcomes should be considered.