The non-target organism Caenorhabditis elegans withstands the impact of sulfamethoxazole.

The widespread usage of antibiotics in agriculture leads to releases into the environment, but there is insufficient knowledge of the side-effects on non-target organisms. Therefore, we investigated the effects of the sulfonamide-antibiotic sulfamethoxazole (SMX) on Caenorhabditis elegans at phenotypic, biochemical and molecular biological levels. Multiple endpoints, including life history traits, thermal stress resistance and lipid peroxidation, as well as gene expression profiles, were determined after exposure of the nematodes to SMX. In contrast to expectations, SMX prolonged the lifespan and increased both the body size and pharynx pumping rate. On the other hand, SMX delayed reproductive timing and caused lipid peroxidation. The total number of offspring and thermal stress resistance were unaffected. The up-regulation of hsp-16.1 indicated stress in general and the increased lipid peroxidation oxidative stress in particular. This oxidative stress indicated that mitohormesis was the likely cause of the longevity and that enhanced pumping frequency was probably the reason for the increased growth. The sole adverse effect was delayed initial reproduction. This delay, however, can be crucial for r-strategists, such as the bacterivorous model animal used, in sustaining their populations in the environment in the presence of predators. Bacterivorous animals, in turn, are essential to maintaining nutrient recycling via the microbial loop. Crown