Animals facing hypoxic or anoxic conditions need a mechanism to obtain energy without using oxygen. A biochemical adaptation of some animals to hypoxia is an alternative mitochondrial electron transport chain (CTEM), in which rhodoquinone (RQ) and not ubiquinone (UQ) is the lipidic electron carrier and fumarate, and not oxygen, is the final electron acceptor. Our results suggest that in C. elegans RQ does not have an essential role in the hypoxia conditions examined, raising the question of whether RQ serves another role in C. elegans. In its natural environment, this organism can encounter high concentrations of hydrogen sulfide (H2S), as well as pathogenic bacteria that kill the worm by the production of hydrogen cyanide (HCN). H2S and HCN are inhibitors of complex IV of the canonical CTEM, preventing oxygen from being used as the final electron acceptor. Therefore, a possible additional role for RQ could be its participation in the worm defense against these toxic compounds. In fact, mutant strains that do not synthesize RQ (and do synthesize UQ) do not survive in the presence of both HCN and H2S high concentration and are more sensitive against the pathogenic bacteria Pseudomonas aeruginosa PA01 (which kills the worm by generating HCN), compared to both the wild type strain and UQ-less worms. These results suggest a new role for RQ in protecting the worm from poisoning with HCN and H2S produced by pathogens present in the worm’s habitat.