Sodium Selenide Toxicity Is Mediated by O2-Dependent DNA Breaks

Hydrogen selenide is a recurrent metabolite of selenium compounds. However, few experiments studied the direct link between this toxic agent and cell death. To address this question, we first screened a systematic collection of Saccharomyces cerevisiae haploid knockout strains for sensitivity to sodium selenide, a donor for hydrogen selenide (H2Se/HSe−/Se2−). Among the genes whose deletion caused hypresensitivity, homologous recombination and DNA damage checkpoint genes were over-represented, suggesting that DNA double-strand breaks are a dominant cause of hydrogen selenide toxicity. Consistent with this hypothesis, treatment of S. cerevisiae cells with sodium selenide triggered G2/M checkpoint activation and induced in vivo chromosome fragmentation. In vitro, sodium selenide directly induced DNA phosphodiester-bond breaks via an O2-dependent reaction. The reaction was inhibited by mannitol, a hydroxyl radical quencher, but not by superoxide dismutase or catalase, strongly suggesting the involvement of hydroxyl radicals and ruling out participations of superoxide anions or hydrogen peroxide. The •OH signature could indeed be detected by electron spin resonance upon exposure of a solution of sodium selenide to O2. Finally we showed that, in vivo, toxicity strictly depended on the presence of O2. Therefore, by combining genome-wide and biochemical approaches, we demonstrated that, in yeast cells, hydrogen selenide induces toxic DNA breaks through an O2-dependent radical-based mechanism

Terrestrial runoff influences white syndrome prevalence in SW Madagascar

Terrestrial runoff and sedimentation have been implicated in a variety of impacts on scleractinian corals. However, despite accumulating evidence, little work has been done to investigate their influence on coral disease development. This study examined the role that river runoff and the associated sedimentation could play in affecting the prevalence of the coral disease "white syndrome" in SW Madagascar. Corals from reefs affected by river discharge and terrestrial sediments were more affected by white syndrome than reefs located far from any source of terrestrial runoff. Terrestrial runoff-affected reefs also displayed a wider diversity of coral species affected by this disease. While much evidence has been pointing in the direction of indirect effects of such runoff on coral disease development, our data corroborates earlier suggestions that pathogens are present within the sediments. As such, sediments released on reefs through river discharge could act as reservoirs of coral pathogens