Effect of Cd2+ and Cu2+ on Desulfovibrio vulgaris strain ATCC 7757: Insights from sulfur isotope fractionation

Microbial sulfate reduction (MSR) is the predominant microbial metabolic process involved in sulfur cycling in metal-sulfide mining areas. In this study, we investigated the effect of Cd2+ and Cu2+ on MSR driven by Desulfovibrio vulgaris strain ATCC 7757, determined the corresponding sulfur isotope compositions to establish a fundamental relationship between toxicity and isotope fractionation. Cd2+ did not cause significant cellular irrecoverable damage until concentrations exceeded 3.5 ppm, and the bacteria would enhance the transfer of SO42- to APS to ensure the bacterial growth. The repair of DNA damage caused by Cd2+ was a gradually stimulated process, which resulted in a tolerance period. Cu2+ inhibited MSR in a dose-dependent manner at concentrations below 1 ppm, and the bacterial growth significantly inhibited. When exposed to 1 ppm Cu2+ for 48 h, ATCC 7757 might enhance the substrates transport to maintain its culturability through up-regulating genes encoding H+-transporting ATPase, ABC transporters and Protein export. Cd2+ had minimal impact on δ34Ssulfate, with an enrichment factor (34ε) ranging from −11.7 ‰ to −12.3 ‰. Conversely, Cu2+ significantly affected the δ34Ssulfate (34ε = −11.1 ‰ to −15.4 ‰), resulting in a substantial decrease in δ34Ssulfide, with the lowest value of δ34Ssulfide recorded as −18.8 ‰ (-11.5 ‰ for control group). The study demonstrated that sulfur isotope fractionation could indicate different toxicity mechanisms of heavy metal on ATCC 7757, aiding in the identification of environmental contamination caused by heavy metals. [Display omitted] •Heavy metals are an important factor affecting sulfur isotope fractionation.•Cu2+ significantly affected the sulfur isotope fractionation, while Cd2+ did not.•Sulfur isotope fractionation can be used to distinguish different toxicities of heavy metals.•Heavy metals affect isotope fractionation by influencing sulfate-reducing related gene expression.