Efficient remedies for living organisms including bacteria to counteract cadmium (Cd 2+ ) toxicity are still highly needed. Plant toxicity studies have showed that exogenous S(-II) (including hydrogen sulfide and its ionic forms, i.e., H 2 S, HS − , and S 2− ) application can effectively alleviate adverse effects of Cd stress, but whether S(-II) could mitigate bacterial Cd toxicity remains unclear. In this study, S(-II) was applied exogenously to Cd-stressed Shewanella oneidensis MR-1 and the results showed that S(-II) can significantly reactivate impaired physiological processes including growth arrest and enzymatic ferric (Fe(III) reduction inhibition. The efficacy of S(-II) treatment is negatively correlated with the concentration and time length of Cd exposure. Energy-dispersive X-ray (EDX) analysis suggested the presence of cadmium sulfide inside cells treated with S(-II). Both compared proteomic analysis and RT-qPCR showed that enzymes associated with sulfate transport, sulfur assimilation, methionine , and glutathione biosynthesis were up-regulated in both mRNA and protein levels after the treatment, indicating S(-II) may induce the biosynthesis of functional low-molecular-weight (LMW) thiols to counteract Cd toxicity. Meanwhile, the antioxidant enzymes were positively modulated by S(-II) and thus the activity of intracellular reactive oxygen species was attenuated. The study demonstrated that exogenous S(-II) can effectively alleviate Cd stress for S. oneidensis likely through inducing intracellular trapping mechanisms and modulating cellular redox status. It suggested that S(-II) may be a highly effective remedy for bacteria such as S. oneidensis under Cd-polluted environments.
Hasan Md. Kamrul,Liu Chen-Xu,Pan Yan-Ting,Ahammed Golam Jalal,Qi Zhen-Yu,Zhou Jie
Despite involvement of melatonin (MT) in plant growth and stress tolerance, its role in sulfur (S) acquisition and assimilation remains unclear. Here we report that low-S conditions cause serious growth inhibition by reducing chlorophyll content, photosynthesis and biomass accumulation. S deficiency evoked oxidative stress leading to the cell structural alterations and DNA damage. In contrast, MT supplementation to the S-deprived plants resulted in a significant diminution in reactive oxygen species (ROS) accumulation, thereby mitigating S deficiency-induced damages to cellular macromolecules and ultrastructures. Moreover, MT promoted S uptake and assimilation by regulating the expression of genes encoding enzymes involved in S transport and metabolism. MT also protected cells from ROS-induced damage by regulating 2-cysteine peroxiredoxin and biosynthesis of S-compounds. These results provide strong evidence that MT can enhance plant tolerance to low-S-induced stress by improving S uptake, metabolism and redox homeostasis, and thus advocating beneficial effects of MT on increasing the sulfur utilization efficiency.