The multiple effects of hydrogen sulfide on cadmium toxicity in tobacco may be interacted with CaM signal transduction

Soilless culture experiments with tobacco were conducted to explore how the signal molecule H2S (0.3, 0.6, 0.9, and 1.2 mu M) alleviated the toxicity of Cd2+ (50 mg/L). The results suggested that photosynthesis was enhanced as H2S improved the tobacco Phi PSII, ETR, Photo, Cond, and Tr, and that by increasing the NPQ, it consumed considerable amount of energy to enhance plant resistances during Cd2+ exposure. Furthermore, H2S increased the gene transcription of NtSOD3, NtPOD1, and CAT1, to enhance antioxidant enzyme activity, which reduces the generation of the reactive oxygen protective membrane integrity. Additionally, H2S increased the gene expression of the tobacco PC genes, Pr2 and Pr8 promoted the formation of the Cd2+ complexes and transportation to the vacuole, resulting in improved Cd-ATPase gene expression, away from organelles, to alleviate the Cd2+ poison. Furthermore, H2S regulated the relative absorption of K+ and Ca2+, which antagonized the Cd2+, and reduced its transportation to the aboveground plant material. Finally, the expression level of CaM increased with the application of H2S, and was highly correlated with the fitted results of a variety of resistance indicators, thereby indicating that H2S regulatory resistance mechanisms might be associated with Ca2+ signal transduction.

Automated summary

H2S alleviates the toxicity of Cd2+ in tobacco by enhancing photosynthesis, increasing antioxidant enzyme activity, and promoting the formation of Cd2+ complexes. Additionally, it regulates the absorption of K+ and Ca2+ to reduce the transportation of Cd2+ to aboveground plant material. The regulatory resistance mechanisms of H2S may be associated with Ca2+ signal transduction.