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

Abstract

Soilless culture experiments with tobacco were conducted to explore how the signal molecule H₂S (0.3, 0.6, 0.9, and 1.2 μM) alleviated the toxicity of Cd²⁺ (50 mg/L). The results suggested that photosynthesis was enhanced as H₂S improved the tobacco ΦPSII, 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.

Keywords: CaM signal; Cadmium; Hydrogen sulfide; Ion antagonist; Resistance genes.