Mitigation of chromium (VI) toxicity by additional sulfur in some vegetable crops involves glutathione and hydrogen sulfide

Abstract

Toxic metals cause substantial reduction in crop yields every year. Therefore, worldwide scientific efforts are being made to reduce such losses in crop productivity by using certain chemical protectants such as nutrients like sulfur (S), hydrogen sulfide (H₂S), glutathione (GSH), etc. Therefore in this study, we have tested potential of additional S, along with probable involvement of H₂S and GSH in mitigating hexavalent chromium (CrVI) toxicity in tomato, pea and brinjal seedlings. Chromium (VI) decreased shoot and root length, endogenous H₂S, and cell viability due to greater Cr accumulation that led to cell death in roots. Chromium (VI) enhanced oxidative stress markers i.e. superoxide radical, hydrogen peroxide, lipid peroxidation and protein oxidation due to down-regulation in ascorbate-glutathione cycle. However, additional S reversed toxic effect of Cr(VI). Chromium (VI) slightly stimulated enzymes of glutathione biosynthesis. Besides this, the results also showed that addition of buthionine sulphoximine (BSO, synthetic inhibitor of glutathione biosynthesis) interestingly further enhanced Cr(VI) toxicity even in the presence of additional S. But this effect of BSO was reversed by the addition of GSH. Interestingly, hydroxylamine (HA, synthetic inhibitor of cysteine desulfhydrase) had also further increased Cr(VI) toxicity even in the presence of additional S but sodium hydrosulfide (NaHS, an H₂S donor) reversed this effect. Furthermore, ameliorative behaviour of NaHS against Cr(VI) toxicity was reversed by the hypotaurine (HT, a H₂S scavenger). All together results suggested that additional S involved GSH and H₂S in mitigating Cr(VI) toxicity in studied vegetables, in which GSH acted downstream of H₂S signal.

Keywords: Ascorbate-glutathione cycle; Cell death; Cell viability; Glutathione biosynthesis; Oxidative stress; Vegetables.