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Salicylic acid‐induced hydrogen sulphide improves lead stress tolerance in pepper plants by upraising the ascorbate‐glutathione cycle
Author(s) -
Kaya Cengiz
Publication year - 2021
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/ppl.13159
Subject(s) - salicylic acid , chemistry , proline , pepper , hypotaurine , glutathione reductase , glutathione , hydrogen peroxide , horticulture , peroxidase , osmoprotectant , ascorbic acid , biochemistry , food science , botany , glutathione peroxidase , enzyme , biology , amino acid , taurine
The contribution of hydrogen sulphide (H 2 S) to salicylic acid (SA) induced lead (Pb) stress tolerance modulated by the ascorbate‐glutathione (AsA‐GSH) cycle was examined in pepper ( Capsicum annuum L.) plants. One week after germination, pepper seedlings were sprayed with 0.5 mM SA once a day for a week. Thereafter, seedlings were grown under control (no Pb) or Pb stress (Pb‐S treatment consisting of 0.1 mM PbCl 2 ) for a further 2 weeks. Lead stress reduced plant growth and leaf water status as well as the activities of dehydroascorbate reductase and monodehydroascorbate reductase. However, lead stress elevated leaf Pb, the proline contents, oxidative stress, activities of glutathione reductase and ascorbate peroxidase, as well as the endogenous H 2 S content. Supplements of SA resulted in improvements in growth parameters, biomass, leaf water status and AsA‐GSH cycle‐related enzyme activities, as well as increasing the H 2 S content. The positive effect of SA was further enhanced when sodium hydrosulphide was added. However, 0.1 mM hypotaurine (HT) treatment reversed the beneficial effect of SA by reducing the plant H 2 S content. Application of NaHS in combination with SA + HT suppressed the adverse effect of HT mainly by restoring the plant H 2 S content, suggesting that higher H 2 S content, induced by exogenous SA supply, resulted in elevated regulation of the AsA‐GSH cycle.