Glutathione and Proline Attenuates Injury Induced by Boron Toxicity in Wheat
Given the increasing importance of boron (B) toxicity, the present study investigates the roles of glutathione (20 mM, GSH) and proline (20 mM) in the improvement of wheat (Triticum aestivum cv. Altindane) resistance to B toxicity (10 mM B). The plants were raised in hydroponic culture with control, B toxicity, B+glutathione, B+proline, glutathione and proline. B+glutathione and B+proline resisted the detrimental influences of B toxicity on the root and shoot lengths, the total chlorophyll, and phenolic contents. B toxicity increased superoxide radicals (O2.-), hydrogen peroxide (H2O2), lipid peroxidation (MDA), and proline contents while B+glutathione and B+proline applications diminished the mentioned parameters with the exception of the proline content. Individual B toxicity and combined B+glutathione and B+proline applications increased generally total ascorbic acid and glutathione levels in the wheat while the B+proline application decreased GSH content. The B toxicity decreased superoxide dismutase, catalase and guaiacol peroxidase activities in compared with control with the exception of the ascorbate peroxidase activity. Exogenous glutathione and proline augmented all enzyme activities in the wheat exposed to B toxicity. As a result, it can be suggested that glutathione and proline mitigates B toxicity; by preventing oxidative damage in the membrane, by increasing enzymatic and non-enzymatic antioxidant and by decreasing O2.-, H2O2, and MDA contents. Glutathione is generally more effective than proline in mitigating the above detrimental effects of B toxicity. The datum submitted in the current work are significant and the first to indicate that effects of exogenous glutathione and proline in improving a culture plant strength to B toxicity.
- Journal
- JOURNAL OF AGRICULTURAL SCIENCES-TARIM BILIMLERI DERGISI
- Year
- 2023
- Volume
- 29
- Issue
- 2
- Pages
- 371-379
- ISSN
- 1300-7580
- eISSN
- 2148-9297
- DOI
- 10.15832/ankutbd.1092217
- WoS UID
- WOS:001012758000001