NADPH oxidase-mediated H2O2 maintains proline concentration under NaCl stress through regulating its biosynthesis and degradation, conferring salt tolerance to wheat plants. Considerable attention has been paid to the specific role of hydrogen peroxide (H2O2) in plant stress responses. Here, using microscopic, pharmacological and biochemical approaches, we explored H2O2 production and its roles in redox control under salt stress in wheat roots. Exogenous H2O2 pretreatment decreased salt-induced lipid peroxidation, while increased proline content in wheat roots. Salt stress led to a transient increase in NADPH oxidase activity accompanied by accumulation of H2O2 and proline in roots. The elevated proline accumulation in the presence of NaCl was significantly suppressed by diphenyleneiodonium, an inhibitor of NADPH oxidase, and dimethylthiourea, a scavenger of H2O2. The rate-limiting enzyme involved in proline biosynthesis, Δ1-pyrroline-5-carboxylate synthetase (P5CS), was induced by NaCl, whereas the house-keeping enzyme in proline degradation, proline dehydrogenase (ProDH), was inhibited. After 6 h, the activity of P5CS increased by 1.5-fold, whereas ProDH decreased by 13.9%. The levels of these enzymes, however, were restored by NADPH oxidase inhibitor or H2O2 scavenger. After treatment with H2O2, the effects of diphenyleneiodonium and or dimethylthiourea on proline content and activities of P5CS and ProDH were reversed. These results suggested that NADPH oxidase-mediated H2O2 alleviates oxidative damage induced by salt stress through regulating proline biosynthesis and degradation.

中文翻译：

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过氧化氢通过增强小麦幼苗中脯氨酸的积累来减轻盐分引起的损害。

NADPH 氧化酶介导的 H2O2 通过调节其生物合成和降解来维持 NaCl 胁迫下的脯氨酸浓度，从而赋予小麦植物耐盐性。过氧化氢 (H2O2) 在植物胁迫反应中的特殊作用引起了相当多的关注。在这里，我们使用微观、药理学和生化方法，探索了小麦根系盐胁迫下 H2O2 的产生及其在氧化还原控制中的作用。外源 H2O2 预处理降低了盐诱导的脂质过氧化，同时增加了小麦根中的脯氨酸含量。盐胁迫导致 NADPH 氧化酶活性的短暂增加，同时伴随着 H2O2 和脯氨酸在根部的积累。NADPH 氧化酶抑制剂二苯碘鎓和二甲基硫脲显着抑制了在 NaCl 存在下升高的脯氨酸积累，H2O2 的清除剂。参与脯氨酸生物合成的限速酶 Δ1-pyrroline-5-carboxylate synthetase (P5CS) 被 NaCl 诱导，而脯氨酸降解中的管家酶脯氨酸脱氢酶 (ProDH) 受到抑制。6 小时后，P5CS 的活性增加了 1.5 倍，而 ProDH 降低了 13.9%。然而，这些酶的水平被 NADPH 氧化酶抑制剂或 H2O2 清除剂恢复。H2O2处理后，二苯碘鎓和/或二甲基硫脲对脯氨酸含量和P5CS和ProDH活性的影响被逆转。这些结果表明，NADPH氧化酶介导的H2O2通过调节脯氨酸的生物合成和降解来减轻盐胁迫引起的氧化损伤。Δ1-pyrroline-5-carboxylate synthetase (P5CS), 由 NaCl 诱导，而脯氨酸降解中的管家酶脯氨酸脱氢酶 (ProDH) 被抑制。6 小时后，P5CS 的活性增加了 1.5 倍，而 ProDH 降低了 13.9%。然而，这些酶的水平被 NADPH 氧化酶抑制剂或 H2O2 清除剂恢复。H2O2处理后，二苯碘鎓和/或二甲基硫脲对脯氨酸含量和P5CS和ProDH活性的影响被逆转。这些结果表明，NADPH氧化酶介导的H2O2通过调节脯氨酸的生物合成和降解来减轻盐胁迫引起的氧化损伤。Δ1-pyrroline-5-carboxylate synthetase (P5CS), 由 NaCl 诱导，而脯氨酸降解中的管家酶脯氨酸脱氢酶 (ProDH) 被抑制。6 小时后，P5CS 的活性增加了 1.5 倍，而 ProDH 降低了 13.9%。然而，这些酶的水平被 NADPH 氧化酶抑制剂或 H2O2 清除剂恢复。H2O2处理后，二苯碘鎓和/或二甲基硫脲对脯氨酸含量和P5CS和ProDH活性的影响被逆转。这些结果表明，NADPH氧化酶介导的H2O2通过调节脯氨酸的生物合成和降解来减轻盐胁迫引起的氧化损伤。P5CS 的活性增加了 1.5 倍，而 ProDH 减少了 13.9%。然而，这些酶的水平被 NADPH 氧化酶抑制剂或 H2O2 清除剂恢复。H2O2处理后，二苯碘鎓和/或二甲基硫脲对脯氨酸含量和P5CS和ProDH活性的影响被逆转。这些结果表明，NADPH氧化酶介导的H2O2通过调节脯氨酸的生物合成和降解来减轻盐胁迫引起的氧化损伤。P5CS 的活性增加了 1.5 倍，而 ProDH 减少了 13.9%。然而，这些酶的水平被 NADPH 氧化酶抑制剂或 H2O2 清除剂恢复。H2O2处理后，二苯碘鎓和/或二甲基硫脲对脯氨酸含量和P5CS和ProDH活性的影响被逆转。这些结果表明，NADPH氧化酶介导的H2O2通过调节脯氨酸的生物合成和降解来减轻盐胁迫引起的氧化损伤。