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Cd~(2+)可提高烟草悬浮细胞脯氨酸的含量,顺序上调脯氨酸合成关键酶鸟氨酸转氨酶(OAT)、精氨酸酶、△~1-吡咯啉-5-羧酸合成酶(P5CS)和谷氨酸脱氢酶(GDH)的活性,降低脯氨酸降解关键酶脯氨酸脱氢酶(ProDH)的活性,表明Cd~(2+)胁迫诱导烟草细胞脯氨酸的积累是脯氨酸合成的鸟氨酸途径和谷氨酸途径顺序激活、而脯氨酸降解途径显著抑制的综合结果。此外,Cd~(2+)能导致烟草细胞H_2O_2的快速产生及H_2O_2产生相关酶(质膜NADPH氧化酶、细胞壁多胺氧化酶及共价结合与离子结合细胞壁过氧化物酶)活性升高和脂质过氧化产物丙二醛(MDA)增加,导致烟草细胞的氧化胁迫。外源脯氨酸预处理显著抑制了Cd~(2+)诱导的烟草细胞H_2O_2的产生与MDA的增加,减轻了Cd~(2+)诱导的氧化胁迫。而脯氨酸抑制Cd~(2+)诱导的H_2O_2产生可能是由于脯氨酸抑制了H_2O_2产生相关酶的活性所致。
Cd 2+ increased the content of proline in tobacco suspension cells and up-regulated the synthesis of key enzymes such as ornithine transaminase (OAT), arginase, △ 1-pyrroline-5-carboxylic acid (P5CS) and glutamate dehydrogenase (GDH), reducing the activity of ProDH, a key enzyme in proline degradation, showed that Cd2 + stress induced proline The accumulation of proline is either synthetic ornithine pathway and the glutamate pathway is activated sequentially, while the proline degradation pathway is significantly inhibited by the combined result. In addition, Cd ~ (2+) could lead to the rapid production of H_2O_2 and the increase of activities of H_2O_2 related enzymes (plasma membrane NADPH oxidase, cell wall polyamine oxidase and covalently bound and ionically bound cell wall peroxidase) Lipid peroxidation product malondialdehyde (MDA) increased, leading to oxidative stress in tobacco cells. Exogenous proline pretreatment significantly inhibited Cd2 + -induced H2O2 production and MDA increase, and reduced Cd2 + -induced oxidative stress. Proline inhibited Cd2 + -induced H2O2 production possibly due to proline’s inhibition of H202-producing enzyme activity.