Aravind Parameswaran, Prasad Majeti Narasimha Vara
Department of Plant Sciences, School of Life Sciences, University of Hyderabad, Hyderabad 500 046, India.
Plant Physiol Biochem. 2005 Feb;43(2):107-16. doi: 10.1016/j.plaphy.2005.01.002.
To understand the interaction between Zn, an essential micronutrient and Cd, a non-essential element, Cd-10 microM and Zn supplemented (10, 50, 100, and 200 microM) Cd 10 microM treated Ceratophyllum demersum L. (Coontail), a free floating freshwater macrophyte was chosen for the study. Cadmium at 10 microM concentration decreased thiol content, enhanced oxidation of ascorbate (AsA) and glutathione (GSH) to dehydroascorbate (DHA) and glutathione disulfide (GSSG), respectively, a clear indication of oxidative stress. Zinc supplementation to Cd (10 microM) treated plants effectively restored thiols, inhibited oxidation of AsA and GSH maintaining the redox molecules in reduced form. Cd-10 microM slightly induced ascorbate peroxidase (APX, E.C. 1.11.1.11) but inhibited monodehydroascorbate reductase (MDHAR, E.C. 1.6.5.4), dehydroascorbate reductase (DHAR, E.C. 1.8.5.1) and glutathione reductase (GR, E.C. 1.6.4.2), enzymes of ascorbate-glutathione cycle (AGC). Zn supplementation restored and enhanced the functional activity of all the AGC enzymes (APX, MDHAR, DHAR and GR). Gamma-glutamylcysteine synthetase (gamma-GCS, E.C. 6.3.2.2) was not affected by Cd as well as Zn, but Zn supplements increased glutathione-S-transferase (GST, E.C. 2.5.1.18) activity to a greater extent than Cd and simultaneously restored glutathione peroxidase (GSH-PX, E.C. 1.11.1.9) activity impaired by Cd toxicity. Zn-alone treatments did not change above investigated parameters. These results clearly indicate the protective role of Zn in modulating the redox status of the plant system through the antioxidant pathway AGC and GSH metabolic enzymes for combating Cd induced oxidative stress.
为了解必需微量元素锌与非必需元素镉之间的相互作用，选用了漂浮水生大型植物金鱼藻，对其进行10微摩尔镉处理，并补充不同浓度（10、50、100和200微摩尔）的锌，以研究镉与锌的相互作用。10微摩尔浓度的镉会降低硫醇含量，分别增强抗坏血酸（AsA）和谷胱甘肽（GSH）氧化为脱氢抗坏血酸（DHA）和谷胱甘肽二硫化物（GSSG），这是氧化应激的明显迹象。向镉（10微摩尔）处理的植物中补充锌可有效恢复硫醇含量，抑制AsA和GSH的氧化，使氧化还原分子保持还原形式。10微摩尔镉轻微诱导抗坏血酸过氧化物酶（APX，E.C. 1.11.1.11），但抑制单脱氢抗坏血酸还原酶（MDHAR，E.C. 1.6.5.4）、脱氢抗坏血酸还原酶（DHAR，E.C. 1.8.5.1）和谷胱甘肽还原酶（GR，E.C. 1.6.4.2），这些都是抗坏血酸-谷胱甘肽循环（AGC）的酶。补充锌可恢复并增强所有AGC酶（APX、MDHAR、DHAR和GR）的功能活性。γ-谷氨酰半胱氨酸合成酶（γ-GCS，E.C. 6.3.2.2）不受镉和锌的影响，但锌补充剂比镉更能提高谷胱甘肽-S-转移酶（GST，E.C. 2.5.1.18）的活性，并同时恢复因镉毒性而受损的谷胱甘肽过氧化物酶（GSH-PX，E.C. 1.11.1.9）的活性。单独的锌处理不会改变上述研究参数。这些结果清楚地表明了锌在通过抗氧化途径AGC和GSH代谢酶调节植物系统的氧化还原状态以对抗镉诱导的氧化应激方面的保护作用。
