Choudhary D, Chandra D, Kale R K
School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Toxicol Lett. 1997 Dec;93(2-3):141-52. doi: 10.1016/s0378-4274(97)00087-8.
The effect of different doses of methylglyoxal (50-400 mg/kg body wt.) were examined using enzymes involved in the antioxidant function, glutathione (GSH) content and lipid peroxidation in the liver and spleen of Swiss albino mice (7-8 week old) after 6, 12 and 24 h. Significant changes were observed predominantly in the liver. The specific activities of superoxide dismutase (SOD), glutathione-S-transferase (GST), catalase, glyoxalase I (gly I) and glyoxalase II (gly II) were found to decrease in the liver. The mode and magnitude of change in the specific activities was seen to depend on the dose of methylglyoxal and the time after its administration. Methylglyoxal also decreased the GSH content and enhanced the lipid peroxidation in the liver. These findings are suggestive of the adverse effect of methylglyoxal on the antioxidant defence system. It is likely that methylglyoxal undergoes a redox cycle and generates the free radicals which in turn lower the antioxidant status in animals. The increased levels of lipid peroxidation provide support for the involvement of free radical processes in the detrimental effects of methylglyoxal. The response of DT-diaphorase (DTD) seems to be adaptive.
研究了不同剂量的甲基乙二醛(50 - 400毫克/千克体重)对7 - 8周龄瑞士白化小鼠肝脏和脾脏中参与抗氧化功能的酶、谷胱甘肽(GSH)含量及脂质过氧化作用的影响,观察时间为给药后6、12和24小时。主要在肝脏中观察到显著变化。发现肝脏中超氧化物歧化酶(SOD)、谷胱甘肽 - S - 转移酶(GST)、过氧化氢酶、乙二醛酶I(gly I)和乙二醛酶II(gly II)的比活性降低。比活性变化的方式和幅度取决于甲基乙二醛的剂量及其给药后的时间。甲基乙二醛还降低了肝脏中的GSH含量并增强了脂质过氧化作用。这些发现提示甲基乙二醛对抗氧化防御系统有不良影响。甲基乙二醛可能经历氧化还原循环并产生自由基,进而降低动物体内的抗氧化状态。脂质过氧化水平的升高为自由基过程参与甲基乙二醛的有害作用提供了支持。DT - 黄递酶(DTD)的反应似乎具有适应性。