N-亚硝基二乙胺对大鼠急性毒性中的肝脏和肾脏氧化应激
Hepatic and renal oxidative stress in acute toxicity of N-nitrosodiethylamine in rats.
作者信息
Bansal A K, Trivedi R, Soni G L, Bhatnagar D
机构信息
Department of Biochemistry, Govt. Medical College, Patiala 147 001, India.
出版信息
Indian J Exp Biol. 2000 Sep;38(9):916-20.
Nitrosoamines such as N-nitrosodiethylamine (NDEA) produce oxidative stress due to generation of reactive oxygen species and may alter antioxidant defence system in the tissues. NDEA was administered ip as a single dose to rats in LD50 or in lower amounts and the animals were sacrificed after 0-48 hr of treatment. The results showed that lipid peroxidation in liver increased, however no significant increase in kidney LPO was observed after NDEA administration. Superoxide dismutase (SOD) and glutathione reductase (GSH-R) activity increased in liver, however, catalase (CAT) activity in liver was inhibited in NDEA treated rats. Kidney showed an increase in SOD activity after an initial decrease along with increase in GSH-R activity in NDEA treated rats. However, kidney CAT activity was not significantly altered in NDEA intoxicated rats. Serum transaminases, serum alkaline phosphatase blood urea nitrogen, serum creatinine and scrum proteins were elevated in NDEA treated rats. The results indicate NDEA-induced oxidative stress and alteration in antioxidant enzymes in liver and kidney to neutralise oxidative stress.
亚硝基胺类物质，如N-亚硝基二乙胺（NDEA），会因活性氧的产生而导致氧化应激，并可能改变组织中的抗氧化防御系统。以LD50剂量或更低剂量给大鼠腹腔注射NDEA，单次给药后在0至48小时处死动物。结果显示，肝脏中的脂质过氧化增加，然而，给予NDEA后未观察到肾脏脂质过氧化有显著增加。肝脏中超氧化物歧化酶（SOD）和谷胱甘肽还原酶（GSH-R）活性增加，但是，在接受NDEA处理的大鼠中，肝脏中的过氧化氢酶（CAT）活性受到抑制。在接受NDEA处理的大鼠中，肾脏在最初下降后SOD活性增加，同时GSH-R活性也增加。然而，在NDEA中毒的大鼠中，肾脏CAT活性没有显著改变。接受NDEA处理的大鼠血清转氨酶、血清碱性磷酸酶、血尿素氮、血清肌酐和血清蛋白升高。结果表明，NDEA诱导氧化应激，并使肝脏和肾脏中的抗氧化酶发生改变以中和氧化应激。
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