目的：观察脑损伤后继发性肾脏自由基损害过程及其抗氧化酶的保护作用．方法：５０只成年雌雄各半Ｗｉｓｔａｒ大鼠，自由落体致伤造成重型颅脑损伤模型．用硫代巴比妥酸比色法，谷胱甘肽过氧化物酶（ＧＳＨｐｘ）活力测定法及铜锌超氧化物歧化酶（Ｃｕ／ＺｎＳＯＤ）放射免疫分析法检测正常对照组、伤后０５，６，２４，７２ｈ肾脏匀浆组织中脂质过氧化产物丙二醛（ＭＤＡ）和抗氧化酶ＧＳＨｐｘ，Ｃｕ／ＺｎＳＯＤ变化．结果：脑损伤后早期（０５ｈ）ＭＤＡ含量即增高（Ｐ＜００５），６，２４ｈ则显著增高（Ｐ＜００１）；ＧＳＨｐｘ和Ｃｕ／ＺｎＳＯＤ则均有所减少，以２４ｈ最为明显（Ｐ＜００１）．结论：脑损伤后继发性肾内自由基产生增多，抗氧化酶保护作用降低，可能是引起继发性肾损害的一个重要因素，也是临床早期使用抗氧化酶的理论依据之一． OBJECTIVE: To observe the process of secondary free radical damage and the protective effect of its antioxidant enzymes after brain injury. Methods: Fifty adult male and female Wistar rats were randomly divided into two groups. The normal control group was detected by thiobarbituric acid colorimetric assay, glutathione peroxidase (GSH-px) activity assay and copper-zinc superoxide dismutase (Cu / ZnSOD) radioimmunoassay. The changes of malondialdehyde (MDA) and antioxidant enzymes GSHpx and Cu / ZnSOD in the kidney homogenates at 05, 6, 24 and 72 hours after injury were observed. Results: The content of MDA increased (P <005) and increased significantly at 6 and 24 hours (P <001) in the early stage of brain injury (05 h), but decreased in both GSHpx and Cu / ZnSOD 24h most obvious (P <0  01). CONCLUSION: Increased production of secondary free radical in the kidney and decreased protection of antioxidant enzymes after brain injury may be one of the important factors that cause secondary renal damage. It is also one of the theoretical bases for early use of antioxidant enzymes.