Agrawal Anju
Division of Biochemistry, Central Drug Institute Lucknow.
J Commun Dis. 2005 Mar;37(1):44-50.
Human cerebral malaria is caused by a protozoan parasitic with no cure till date. The isolation of brain capillaries i.e. microvessels has permitted the in vitro study related to cerebral function. Microvessels were isolated from normal and P. yoelii infected mice brain cortex and subjected to biochemical characterization by the following enzyme markers viz alkaline phosphatase, gamma-glutamyI transpeptidase and monoamine oxidase and electron microscopically. Limited studies have been carried out in relation to drug metabolizing enzymes in cerebral microvessels of rodents. The present studies have been carried out in relation to status of drug metabolizing enzymes during P. yoelii infection in cerebral microvessels of mice. The data obtained depicted a clear cut impairment of cytochrome P450 (a terminal monooxygenase) and related indices viz b5, benzopyrene hydroxylase, aminopyrene-n-demethylase, aniline hydroxylase except NADH cytochrome e reductase which increased during P. yoelii infection in mice as compared to normal. Further the oral drug administration (arteether) treatment brought back the altered MFO system normal a week alter cessation of drug treatment.
人类脑型疟疾由一种原生动物寄生虫引起，至今仍无治愈方法。脑毛细血管即微血管的分离使得与脑功能相关的体外研究成为可能。微血管从正常和感染约氏疟原虫的小鼠脑皮质中分离出来，并通过以下酶标记物进行生化表征，即碱性磷酸酶、γ-谷氨酰转肽酶和单胺氧化酶，并进行电子显微镜观察。关于啮齿动物脑微血管中药物代谢酶的研究有限。目前的研究是关于小鼠脑微血管中约氏疟原虫感染期间药物代谢酶的状态。所获得的数据显示，细胞色素P450（一种末端单加氧酶）及相关指标即b5、苯并芘羟化酶、氨基芘-N-脱甲基酶、苯胺羟化酶明显受损，除了NADH细胞色素e还原酶，与正常相比，其在小鼠约氏疟原虫感染期间增加。此外，口服药物（蒿乙醚）治疗在停药一周后使改变的混合功能氧化酶系统恢复正常。
