Areekul S, Churdchu K, Thanomsak W, Pattanamatum S, Suphadtanaphongs V, Pojjiaroenanant C
Department of Tropical Radioisotopes, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
Southeast Asian J Trop Med Public Health. 1988 Dec;19(4):601-7.
It has already shown that catalase activity is significantly decreased in red cells of patients with P. falciparum. The mechanism suggested was by this enzyme inactivation through increased H2O2 generated during malarial infection. The present study was performed to verify this hypothesis. Catalase activities of red cells with high or low parasitemia in patients with P. falciparum were found to be lower than those of normal red cells. However, P. falciparum-infected red cells cultured for one week showed similar SOD and catalase levels to normal red cells. There was also no significant difference in the catalase levels between the parasitized and non-parasitized red cells. The difference in catalase activity of infected red cells before and after culture could be explained in terms of the activation of mononuclear cells and macrophages in vivo. During the sojourn of the parasitized red cells in close proximity to the macrophages of the spleen, they might trigger oxidative bursts resulting in increased H2O2. In order to protect themselves from oxidant damage, the catalase in the infected red cells could be inactivated by H2O2 resulting in the reduction of this enzyme.
已经表明，恶性疟原虫患者红细胞中的过氧化氢酶活性显著降低。提出的机制是，在疟疾感染期间产生的过氧化氢增加，导致该酶失活。本研究旨在验证这一假设。发现恶性疟原虫患者高或低疟原虫血症的红细胞中的过氧化氢酶活性低于正常红细胞。然而，培养一周的恶性疟原虫感染红细胞的超氧化物歧化酶和过氧化氢酶水平与正常红细胞相似。被寄生和未被寄生的红细胞之间的过氧化氢酶水平也没有显著差异。感染红细胞培养前后过氧化氢酶活性的差异可以用体内单核细胞和巨噬细胞的激活来解释。在被寄生的红细胞靠近脾脏巨噬细胞停留期间，它们可能引发氧化爆发，导致过氧化氢增加。为了保护自己免受氧化损伤，感染红细胞中的过氧化氢酶可能会被过氧化氢失活，从而导致该酶减少。
