Effect of nifedipine on oxidative damage of erythrocytes in Plasmodium berghei-infected mice.
Effect of nifedipine on oxidative damage of erythrocytes in Plasmodium berghei-infected mice.
复制标题
硝苯地平对伯氏疟原虫感染小鼠红细胞氧化损伤的影响。
DOI：
10.1006/clin.1993.1175
复制
发表时间：
1993
期刊：
影响因子：
--
通讯作者：
R. Mahajan
中科院分区：
文献类型：
--
作者：
K. Mohan;M. Dubey;N. Ganguly;A. Kalra;R. Mahajan
钙离子通道阻滞剂硝苯地平能抑制伯氏疟原虫感染小鼠吞噬细胞的氧化爆发。在不同的寄生虫负荷与未处理的小鼠相比，在硝苯地平治疗的小鼠的感染和膜脂质过氧化反应的过程中看到的免疫病理变化的程度进行了检查。还在这些动物中研究了谷胱甘肽抗氧化系统，以评估其中和感染红细胞中活性氧（ROS）的能力。硝苯地平治疗的感染小鼠的存活期显著缩短。据观察，还原型谷胱甘肽的积累更大，谷胱甘肽过氧化物酶活性的下降是不太明显的药物治疗的动物，这表明更好地保护寄生虫免受氧化损伤。脂质过氧化产物丙二醛的积累显着降低硝苯地平治疗的动物在所有寄生虫血症水平的研究，表明减少ROS的产生和寄生虫的损害。这些观察结果揭示了使用CCB逆转疟疾中氯喹抗性的缺点，因为这将使寄生红细胞的氧化损伤和吞噬细胞介导的寄生虫杀伤最小化。
It is known that the calcium channel blocker (CCB), nifedipine, can inhibit phagocyte oxidative burst in Plasmodium berghei-infected mice. The extent of immunopathological changes as seen by the course of infection and membrane lipid peroxidation in nifedipine-treated mice was examined in comparison with untreated mice at different parasite loads. The glutathione antioxidant system was also studied in these animals to assess its capacity to neutralize reactive oxygen species (ROS) in infected erythrocytes. The survival period of nifedipine-treated, infected mice decreased significantly. It was observed that the accumulation of reduced glutathione was greater and the decrease in glutathione peroxidase activity was less marked in drug-treated animals, suggesting better protection of the parasites against oxidative injury. The accumulation of the lipid peroxidation product, malonyldialdehyde was significantly lower in nifedipine-treated animals at all parasitemia levels studied, indicating decreased ROS generation and parasite damage. These observations reveal the shortcomings of using CCB to reverse the chloroquine resistance in malaria as this would minimize oxidative damage of parasitized red cells and phagocyte-mediated parasite killing.