Mishra N C, Kabilan L, Sharma A
Malaria Research Centre, Delhi, India.
Indian J Malariol. 1994 Jun;31(2):77-87.
This paper presents several mechanisms/pathways by which oxidative stress could cause damage to the parasites. During developmental stages of plasmodia profound alterations of the structure and function of host erythrocytes take place, in order to support the development and/or survival of the parasite. In addition an oxidant stress is also induced by the parasite. There is also an increased production of reactive oxygen species (ROS) by the parasite. This may deplete the erythrocyte of its defense mechanisms namely, superoxide dismutase (SOD), catalase, glutathione peroxidase, NADPH, NADH, glutathione (GSH) and glutathione reductase etc. Thus oxidative stress may be exerted by the growing parasite in red blood cells which are highly sensitive to such a challenge. These enhanced alterations may result in a retarded development of the parasite. Thus, the coexistence of both parasite and erythrocyte is a matter of a delicate balance. However, one cannot rule out the role of external modulations (immune pressure) inhibiting the vitality of the parasites.
本文介绍了氧化应激可能对寄生虫造成损害的几种机制/途径。在疟原虫的发育阶段，宿主红细胞的结构和功能会发生深刻改变，以支持寄生虫的发育和/或存活。此外，寄生虫还会诱导氧化应激。寄生虫产生的活性氧（ROS）也会增加。这可能会耗尽红细胞的防御机制，即超氧化物歧化酶（SOD）、过氧化氢酶、谷胱甘肽过氧化物酶、NADPH、NADH、谷胱甘肽（GSH）和谷胱甘肽还原酶等。因此，生长中的寄生虫可能会在对这种挑战高度敏感的红细胞中施加氧化应激。这些增强的改变可能会导致寄生虫发育迟缓。因此，寄生虫和红细胞的共存是一个微妙的平衡问题。然而，不能排除外部调节（免疫压力）抑制寄生虫活力的作用。
