Ayi K, Cappadoro M, Branca M, Turrini F, Arese P
Dipartimento di Genetica, Biologia e Biochimica, Università di Torino, Turin, Italy.
FEBS Lett. 1998 Mar 13;424(3):257-61. doi: 10.1016/s0014-5793(98)00185-9.
Plasmodium falciparum parasites grew normally in glutathione (GSH)-depleted normal and G6PD-deficient (Mediterranean variant) erythrocytes (RBC). Growth inhibition was observed only at less than approximately 6-12% residual GSH. Parasites studied separately with the Sendai virus technique synthesized GSH de novo and regenerated reduced GSH 10-20 times faster than non-parasitized RBC. Electron spin resonance measurement of Tempol reduction indicated that the ability to reduce free radicals was restricted to the parasite. The marked efflux of oxidized GSH was mainly derived from the parasite. In conclusion, parasites are endowed with powerful and host-independent mechanisms which de novo synthesize or regenerate GSH and allow undisturbed parasite development in GSH-depleted RBC.
恶性疟原虫在谷胱甘肽（GSH）耗竭的正常红细胞和葡萄糖-6-磷酸脱氢酶（G6PD）缺乏（地中海变异型）红细胞中生长正常。仅在残余GSH低于约6%-12%时才观察到生长抑制。用仙台病毒技术单独研究的寄生虫能从头合成GSH，其还原型GSH的再生速度比未感染寄生虫的红细胞快10-20倍。电子自旋共振测量Tempol还原表明，自由基还原能力仅限于寄生虫。氧化型GSH的显著外流主要源自寄生虫。总之，寄生虫具有强大且不依赖宿主的机制，可从头合成或再生GSH，并能在GSH耗竭的红细胞中不受干扰地发育。
