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Plasmodium berghei Resists Killing by Reactive Oxygen Species

机译：伯氏疟原虫抵抗活性氧的杀灭

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Reactive oxygen species (ROS) are widely believed to kill malarial parasites. C57BL/6 mice injected with P. berghei inocula incubated with supraphysiological doses of NO (≤150 μM) or with peroxynitrite (220 μM), however, exhibited parasitemia similar to that seen with those given control inocula, and there was no difference in disease development. Only treatment of inocula with NO doses nearing saturation (≥1.2 mM) resulted in no detectable parasitemia in the recipients; flow cytometric analysis with a vital dye (hydroethidine) indicated that 1.5 mM NO lysed the erythrocytes rather than killing the parasites. The hemoglobin level in the inocula was about 8 μM; the hemoglobin was mainly oxyhemoglobin (oxyHb) (96%), which was converted to methemoglobin (>95%) after treatment with 150 μM NO. The concentrations of 150 μM of NO and 220 μM of peroxynitrite were far in excess of the hemoglobin concentration (～8 μM), and yet no parasite killing was detected. We therefore conclude that hemoglobin protects Plasmodium parasites from ROS, but the parasite likely possesses intrinsic defense mechanisms against ROS.
机译：人们普遍认为活性氧（ROS）可以杀死疟疾寄生虫。注射 P的C57BL / 6小鼠。与超生理剂量的NO（≤150μM）或过氧亚硝酸盐（220μM）孵育的伯氏菌接种物显示出与对照接种者相似的寄生虫血症，并且疾病发展没有差异。仅在NO剂量接近饱和（≥1.2mM）的情况下接种接种物，才能在接受者中检测不到寄生虫病。活体染料（氢乙啶）的流式细胞仪分析表明1.5 mM NO溶解红细胞而不是杀死寄生虫。接种物中的血红蛋白水平约为8μM;血红蛋白主要为氧合血红蛋白（oxyHb）（96％），经150μMNO处理后转化为高铁血红蛋白（> 95％）。 150μM的NO和220μM的过氧亚硝酸盐的浓度远远超过血红蛋白浓度（〜8μM），但未检测到寄生虫杀死。因此，我们得出的结论是，血红蛋白可以保护ROS免受

Plasmodium 寄生虫的侵害，但该寄生虫可能具有针对ROS的内在防御机制。

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