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正常小鼠和感染疟疾小鼠血液中维生素C的氧化还原代谢

Redox metabolism of vitamin C in blood of normal and malaria-infected mice.

作者信息

Iheanacho E N, Stocker R, Hunt N H

机构信息

Department of Pathology, University of Sydney, Australia.

出版信息

Biochim Biophys Acta. 1993 Aug 4;1182(1):15-21. doi: 10.1016/0925-4439(93)90147-s.

DOI:10.1016/0925-4439(93)90147-s
PMID:8347682
Abstract

As oxidative mechanisms have been suggested to be part of the host immune reaction against malarial parasites, we investigated the redox metabolism of the antioxidant vitamin C in the blood of control and malaria-infected mice. At the peak of infection (day 6) with the malaria parasite P. vinckei, plasma levels of ascorbate (AH-) were 10.8 +/- 0.9 micrograms/ml compared to 5.7 +/- 0.7 micrograms/ml in control mice, though no significant change was observed in the plasma concentration of dehydroascorbate (DHA). The plasma redox ratio of vitamin C, [AH-]:[DHA], was 7.4 in control mice and 18.5 in infected mice on day 6 post-inoculation. The increased AH- level in plasma of P. vinckei-infected mice was not due to differences in stabilities of either AH- or DHA in plasmas from control or P. vinckei-infected mice. DHA added to plasma was lost rapidly. In contrast, when added to whole blood. DHA was rapidly taken up and reduced to AH by blood cells from both normal mice and P. vinckei-infected mice. Most of the intracellular AH- derived from the exogenously added DHA was released into the plasma by blood cells from the infected but not normal mice. The observed release of AH- into the plasma by blood cells from infected mice was not caused by a plasma factor. Depletion of leukocytes from erythrocytes had no effect on the uptake and reduction of DHA by red blood cells, but the subsequent release of intracellular AH- occurred more rapidly.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

由于氧化机制被认为是宿主针对疟原虫的免疫反应的一部分,我们研究了对照小鼠和感染疟疾小鼠血液中抗氧化维生素C的氧化还原代谢。在用文氏疟原虫感染的高峰期(第6天),感染小鼠血浆中抗坏血酸盐(AH-)水平为10.8±0.9微克/毫升,而对照小鼠为5.7±0.7微克/毫升,不过脱氢抗坏血酸盐(DHA)的血浆浓度未观察到显著变化。接种后第6天,对照小鼠维生素C的血浆氧化还原比[AH-]:[DHA]为7.4,感染小鼠为18.5。文氏疟原虫感染小鼠血浆中AH-水平升高并非由于对照小鼠或感染小鼠血浆中AH-或DHA稳定性的差异。添加到血浆中的DHA迅速消失。相反,添加到全血中时,DHA被正常小鼠和文氏疟原虫感染小鼠的血细胞迅速摄取并还原为AH-。外源性添加的DHA衍生的大部分细胞内AH-由感染小鼠而非正常小鼠的血细胞释放到血浆中。观察到感染小鼠的血细胞将AH-释放到血浆中并非由血浆因子引起。从红细胞中去除白细胞对红细胞摄取和还原DHA没有影响,但随后细胞内AH-的释放发生得更快。(摘要截短于250字)

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