Varani J, Ginsburg I, Gibbs D F, Mukhopadhyay P S, Sulavik C, Johnson K J, Weinberg J M, Ryan U S, Ward P A
Department of Pathology, University of Michigan, Ann Arbor.
Inflammation. 1991 Aug;15(4):291-301. doi: 10.1007/BF00917314.
Recent evidence indicates that under in vitro conditions, superoxide anion and hydrogen peroxide (H2O2) are unstable in the presence of manganese ion (Mn2+). The current studies show that in the presence of Mn2+, H2O2-mediated injury of endothelial cells is greatly attenuated. A source of bicarbonate ion and amino acid is required for Mn2+ to exert its protective effects. Injury by phorbol ester-activated neutrophils is also attenuated under the same conditions. EDTA reverses the protective effects. Acute lung injury produced in vivo in rats by intratracheal instillation of glucose-glucose oxidase is almost completely blocked in rats treated with Mn2+ and glycine. Conversely, treatment of rats with EDTA, a chelator of Mn2+, markedly accentuates lung injury caused by glucose-glucose oxidase. These data are consistent with the findings of others that Mn2+ can facilitate direct oxidation of amino acids with concomitant H2O2 disproportionation. This could form the basis of a new therapeutic approach against oxygen radical-mediated tissue injury.
最近有证据表明，在体外条件下，超氧阴离子和过氧化氢（H2O2）在锰离子（Mn2+）存在时不稳定。当前研究表明，在Mn2+存在时，H2O2介导的内皮细胞损伤会大大减轻。Mn2+发挥其保护作用需要碳酸氢根离子和氨基酸来源。在相同条件下，佛波酯激活的中性粒细胞造成的损伤也会减轻。乙二胺四乙酸（EDTA）会逆转这种保护作用。通过气管内滴注葡萄糖-葡萄糖氧化酶在大鼠体内产生的急性肺损伤，在用Mn2+和甘氨酸治疗的大鼠中几乎完全被阻断。相反，用Mn2+的螯合剂EDTA治疗大鼠，会明显加重由葡萄糖-葡萄糖氧化酶引起的肺损伤。这些数据与其他人的研究结果一致，即Mn2+可促进氨基酸的直接氧化并伴有H2O2歧化反应。这可能构成一种针对氧自由基介导的组织损伤的新治疗方法的基础。
