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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Introduction of an additional pathway for lactate oxidation in the treatment of lactic acidosis and mitochondrial dysfunction in Caenorhabditis elegans.
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Introduction of an additional pathway for lactate oxidation in the treatment of lactic acidosis and mitochondrial dysfunction in Caenorhabditis elegans.

机译：引入另一种乳酸氧化途径来治疗秀丽隐杆线虫的乳酸性酸中毒和线粒体功能障碍。

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摘要

Mitochondrial dysfunction, with an estimated incidence of 1 in 5,000 births, is associated with a wide variety of multisystem degenerative diseases. Among the most prevalent forms of dysfunction are defects in the NADH:ubiquinone oxidoreductase (complex I). Caenorhabditis elegans strains with complex I mutations exhibit characteristic features of human mitochondrial disease including decreased rates of respiration and lactic acidosis. We hypothesized that introducing an additional pathway for the direct oxidation of lactate would be beneficial for energy metabolism. The yeast CYB2 gene encodes an L-lactate:cytochrome c oxidoreductase that oxidizes lactate, donates electrons directly into the mitochondrial respiratory chain, and supports lactate-dependent respiration. Cyb2p expression markedly increases lifespan, fertility, respiration rates, and ATP content in complex I-deficient animals. Our results indicate that metabolic imbalance leading to lactic acidosis and energy depletion are central mechanisms of pathogenesis in mitochondrial dysfunction and that introduction of an additional pathway for lactate oxidation should be considered as a treatment.
机译：线粒体功能障碍估计有5,000例新生儿中有1例发生，与多种多系统退行性疾病相关。功能障碍的最普遍形式是NADH：泛醌氧化还原酶（复合体I）的缺陷。具有复杂I突变的秀丽隐杆线虫菌株表现出人类线粒体疾病的特征，包括呼吸频率降低和乳酸性酸中毒。我们假设为乳酸的直接氧化引入额外的途径将有益于能量代谢。酵母CYB2基因编码一个L-乳酸：细胞色素C氧化还原酶，该酶氧化乳酸，将电子直接捐赠给线粒体呼吸链，并支持乳酸依赖性呼吸。 Cyb2p的表达显着增加了复杂I缺陷动物的寿命，生育力，呼吸频率和ATP含量。我们的结果表明，导致乳酸性酸中毒和能量消耗的代谢失衡是线粒体功能障碍发病机理的主要机制，因此应考虑引入其他途径进行乳酸氧化作为治疗方法。

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