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沙蠋线粒体中的硫化物氧化。替代电子途径的证据。

Mitochondrial sulfide oxidation in Arenicola marina. Evidence for alternative electron pathways.

作者信息

Völkel S, Grieshaber M K

机构信息

Institut für Zoophysiologie, Lehrstuhl für Stoffwechselphysiologie, Heinrich-Heine-Universität, Düsseldorf, Germany.

出版信息

Eur J Biochem. 1996 Jan 15;235(1-2):231-7. doi: 10.1111/j.1432-1033.1996.00231.x.

DOI:10.1111/j.1432-1033.1996.00231.x
PMID:8631334
Abstract

Sulfide is oxidized in the mitochondria of the lugworm Arenicola marina. Mitochondrial sulfide oxidation is coupled with oxygen consumption and with an equimolar production of thiosulfate [Völkel, S. & Grieshaber, M. K. (1994) Mar. Biol. 118, 137-147]. Mitochondrial respiration in the presence of malate (or succinate) and ADP but without sulfide could be completely inhibited by rotenone, antimycin, cyanide, and sulfide. Only 40% inhibition was achieved by salicylhydroxamic acid. Sulfide oxidation (with sulfide as the only substrate) was fully inhibited by antimycin and by salicylhydroxamic acid but not by rotenone or sulfide. Moreover, sulfide oxidation was 3-4-fold less sensitive to cyanide as compared to normal respiration. The data indicate that sulfide oxidation in A. marina is linked to the respiratory electron transport chain. We suggest that electrons from sulfide enter the respiratory chain via ubiquinone or at the ubiquinol-cytochrome-c oxidoreductase. At sulfide concentrations higher than 10 microM, the cytochrome-c oxidase is blocked and electrons from sulfide are transferred to oxygen via an alternative terminal oxidase.

摘要

硫化物在沙蠋(Arenicola marina)的线粒体中被氧化。线粒体硫化物氧化与氧气消耗以及硫代硫酸盐的等摩尔生成相关联[Völkel, S. & Grieshaber, M. K. (1994) 《海洋生物学》118, 137 - 147]。在存在苹果酸(或琥珀酸)和ADP但不存在硫化物的情况下,线粒体呼吸可被鱼藤酮、抗霉素、氰化物和硫化物完全抑制。水杨羟肟酸仅能实现40%的抑制。硫化物氧化(以硫化物作为唯一底物)可被抗霉素和水杨羟肟酸完全抑制,但不受鱼藤酮或硫化物抑制。此外,与正常呼吸相比,硫化物氧化对氰化物的敏感性低3 - 4倍。数据表明沙蠋中的硫化物氧化与呼吸电子传递链相关。我们认为来自硫化物的电子通过泛醌或在泛醇 - 细胞色素 - c氧化还原酶处进入呼吸链。在硫化物浓度高于10微摩尔时,细胞色素 - c氧化酶被阻断,来自硫化物的电子通过一种替代末端氧化酶转移至氧气。

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