Jones D P
Department of Biochemistry, Emory University, Atlanta, GA 30322, USA.
Biochim Biophys Acta. 1995 May 24;1271(1):29-33. doi: 10.1016/0925-4439(95)00006-p.
Mitochondrial function is closely linked to the maintenance of mitochondrial integrity. During short-term anoxia, ion-transport systems in the inner membrane are inhibited to protect against loss of the promotive force and associated osmotic imbalance that can cause irreversible loss of mitochondrial integrity and function. In two models of chemically induced mitochondrial failure, a prostaglandin B1 derivative, di-calciphor, protected against mitochondrial failure and prevented cell death. Characteristics were similar to those observed in mitochondria during short-term anoxia. Thus, the results indicate that di-calciphor may represent a new type of mitochondrial protectant that inhibits ion transport and thus slows the loss of osmotic stability and delays mitochondrial dysfunction under traumatic and toxicologic conditions.
线粒体功能与线粒体完整性的维持密切相关。在短期缺氧期间，内膜中的离子转运系统受到抑制，以防止促进力丧失和相关的渗透失衡，后者可导致线粒体完整性和功能的不可逆丧失。在两种化学诱导的线粒体功能衰竭模型中，一种前列腺素B1衍生物二钙磷保护线粒体功能衰竭并防止细胞死亡。其特征与短期缺氧期间线粒体中观察到的特征相似。因此，结果表明二钙磷可能代表一种新型的线粒体保护剂，它抑制离子转运，从而减缓渗透稳定性的丧失，并在创伤和毒理学条件下延迟线粒体功能障碍。
