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首页> 外文期刊>Biochemistry >Ceramide interaction with the respiratory chain of heart mitochondria.
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Ceramide interaction with the respiratory chain of heart mitochondria.

机译：神经酰胺与心脏线粒体的呼吸链相互作用。

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A study is presented on the interaction of ceramide with the respiratory chain of rat heart mitochondria, and a comparison is made between the effects elicited by short- and long-chain ceramides. N-Acetylsphingosine (C(2)-ceramide) and N-palmitoylsphingosine (C(16)-ceramide) inhibited to the same extent the pyruvate+malate-dependent oxygen consumption. Succinate-supported respiration was also inhibited by ceramides, but this activity was substantially restored upon the addition of cytochrome c, which, on the contrary, was ineffective toward the ceramide-inhibited NADH-linked substrate oxidation. Direct measurements showed that short- and long-chain ceramides caused a large release of cytochrome c from mitochondria. The ceramide-dependent inhibition of pyruvate+malate and succinate oxidation caused reactive oxygen species to be produced at the level of either complex I or complex III. The activity of the cytochrome c oxidase, measured as ascorbate/TMPD oxidase activity, was significantly stimulated and inhibited by C(2)- and C(16)-ceramide, respectively. Similar effects were observed on the activity of the individual respiratory complexes isolated from bovine heart. Short- and long-chain ceramides had definitely different effects on the mitochondrial membrane potential. C(2)-ceramide caused an almost complete collapse of the respiration-dependent membrane potential, whereas C(16)-ceramide had a negligible effect. Similar results were obtained when the potential was generated in liposome-reconstituted complex III respiring at the steady-state. Furthermore, C(2)-ceramide caused a drop of the membrane potential generated by ATP hydrolysis instead of respiration, whereas C(16)-ceramide did not. Finally, only short-chain ceramides inhibited markedly the reactive oxygen species generation associated with membrane potential-dependent reverse electron flow from succinate to complex I. The emerging indication is that the short-chain ceramide-dependent collapse of membrane potential is a consequence of their ability to perturb the membrane structure, leading to an unspecific increase of its permeability.
机译：开展了关于神经酰胺与大鼠心脏线粒体呼吸链相互作用的研究，并比较了短链和长链神经酰胺引起的作用。 N-乙酰鞘氨醇（C（2）-神经酰胺）和N-棕榈酰鞘氨醇（C（16）-神经酰胺）抑制丙酮酸+苹果酸依赖的耗氧量相同。琥珀酸支持的呼吸也被神经酰胺抑制，但是这种活性在加入细胞色素c后基本上得以恢复，相反，它对神经酰胺抑制的NADH连接的底物氧化无效。直接测量表明，短链和长链神经酰胺引起线粒体细胞色素c大量释放。丙酮酸+苹果酸和琥珀酸氧化的神经酰胺依赖性抑制导致在复合物I或复合物III的水平产生活性氧。以抗坏血酸盐/ TMPD氧化酶活性衡量的细胞色素c氧化酶的活性分别被C（2）-和C（16）-神经酰胺显着刺激和抑制。对从牛心脏分离的单个呼吸复合物的活性观察到相似的作用。短链和长链神经酰胺对线粒体膜电位的影响肯定不同。 C（2）-神经酰胺引起呼吸依赖的膜电位几乎完全崩溃，而C（16）-神经酰胺的作用可忽略不计。当脂质体重构的复合物III在稳态呼吸时产生了电势时，获得了相似的结果。此外，C（2）-神经酰胺引起ATP水解而不是呼吸作用所产生的膜电位下降，而C（16）-神经酰胺则没有。最后，只有短链神经酰胺能显着抑制与琥珀酸到复合物I的膜电势依赖的反向电子流相关的活性氧的产生。新出现的迹象是，短链神经酰胺依赖的膜电势的崩溃是它们的结果。扰动膜结构的能力，导致其渗透性的非特异性增加。

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