Serebrov V Iu, Kuz'menko D I, Burov P G, Sapugol'tseva O B
Biomed Khim. 2010 Mar-Apr;56(2):283-9.
Activity of key enzymes of a sphingomyelin cycle and the maintenance of its components (sphingomyelin, ceramide and sphingosine-1-phosphate) have been studied in livers of rats in dynamics of the acute toxic hepatitis caused by hypodermic introduction of an oil solution of CCl4. Sphingomyelinase activity significally increased already on early terms and remained increased over the whole period of observation. Activity of ceramidase insignificantly differed from the control level. The levels of sphingomyelin and sphingosine-1-phosphate did not undergo marked changes while ceramide content significally increased. Thus, balance between liver content of ceramide (proapoptotic) and the sphingosine-1-phosphate, being the antiapoptotic factor, was shifted towards ceramide. In sphingomyelin molecules there was a significant decrease in the content of fatty acids C18: and C22:2, while in ceramide molecules and sphingosine-1-phosphate only fatty acid C22:2 changed. In spite of significant decrease in content of some unsaturated fatty acids, calculated unsaturation coefficients of the fatty acid component of the sphingomyelin cycle metabolites. Thus, our results together with literature data suggests involvement of ceramide-mediated apoptosis in the pathogenesis of acute toxic hepatitis. Elimination of damaged hepatocytes facilitates realization of repair processes and optimization of cellular community of a liver.
在皮下注射四氯化碳油溶液所致急性中毒性肝炎动态过程中，对大鼠肝脏中鞘磷脂循环关键酶的活性及其成分（鞘磷脂、神经酰胺和鞘氨醇-1-磷酸）的维持情况进行了研究。鞘磷脂酶活性在早期就显著增加，并在整个观察期内持续升高。神经酰胺酶活性与对照水平无明显差异。鞘磷脂和鞘氨醇-1-磷酸水平未发生明显变化，而神经酰胺含量显著增加。因此，肝脏中神经酰胺（促凋亡）与作为抗凋亡因子的鞘氨醇-1-磷酸之间的平衡向神经酰胺方向偏移。在鞘磷脂分子中，C18:和C22:2脂肪酸含量显著降低，而在神经酰胺分子和鞘氨醇-1-磷酸中，只有C22:2脂肪酸发生了变化。尽管某些不饱和脂肪酸含量显著降低，但鞘磷脂循环代谢产物脂肪酸成分的计算不饱和系数并未改变。因此，我们的结果与文献数据共同表明，神经酰胺介导的细胞凋亡参与了急性中毒性肝炎的发病机制。清除受损肝细胞有助于修复过程的实现和肝脏细胞群落的优化。
