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首页> 外文期刊>Biochemistry (Moscow). Supplement, Series B. Biomedical chemistry >A functional state of the sphingomyelin cycle and activity of free radical oxidation of rat liver lipids at different phases of starvation
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A functional state of the sphingomyelin cycle and activity of free radical oxidation of rat liver lipids at different phases of starvation

机译:饥饿不同时期大鼠鞘磷脂循环的功能状态和大鼠脂质的自由基氧化活性

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A functional state of the sphingomyeline cycle and its links with processes of free radical lipid oxidation have been investigated in rat liver during starvation of animals without any restriction of access to drinking water at day 1, 2, 3 (phase I) and day 6 (phase II of starvation). The maximal values of the ceramide/sphingomyelin ratio and activities of neutral sphingomyelinase and executive caspase-3 were found in rat livers at day 3 of starvation. Since day 3 of starvation an increase of tumour necrosis factor-α, one of neutral sphingomyelinase activators, was detected in serum. During the major part of phase I of starvation the intensity of liver free radical lipid peroxidation was comparable to that of control due to competent functioning of the antioxidant defense system. Transition of phase I to phase II of starvation (day 6 of the experiment) was accompanied by the development of oxidative stress associated with depletion of the antioxidant defense system. The results obtained in this study suggest that phase I of starvation favors realization of the ceramide-mediated proapoptotic signaling in the liver. In our viewpoint, ceramide-mediated apoptosis is one of mechanisms used optimization of liver cellular population within the frame of metabolic adaptation. In rat liver phase I of starvation was characterized by prevailing of the ceramide-mediated proapoptotic signaling, while in phase II oxidative stress dominated.
机译:在动物饥饿期间,在大鼠肝脏中研究了鞘磷脂循环的功能状态及其与自由基脂质氧化过程的联系,在第1、2、3天(I期)和第6天(没有任何限制地获得饮用水)(饥饿的第二阶段)。在饥饿的第3天,在大鼠肝脏中发现了神经酰胺/鞘磷脂比例的最大值以及中性鞘磷脂酶和执行胱天蛋白酶3的活性。自饥饿的第3天起,在血清中检测到肿瘤坏死因子-α(一种中性鞘磷脂酶激活剂)的增加。在饥饿的第一阶段的主要阶段,由于抗氧化剂防御系统的有效功能,肝脏自由基脂质过氧化的强度与对照的强度相当。从饥饿的I期到II期的过渡(实验的第6天)伴随着与抗氧化剂防御系统耗竭相关的氧化应激的发展。在这项研究中获得的结果表明,饥饿的第一阶段有利于在肝脏中实现神经酰胺介导的促凋亡信号传导。在我们看来,神经酰胺介导的细胞凋亡是在代谢适应性框架内优化肝细胞种群的机制之一。在大鼠肝中,饥饿的I期的特征是神经酰胺介导的促凋亡信号转导占主导,而在II期中,氧化应激占主导。

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