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Vitamin E prevents the age-dependent and palmitate-induced disturbances of sphingolipid turnover in liver cells

机译:维生素E可防止年龄依赖性和棕榈酸酯诱导的肝细胞鞘脂代谢紊乱

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摘要

Sphingolipid turnover has been shown to be activated at old age and in response to various stress stimuli including oxidative stress. Reduction of vitamin E content in the liver under the pro-oxidant action is associated with enhanced sphingolipid turnover and ceramide accumulation in hepatocytes. In the present paper, the correction of sphingolipid metabolism in the liver cells of old rats and in the palmitate-treated young hepatocytes using α-tocopherol has been investigated. 3- and 24-month-old rats, [14 C]palmitic acid, [methyl−14 C-choline]sphingomyelin (SM), and [14 C]serine were used. α-Tocopherol administration to old rats or addition to the culture medium of old liver slices or hepatocytes prevented age-dependent increase of ceramide synthesis and lipid accumulation, and increased SM content in liver tissue and cells. α-Tocopherol treatment of old cells decreased the neutral and acid sphingomyelinase (SMase) activities in hepatocytes and serine palmitoyl transferase activity in the liver cell microsomes. Effect of α- or γ-tocopherol, but not of δ-tocopherol, on the newly synthesized ceramide content in old cells was correlated with the action of inhibitor of serine palmitoyl transferase (SPT) activity (myriocin) and SMase inhibitors (glutathione, imipramine). Addition of α-tocopherol as well as myriocin to the culture medium of young hepatocytes, treated by palmitate, abolished ceramide accumulation and synthesis. The data obtained demonstrate that α-tocopherol normalized elevated ceramide content in the old liver cells via inhibition of acid and neutral SMase activities and lipid synthesis de novo. α-Tocopherol, reducing ceramide synthesis, prevented palmitate-induced aging-like ceramide accumulation in young liver cells.
机译:鞘脂代谢被证明在年老时被激活并且响应包括氧化应激在内的各种应激刺激。在前氧化剂作用下肝脏中维生素E含量的减少与鞘脂代谢的增加和肝细胞中神经酰胺的积累有关。在本文中,已经研究了使用α-生育酚对老年大鼠肝细胞和经棕榈酸酯处理的年轻肝细胞中鞘脂代谢的校正。 3和24个月大的大鼠,[ 14 C]棕榈酸,[methyl- 14 C-胆碱]鞘磷脂(SM)和[ 14 使用C]丝氨酸。对老龄大鼠施用α-生育酚或在老肝切片或肝细胞的培养基中添加,可预防神经酰胺合成和脂质蓄积的年龄依赖性增加,并防止肝组织和细胞中SM含量增加。 α-生育酚处理旧细胞降低了肝细胞中性和酸性鞘磷脂酶(SMase)的活性,并降低了肝细胞微粒体中丝氨酸棕榈酰转移酶的活性。 α-或γ-生育酚对δ-生育酚的影响不大,而对旧细胞中新合成的神经酰胺含量的影响与丝氨酸棕榈酰转移酶(SPT)活性抑制剂(myriocin)和SMase抑制剂(谷胱甘肽,丙咪嗪)的作用有关。 )。经棕榈酸酯处理后,在年轻的肝细胞培养基中添加α-生育酚和myriocin可以消除神经酰胺的积累和合成。获得的数据表明,α-生育酚可通过抑制酸和中性SMase活性以及从头进行脂质合成来规范旧肝细胞中神经酰胺的含量升高。 α-生育酚减少了神经酰胺的合成,阻止了棕榈酸酯诱导的衰老样神经酰胺在年轻肝细胞中的积累。

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