Relationship between cellular calcium and vitamin E metabolism during protection against cell injury.
Relationship between cellular calcium and vitamin E metabolism during protection against cell injury.
复制标题
细胞钙和维生素 E 代谢在防止细胞损伤过程中的关系。
DOI：
10.1016/0003-9861(87)90181-0
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发表时间：
1987
影响因子：
3.9
通讯作者：
Reed,DJ
中科院分区：
文献类型：
--
作者：
Pascoe,GA;Reed,DJ
先前已证明，化学诱导的对分离的下红细胞的损伤程度取决于细胞中α-生育酚的含量，其水平受细胞外钙浓度的影响。钙对非化学暴露细胞α-生育酚含量影响的研究表明，在钙缺乏培养基中孵育分离的肝细胞可使细胞钙含量降至初始水平的10%，并导致内源性α-生育酚耗竭。α-生育酚的这种损失不能通过α-生育酚醌的形成来解释。在细胞孵育培养基中补充α-生育酚琥珀酸酯后，细胞钙含量降低与细胞α-生育酚水平高于钙充足细胞相关。这是钙耗竭细胞中生育酚酯的细胞内水解增加的结果，而不是细胞外钙浓度对α-生育酚琥珀酸酯摄入细胞或酯的细胞外水解的影响。摄取研究表明，与α-生育酚孵育后，肝细胞中α-生育酚的可达到水平远高于α-生育酚酯。这些数据为以下假设提供了实质性支持：细胞外钙含量本身不是肝细胞毒性损伤的决定因素，但细胞钙含量影响α-生育酚及其酯的细胞内代谢，这可能随后控制毒性挑战的结果。
The extent of chemically induced injury to isolated hypatocytes has been previously shown to depend on the content of α-tocopherol in the cells, the levels of which are influenced by the concentration of extracellular calcium. Investigations into the effect of calcium on the α-tocopherol content of nonchemically exposed cells demonstrated that incubation of isolated hepatocytes in a calcium-deficient medium decreased cell calcium content to 10% of initial levels, and resulted in the depletion of endogenous α-tocopherol. This loss in α-tocopherol was not accounted for by α-tocopherylquinone formation. After supplementation of the cell incubation medium with α-tocopheryl succinate, the decreased cell calcium content was associated with higher levels of cellular α-tocopherol than in calcium-adequate cells. This was the result of greater intracellular hydrolysis of the tocopheryl ester in the calcium-depleted cells, and not an effect of extracellular calcium concentration on the uptake of α-tocopheryl succinate into the cells or on the extracellular hydrolysis of the ester. Uptake studies indicated a much greater achievable level of α-tocopherol in hepatocytes after incubation with α-tocopherol than with the α-tocopheryl ester. These data provide substantial support for the hypotheses that the content of extracellular calcium per se is not the determinant in toxic injury to hepatocytes, but that cell calcium content affects the intracellular metabolism of α-tocopherol and its esters, which may subsequently govern the outcome of a toxic challenge.