A possible role for plasmalogens in protecting animal cells against photosensitized killing.
A possible role for plasmalogens in protecting animal cells against photosensitized killing.
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DOI：
10.1016/s0021-9258(18)38000-1
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发表时间：
1988-08
期刊：
影响因子：
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通讯作者：
Photosensitized Killing;Raphael;-A.;ZoellerS;Olivier;-H.;MorandQ;Christian R. H Raetzll
中科院分区：
文献类型：
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作者：
Photosensitized Killing;Raphael;-A.;ZoellerS;Olivier;-H.;MorandQ;Christian R. H Raetzll
中国仓鼠卵巢(CHO)细胞在膜脂中掺入12-(1‘-芘)十二酸(P12)。P12标记的细胞暴露在长波紫外线下会导致细胞死亡，这可能是因为芘部分(一种光敏剂)的激发导致了活性氧物种的产生。细胞毒性取决于用于标记细胞的P12的浓度、紫外线照射的时间以及照射期间氧气的存在。缺乏血浆蛋白原生物合成和过氧化体组装的CHO突变细胞(Zoeller，R.A.和Raetz，C.R.H.(1986)过程。娜塔莉。阿卡德。SCI。美国83,5170-5174)对P12/UV处理的敏感性比野生型细胞高几个数量级，允许在1×10(4)突变细胞中直接选择一个野生型细胞。导致这些突变体对P12/UV过敏的一个主要因素似乎是缺乏血浆原。向突变体添加1-O-十六烷基-sn-甘油可恢复血浆蛋白原水平，并恢复对P12/UV处理的几乎正常的抗性，而过氧化体的生物发生不能恢复。P12/UV突变体的P12/UV敏感性，以及P12/UV诱导的野生型细胞中血浆原的选择性分解，在随附的手稿中记录下来，表明血浆原的乙烯基醚连接在保护动物细胞膜免受某些氧化应激中起着直接作用。
Chinese hamster ovary (CHO) cells incorporate 12-(1′-pyrene) dodecanoic acid (P12) into membrane lipids. Exposure of P12-labeled cells to long wavelength ultraviolet light causes cell killing, presumably because excitation of the pyrene moiety (a photosensitizer) leads to the generation of reactive oxygen species. Cytotoxicity is dependent upon the concentration of P12 used to label the cells, and time of UV exposure, and the presence of oxygen during irradiation. CHO mutant cells deficient in plasmalogen biosynthesis and peroxisome assembly (Zoeller, R.A., and Raetz, C.R.H. (1986) Proc. Natl. Acad. Sci. U.S.A. 83, 5170-5174) are several orders of magnitude more sensitive to P12/UV treatment than wild-type cells, permitting direct selection of one wild-type cell in 1 X 10(4) mutant cells. A major factor responsible for the P12/UV hypersensitivity of these mutants appears to be the absence of plasmalogens. Supplementation of the mutants with 1-O-hexadecyl-sn-glycerol restores plasmalogen levels and nearly normal resistance to P12/UV treatment, whereas the biogenesis of peroxisomes is not restored. The P12/UV hypersensitivity of the plasmalogen-deficient mutants, together with the selective, P12/UV-induced decomposition of plasmalogens in wild-type cells, documented in the accompanying manuscript, suggest that the vinyl ether linkage of plasmalogens plays a direct role in protecting animal cell membranes against certain oxidative stresses.