Volden G, Haugen H F, Skrede S
Arch Dermatol Res. 1980;268(3):225-30. doi: 10.1007/BF00404282.
Experimental blisters were produced with suction on normal human skin and simultaneously on skin inflamed after exposure to middle wave ultraviolet light. Total proteins and marker enzymes for the plasma membrane, cytosol, lysosomes, peroxisomes, mitochondria, and microsomes were assayed in the blister fluid. In blisters on erythematous skin, a large increase of lactate dehydrogenase from cytosol was noted. A small increase of the plasma membrane marker phosphodiesterase I and some increase of alpha-mannosidase from lysosomes was found. No significant increase in total proteins or in microsomal marker enzymes were not detectable. It is concluded that cutaneous cells to some extent may lose intracellular enzymes without visible signs of irreversible damage (necrosis), but that an UVB-induced injury/regeneration cycle probably explains the enzyme release.
在正常人体皮肤以及暴露于中波紫外线后发炎的皮肤上通过抽吸产生实验性水疱。对水疱液中的总蛋白以及质膜、胞质溶胶、溶酶体、过氧化物酶体、线粒体和微粒体的标记酶进行了测定。在红斑皮肤的水疱中,发现胞质溶胶中的乳酸脱氢酶大幅增加。质膜标记物磷酸二酯酶I略有增加,溶酶体中的α-甘露糖苷酶有所增加。未检测到总蛋白或微粒体标记酶有显著增加。得出的结论是,皮肤细胞在一定程度上可能会失去细胞内酶而没有不可逆损伤(坏死)的明显迹象,但紫外线B诱导的损伤/再生循环可能解释了酶的释放。