Schallreuter K U, Pittelkow M P
Department of Dermatology, University of Hamburg, FRG.
Arch Dermatol Res. 1988;280(3):137-9. doi: 10.1007/BF00456842.
45Ca2+ has been used to measure kinetics for the uptake, efflux, and "steady state" of this regulatory cation in keratinocytes grown from the involved and uninvolved skin of one donor (JM) with vitiligo. Cells grown from uninvolved skin yielded a very rapid uptake and efflux of this isotope before reaching "steady state". A similar profile has been found for keratinocytes from normal healthy adult controls. However, cells established from vitiliginous skin showed a slow uptake of 45Ca2+ before reaching the same "steady state" as the controls. 45Ca2+ efflux has not been observed in vitiliginous keratinocytes. Furthermore, vitiliginous keratinocytes yielded a higher concentration of extracellular bound 45Ca2+ compared with keratinocytes from uninvolved skin. Since Ca2+ has been found to be an allosteric inhibitor of membrane-associated thioredoxin reductase, this defect in Ca2+ transport may explain the proposed breakdown in free radical defense in vitiligo. These findings may also shed more light on the etiology of this disorder.
45Ca2+已被用于测量从一名白癜风患者（JM）的受累皮肤和未受累皮肤培养的角质形成细胞中这种调节性阳离子的摄取、流出和“稳态”动力学。从未受累皮肤培养的细胞在达到“稳态”之前对这种同位素的摄取和流出非常迅速。在正常健康成人对照组的角质形成细胞中也发现了类似的情况。然而，从白癜风皮肤建立的细胞在达到与对照组相同的“稳态”之前对45Ca2+的摄取较慢。在白癜风角质形成细胞中未观察到45Ca2+流出。此外，与未受累皮肤的角质形成细胞相比，白癜风角质形成细胞产生的细胞外结合45Ca2+浓度更高。由于已发现Ca2+是膜相关硫氧还蛋白还原酶的变构抑制剂，Ca2+转运的这种缺陷可能解释了白癜风中自由基防御的推测性破坏。这些发现也可能为这种疾病的病因提供更多线索。
