Rhoda M D, Apovo M, Beuzard Y, Giraud F
INSERM CIF 8814, Centre hospitalier, Pointe-à-Pitre, Guadeloupe, France.
Blood. 1990 Jun 15;75(12):2453-8.
Deoxygenation of sickle cells is known to increase cation permeabilities (Na+, K+, and Ca2+). The possible mechanisms involved in the increased uptake of Ca2+ were investigated: activation of Ca2+ channels, involvement of the anion channel, and the formation of endocytic vacuoles. The Ca2+ channel blocker nifedipine reduced the deoxy-stimulated Ca2+ uptake by about 30% to 40%. The anion channel inhibitor DIDS (4,4' diisothiocyanate stilbene 2,2' disulfonate) inhibited the deoxy-stimulated Ca2+ uptake by approximately 50%. Maximal possible endocytic uptake, measured by using an impermeant marker ([3H] inuline), accounted for 6% to 9% of the total Ca2+ uptake. These data indicate that the deoxygenation-induced increase in Ca2+ permeability could result from both the activation of a Ca2+ channel and of a transport system for cations involving interactions between polymerized hemoglobin S, band 3 and other membrane components. Endocytosis appears to play only a minor role in the Ca2+ uptake of deoxygenated sickle cells.
已知镰状细胞的脱氧会增加阳离子通透性（Na⁺、K⁺和Ca²⁺）。对Ca²⁺摄取增加可能涉及的机制进行了研究：Ca²⁺通道的激活、阴离子通道的参与以及内吞泡的形成。Ca²⁺通道阻滞剂硝苯地平使脱氧刺激的Ca²⁺摄取减少了约30%至40%。阴离子通道抑制剂DIDS（4,4'-二异硫氰酸根合芪-2,2'-二磺酸盐）抑制脱氧刺激的Ca²⁺摄取约50%。通过使用非渗透性标记物（[³H]菊粉）测量的最大可能内吞摄取占总Ca²⁺摄取的6%至9%。这些数据表明，脱氧诱导的Ca²⁺通透性增加可能是由于Ca²⁺通道的激活以及涉及聚合血红蛋白S、带3和其他膜成分之间相互作用的阳离子转运系统的激活。内吞作用在脱氧镰状细胞的Ca²⁺摄取中似乎仅起次要作用。
