Requirements of drug-induced endocytosis by intact human erythrocytes.
Requirements of drug-induced endocytosis by intact human erythrocytes.
复制标题
完整人红细胞药物诱导的内吞作用的要求。
DOI：
--
复制
发表时间：
1978
期刊：
影响因子：
--
通讯作者：
M. Johnson
中科院分区：
文献类型：
--
作者：
S. Schrier;I. Junga;J. Krueger;M. Johnson
完整人红细胞中药物诱导的内吞作用的研究继续为将膜功能（如内陷和融合）与红细胞能量学和质膜功能的其他决定因素（如Ca++）相关联提供了机会。报告的研究表明，即使在ATP严重耗竭的红细胞中，高浓度的长春碱和氯丙嗪也可产生内吞空泡，尽管数量减少。与此相反，伯氨喹诱导的内吞作用似乎肯定依赖于持久性的红细胞ATP商店。离子载体介导的Ca ~（++）进入红细胞增强伯氨喹的内吞作用，抑制长春碱的内吞作用，而对氯丙嗪的内吞作用没有规律性的影响。乳酸钠可能通过增加伯氨喹进入红细胞而增强伯氨喹的内吞作用。细胞松弛素B既不增强也不抑制红细胞内吞作用，从而表明红细胞中的微纤维或微纤维类似物不参与内吞作用。环核苷酸对内吞作用的抑制作用仅限于培养基中核苷酸的极高浓度范围。伯氨喹和氯丙嗪的内吞作用被环核苷酸抑制，长春碱的内吞作用也是如此。
Study of drug-induced endocytosis in intact human erythrocytes continues to provide an opportunity for correlating membrane functions such as invagination and fusion with erythrocytic energetics and other determinants of plasma membrane function like Ca++. The studies reported indicate that high concentrations of vinblastine and chlorpromazine can produce endocytic vacuoles, albeit in reduced amounts, even in severely ATP depleted erythrocytes. In contrast, primaquine-induced endocytosis seems definitely dependent upon persistence of erythrocytic ATP stores. The ionophore mediated entry of Ca++ into erythrocytes potentiates primaquine endocytosis, inhibits vinblastine endocytosis, and has no regular effect on chlorpromazine endocytosis. Sodium lactate enhances primaquine endocytosis, probably by causing an increase in the entry of primaquine into erythrocytes. Cytochalasin B neither enhances nor inhibits erythrocytic endocytosis, thereby suggesting that microfibrils or analogues of microfibrils in erythrocytes are not involved in endocytosis. Cyclic nucleotide inhibition of endocytosis is confined to a very high concentration range of nucleotides in the medium. Primaquine and chlorpromazine endocytosis are inhibited by cyclic nucleotides as is vinblastine endocytosis.