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原位大鼠肠道制剂对铝的摄取。

Aluminum uptake by the in situ rat gut preparation.

作者信息

Provan S D, Yokel R A

机构信息

College of Pharmacy, University of Kentucky, Lexington.

出版信息

J Pharmacol Exp Ther. 1988 Jun;245(3):928-31.

PMID:2455041
Abstract

An in situ rat gut preparation was used to elucidate the mechanisms of gastrointestinal aluminum (Al) absorption. Al uptake rate at the mucosal surface was decreased by the paracellular pathway blockers kinetin (1 mM) and 2,4,6-triaminopyrimidinium (10 mM), by sodium removal with choline substitution and by treatment with amiloride (1 mM), an epithelial sodium transport blocker. The rate of Al uptake was unchanged by 2,4-dinitrophenol (0.1 mM), 4-aminopyridine (0.1 mM, 0.5 mM) and verapamil (0.1 mM). The rate of Al uptake was increased from a medium containing no added calcium, a treatment which decreases resistance to flux in the paracellular pathway. These results suggest that gastrointestinal Al uptake occurs by an energy-independent, sodium-dependent, paracellular pathway-mediated process.

摘要

采用大鼠原位肠道制备法来阐明胃肠道铝(Al)吸收的机制。在黏膜表面,铝的摄取率因细胞旁途径阻滞剂激动素(1 mM)和2,4,6 - 三氨基嘧啶鎓(10 mM)、用胆碱替代去除钠以及用上皮钠转运阻滞剂氨氯吡脒(1 mM)处理而降低。铝的摄取率不受2,4 - 二硝基苯酚(0.1 mM)、4 - 氨基吡啶(0.1 mM、0.5 mM)和维拉帕米(0.1 mM)的影响。从不添加钙的培养基中摄取铝的速率增加,这种处理会降低细胞旁途径中的通量阻力。这些结果表明,胃肠道铝的摄取是通过能量非依赖性、钠依赖性、细胞旁途径介导的过程发生的。

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