A noninducible cystine transport system in rat alveolar type II cells

• Published in: The American journal of physiology Vol. 268; no. 1 Pt 1; p. L21
• Main Authors: Bukowski, D M, Deneke, S M, Lawrence, R A, Jenkinson, S G
• Format: Journal Article
• Language: English
• Published: United States 01.01.1995
• Subjects: Animals; Arsenites - pharmacology; Biological Transport; Cattle; Cystine - metabolism; Endothelium, Vascular - cytology; Endothelium, Vascular - metabolism; Epithelial Cells; Epithelium - metabolism; Maleates - pharmacology; Pulmonary Alveoli - cytology; Pulmonary Alveoli - metabolism; Pulmonary Artery - cytology; Pulmonary Artery - metabolism; Rats; Rats, Sprague-Dawley
• ISSN: 0002-9513
• DOI: 10.1152/ajplung.1995.268.1.l21

Type II lung epithelial cells are different from other lung cell types in their means of processing and regulating intracellular glutathione (GSH) levels. In lung cell types, including endothelial cells, fibroblasts, smooth muscle cells, and macrophages, oxidants, sulfhydryl reagents, and electrophilic agents have been shown to induce cystine uptake and concomitantly increase GSH levels, suggesting that cysteine, formed by intracellular reduction of cystine, is a rate-limiting substrate for GSH synthesis. The cystine transport increase was reportedly due to increase in activity of a sodium-independent transport system designated xc-. We have now examined cultures of rat lung type II cells exposed to diethylmaleic acid and arsenite. Although a rise in cellular GSH occurred, cystine transport was not induced. Cystine transport in type II cells was found to differ from the xc- system previously described. Type II cell cystine transport is primarily sodium dependent and is inhibitable by aspartate as well as glutamate and homocysteate. We conclude that the type II cell differs from other lung cell types in both its cystine transport mechanism and method of GSH regulation.