Detail of "19771-63-2"

Reference

L-2-oxothiazolidine-4-carboxylic acid protection against tridiphane toxicity

Correction of: L-2-oxothiazolidine-4-carboxylic acid protection against tridiphane toxicity. Hilton, James L.; Pillai, Parthasarathy (Agric. Res. Serv., U.S. Dep. Agric., Beltsville, MD 20705, USA). Weed Sci., 34(5), 669-75 (English) 1986. CODEN: WEESA6. ISSN: 0043-1745. DOCUMENT TYPE: Journal CA Section: 5 (Agrochemical Bioregulators) Tridiphane [58138-08-2] inhibited growth of corn (Zea mays), wheat (Triticum aestivum), and sorghum (Sorghum vulgare) in growth chamber expts. These inhibitions were partially circumvented by simultaneous treatment with L-2-oxothiazolidine-4-carboxylic acid (OTC) [19771-63-2]. Tridiphane, atrazine [1912-24-9], and OTC each increased levels of low mol. wt. thiols (glutathione [70-18-8]) in intact roots of treated corn seedlings, but only OTC did in excised roots. Tridiphane and atrazine caused a decrease in thiol content of excised roots. Tridiphane treatments reduced the amt. of glutathione S-transferase [50812-37-8] activity extractable from corn roots, and this redn. was circumvented partially by OTC applied in combination with tridiphane. Thus, tridiphane interference with cysteine or glutathione metab. can be reversed by increasing cellular content of cysteine [52-90-4].

Enhancement of intracellular glutathione protects endothelial cells against oxidant damage

Enhancement of intracellular glutathione protects endothelial cells against oxidant damage. Tsan, Min Fu; Danis, Ellen H.; Del Vecchio, Peter J.; Rosano, Carmen L. (Dep. Physiol., Albany Veterans Adm. Med. Cent., Albany, NY 12208, USA). Biochem. Biophys. Res. Commun., 127(1), 270-6 (English) 1985. CODEN: BBRCA9. ISSN: 0006-291X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The role of GSH [70-18-8] in the endothelial cell defense against H2O2 damage was studied. Treatment of endothelial cells with buthionine sulfoximine [5072-26-4], an irreversible inhibitor of g-glutamylcysteine synthetase, depleted the cells of GSH, whereas L-2-oxothiazolidine-4-carboxylate [19771-63-2], an effective intracellular cysteine delivery agent, markedly enhanced endothelial cell GSH concn. Depletion of intracellular GSH sensitized the endothelial cells to injury by H2O2 either preformed or generated by the glucose-glucose oxidase system. In contrast, an increase of intracellular GSH protected the cells from H2O2 damage. There was an inverse, linear relation between the intracellular GSH concns. and killing of endothelial cells by H2O2. Evidently, enhancement of endothelial cell GSH may be an alternative approach toward the prevention of oxidant-induced endothelial damage such as adult respiratory distress syndrome.