Reference

On the possible role of thiol groups in the insulin-releasing action of mercurials, organic disulfides, alkylating agents, and sulfonylureas

On the possible role of thiol groups in the insulin-releasing action of mercurials, organic disulfides, alkylating agents, and sulfonylureas. Hellman, B.; Lernmark, A.; Sehlin, J.; Soderberg, M.; Taljedal, I. B. (Dep. Histol., Univ. Umea, Umea, Swed.). Endocrinology (Philadelphia), 99(5), 1398-406 (English) 1976. CODEN: ENDOAO. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) The SH activity of pancreatic islets was spectrophotometrically assayed as the formation of 6-mercaptonicotinic acid from the org. disulfide, 6,6'-dithiodinicotinic acid. Islets contg. more than 90% .beta.-cells were microdissected from non-inbred ob/ob-mice. Comparisons of intact with homogenized islets indicated that the org. sidulfide penetrates relatively slowly into the .beta.-cells. When tested at concns. known to enhance insulin release, p-chloromercuribenzene-sulfonic acid [554-77-8] almost completely blocked the thiol activity of intact islets, whereas no significant effect was obsd. with iodoacetamide [144-48-9], D-glucose [50-99-7], or glibenclamide [10238-21-8]. Although glibenclamide had no demonstrable effect on the thiol activity of free L-cysteine [52-90-4], the binding of glibenclamide to serum albumin was decreased by blocking the albumin thiols with azobenzene-2-sulfenyl bromide [2849-62-9]. The uptake of glibenclamide by pancreatic islets was inhibited by cysteine or reduced glutathione [70-18-8]. Cysteine, as well as 6,6'-dithiodinicotinic acid, also seemed to interact neg. with glibenclamide as insulin [9004-10-8] secretagogue. The results support the hypothesis that org. 50-99-7 and 10238-21-8 which are cas registry numbers of substances are two of reagents here. mercurials and disulfides stimulate insulin release by blocking SH groups in the .beta.-cell plasma membranes. The SH groups involved in iodoacetamide-induced secretion may escape detection by the assay employed, or target groups other than SH may be involved. The data on glibenclamide are compatible with, but do not unequivocally support, the notion that SH groups may play a role in sulfonylurea-induced insulin release. .

Evidence for a membrane sulfhydryl associated with resistance to melphalan in a murine L1210 leukemia line

Evidence for a membrane sulfhydryl associated with resistance to melphalan in a murine L1210 leukemia line. Fisher, J. M.; Naujokaitis, A. S.; Uehara, Y.; Rabinovitz, M. (Lab. Med. Chem. Pharmacol., Natl. Cancer Inst., Bethesda, MD 20205, USA). Biochem. Biophys. Res. Commun., 117(3), 670-6 (English) 1983. CODEN: BBRCA9. ISSN: 0006-291X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Murine L1210 leukemia cells, which display sensitivity or resistance to the chemotherapeutic alkylating agent, melphalan [148-82-3], are equiv. sensitive or resistant to the poorly permeable mercurial, p-chloromercuribenzenesulfonate [554-77-8]. Cells of both lines do not differ in sensitivity to the sulfhydryl reagents, N-ethylmaleimide [128-53-0], iodoacetamide [144-48-9], and iodoacetate [64-69-7] or to the glutathione transferase substrates 1-chloro-2,4-dinitrobenzene [97-00-7] and p-nitrobenzyl chloride [100-14-1]. The results are interpreted in terms of the known biol. reactivity of p-chloromercuribenzenesulfonate as a selective reagent for sulfhydryl groups of membrane proteins assocd. with monovalent cation permeability.