Interaction of zinc of pancreatic ß-cells with cystein as possible cause of its protective activity

Abstract

It is known that zinc, contained in β-cells of the pancreas, takes an important part in the formation of its deposited storage form in the cell, due to which not all of the cell-synthesized hormone, but only a certain amount of it, enters the blood, regulating carbohydrate metabolism and providing maintenance of blood glucose level at a constant level. It is also known that there are zinc-binding diabetogenic substances that, when ingested, bind to zinc of β-cells, forming toxic complexes, leading to destruction and cell death within 15-30 minutes. A total of 18 such substances are known, and 17 of them refer to derivatives of 8-hydroxyquinoline, some of whose representatives are components of 12 drugs (in 1970 there were 2 of them). It is also known that the preliminary introduction of the amino acid cysteine completely prevents the development of diabetes caused by zinc-binding diabetogenic substances. Presumably, this is justified by its ability to block zinc in the doses used for 24-36 h, preventing it from interacting with zinc-binding diabetogenic substances. Authors using sensitive and strictly specific methods have established that indeed, cysteine blocks islet zinc, preventing its interaction with zinc-binding diabetogenic substances. The authors believe that the blocked zinc atoms are fixed between the sulfur atom that is part of the SH group in the cysteine molecule and the oxygen atom of the carboxyl group, or between the sulfur atom and the nitrogen atom of the amino group of the cysteine molecule, as is also the case with the interaction of zinc with zinc-binding diabetogenic substances, where chelates with zinc are formed only as a result of fixing them between these atoms