Histochemical Investigation of Influence of Diabetogenic Zinc Binding Chemicals In Vitro on Human Pancreatic Β-Cells and its Prevention

Abstract

BACKGROUND: Amount of zinc-ions is correspond to insulin content in cytoplasm of β-cells. Diabetogenic zinc binding chemicals (DZC) formed with zinc in β-cells chelat complex that result destruction and death of β-cells within 10–15 min in animals. AIM: The aim of the study was to investigate using of specific histochemical methods the content of zinc and insulin in β-cells of pancreatic islets of human intact fetal pancreas tissue and under action of diabetogenic and non-diabetogenic zinc-binding substances diabetogenic zinc diethyldithiocarbamate (DZ and DDC). METHODS: Pancreas from 8-week-old human embryos and adult rabbits were used. Fixed or frozen islets were used in vitro effect. Histochemical methods for insulin and zinc in β-cells were used. RESULTS: Results showed that zinc in human β-cells is clearly revealed using of histochemical methods. In embryo pancreas, not integral islets were found as clusters of cells or even individual β-cells. Insulin content in ß-cells is for 7–20% lower and Zn2+ by 16–18% in compared with rabbits; Zinc in human ß-cells formed chelat complexes with 8PTSQ and DZ as Zn2+ –8PTSQ and Zn2+–DZ. Sodium DDC, a non-diabetogenic Zn2+ chelator, formed not toxic complexes with Zn2+ in fetal β-cells that protect cells of destruction caused by DZC as in animal’s pancreas. CONCLUSION: (1) Intracellular reactive zinc contained in human fetal pancreatic ß-cells clearly revealed using of histochemical methods and also (2) demonstrated that DZC in human ß-cells result formation with zinc of chelat complexes. (3) As in animals, non-toxic chemical as DDC is able to block zinc in ß-cells that result prevention of its destruction caused by DZC.