The β‐cells of pancreatic islets, dying after injury by alloxan, were studied (1) by staining with oxidized tannin‐azo (OTA), which colours well the tannophilic protein both in islet and acinar cells, and (2) by successive treatment with neutral permanganate, Gomori's paraldehyde‐fuchsin and methylene blue, a method which effectively differentiates the β‐cells from the other cells of the pancreas. There was no rapid loss of tannophilic protein from the injured β‐cells which retained their granules stainable by paraldehyde‐fuchsin in the early stages of necrosis. The injured β‐cells were rapidly dissevered from one another and from the capillaries, which they normally encompass, and were thus transformed from mutually coherent epithelial units into isolated separate cells. It is suggested that alloxan may react with an external film of protein on the surface of the β‐cells so as to sever their mutual coherence and also their adherence to the walls of the capillaries. After separation from their vascular supply, the isolated β‐cells may then undergo ischæmic necrosis. Pyknosis was conspicuous in the nuclei of the dying β‐cells and was accompanied by an increase in tannophilic protein. The capacity of the cytoplasm of the injured β‐cells to stain with paraldehyde‐fuchsin and with OTA later declined, when the necrotic remnants had swollen and coalesced into indistinct cellular phantoms. Finally all remnants of the β‐cells disappeared and the islets were reoccupied by epithelial cells rich in tannophilic protein but devoid of granules stainable by paraldehyde‐fuchsin.
|Original language||English (US)|
|Number of pages||11|
|Journal||Quarterly Journal of Experimental Physiology and Cognate Medical Sciences|
|State||Published - Apr 7 1960|
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