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The acute toxicity of some organolead and organotin compounds in the rat, with particular reference to a gastric lesion
Author(s) -
Verschoyle R. D.,
Little R. A.
Publication year - 1981
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550010503
Subject(s) - chemistry , toxicity , desquamation , gastric mucosa , oral administration , lesion , stomach , pharmacology , acute toxicity , medicine , pathology , biochemistry , organic chemistry
The acute toxicity of triphenyl, tributyl and dibutyllead in the rat appears to result from their irritating properties to membranes regardless of their route of administration. A more detailed examination of their oral toxicity has shown that a single dose inhibits gastric emptying with resulting fluid distension. A similar effect was observed with a number of other organolead and organotin compounds. Analysis of gastric fluid from pyloric ligated rats following an oral organolead dose showed increased concentrations of Na + and glucose and decreased concentrations of H + and K + . Dilation of the gastic mucosal microcirculation was also observed along with desquamation of surface mucous cells which resulted in shallow erosions of the upper portions of the gastric glands. It is suggested that oral dosing with a number of organoleads and, possibly, organotins has an effect on mucosal membranes that results in erosion of the gastric mucosa and increases permeability of the mucosal microcirculation. This would allow leakage of plasma constituents into interstitial fluid and ultimately the gastric lumen with back‐diffusion of H + into the gastric mucosa. Such a lesion would impair gastric function and reduce normal food and water consumption. The starvation and dehydration may then be the important factors for death that follows oral dosing with organolead and organotin compounds.