HISTOCHEMISTRY OF RAT SMALL INTESTINE MUCOSA AFTER ORAL ADMINISTRATION SILVER NITRATE

Abstract

The investigations making up the thesis were aimed towards elucidating the structural and histochemical effects of toxic doses of silver nitrate on rat small intestinal mucosa at three different sites. The studies were also an attempt to find out

1. the relationship between dose of silver nitrate and the degree of histological damage; 2. the relationship between dose and magnitude of the biochemical change; 3. changes if any, in the biochemical and morphological patterns following the replacement of silver nitrate by water; 4. the uptake of silver at various sites following the ingestion of silver nitrate. To provide background to these studies, it was necessary first of all to establish normal distribution patterns in terms of the enzymes and histology of the various sites. The enzymes investigated include Acid phosphatase; Alkaline phosphatase; /β-glucuronidase; Lactate dehydrogenase and /β -Hydroxybutyric dehydrogenase. The results of the background studies suggest that the height of the villi decreases progressively from the 10% point to the 95% point. The volume of the lamina propria of the epithelia decreased progressively from the 95% point to the 10% point. There was point-to-point variation in the levels of activities of Acid phosphatase; Alkaline phosphatase; β -glucuronides and Lactate dehydrogenase. The activity of dehydrogenase was uniform at all the sites. Following the ingestion of silver nitrate there were marked changes in the villi; crypts and lamina propria. Silver nitrate produced histological damage of the mucosa. The extent of damage was directly proportional to the dose. The 10% point appeared most vulnerable to silver toxicity; followed by the 50% point and the 95% point. The activities of Acid phosphatase; Alkaline phosphatase and β -glucuronidase were stimulated following silver nitrate ingestion. The magnitude of stimulation was directly proportional to the dose of silver nitrate. The activities of Lactate dehydrogenase and β -Hydroxybutyric dehydrogenase were inhibited following silver nitrate ingestion. The magnitude of Inhibition was directly proportional to the dose of silver nitrate. When the silver nitrate was replaced by water there were changes in biochemical and morphological patterns. There was evidence of histologic and enzymic recovery. The absorptive capacity for silver varies in different regions of rat small Intestine. The 10% point is the most active for silver uptake, followed by the 50% point. The 95% point has the least capacity for silver uptake. When all of the data obtained by the different methods are pooled together, they provide basic Information on the reaction of rat small Intestinal mucosa to silver toxicity. The experimental methods utilised in this work probably have potential as a model for the investigation of the mechanism of Intestinal damage in experimental animal. They can also be used for the investigation of epithelial turnover and repair; and for the study of potential agents for the prevention and treatment of ulceration of the small intestinal mucosa. Furthermore, correlated studies of functional capacity and enzyme levels as reported in this work might be useful in identifying the nature of the enzymic systems concerned in the absorption process.