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C ALLARD

Publications and source records attributed to C ALLARD.

At least 19 recordsLinked to original sources

A LIGHT AND ELECTRON MICROSCOPE STUDY OF THE MORPHOLOGICAL CHANGES INDUCED IN RAT LIVER CELLS BY THE AZO DYE 2-ME-DAB.

The cytological changes induced in rat liver cells by the aminoazo dye 2-Me-DAB have been examined by light and electron microscopy. It is observed that this non-carcinogenic compound duplicates most of the morphological alterations produced by other hepatotoxins, some of which, such as the closely related aminoazo dye 3'-Me-DAB, are potent carcinogens. These non-specific effects involve both the granular and agranular forms of the endoplasmic reticulum as well as the glycogen content of hepatic cells. The arrays of cisternal profiles of the granular reticulum in normal hepatic cells become disorganized and the dispersed cisternae often appear fragmented and irregular. Large cytoplasmic inclusions, consisting of loosely organized tubules and vesicles, are also observed which result from a hypertrophy of the agranular reticulum. The glycogen in the cells progressively decreases in amount. The most specific effect of 2-Me-DAB is to induce an increase in the number of mitochondria per cell. Many of these organelles are characterized by the presence of a median double membrane continuous with the inner limiting membrane of the mitochondrial envelope. Evidence is presented in favor of the view that this partition is directly related to the phenomenon of mitochondrial division. It was noted also in the course of the experiment that an increasing number of cells appear which stain quite intensely with methylene blue and appear denser than normal under electron microscopy. The significance of these cells is not known.

Animals↗

Hypertension, thrombosis, and atherosclerosis in the rat.

A simple high fat diet containing cholic acid has been devised for producing hyperlipemia and an increased incidence of thrombosis in the small coronary vessels of the rat, but without producing significant atherosclerotic lesions. The influence on this syndrome induced by six weeks of desoxycorticosterone administration, 2 mg. daily, and 10 weeks of oral saline (1%) ingestion was investigated in 30 115-g. male rats. Marked hypertension developed only when it was induced prior to beginning the dietary feeding. In comparison to the control groups, the group that was both hyperlipemic and hypertensive had severer hypertension, severer hyperlipemia, double the mortality due to thrombosis and fatty streaks in the aorta but very few lesions of periarteritis nodosa. However, the early atherosclerotic lesions did not seem to be responsible for the increased production of thrombosis. It is therefore probable that under these experimental conditions hypertension has a more direct action on the production of thrombotic effect than that of worsening the atherosclerotic lesions.

Animals↗