Influence of chronic carbon disulphide intoxication on the development of experimental atherosclerosis in rats.

Rats fed on atherogenic diets containing 2% cholesterol and 0.5% cholic acid with or without 0.15% thiouracil were exposed to carbon disulphide (CS2) vapours (1 mg/l of air), five hours a day, six days a week for 6-10 months.

Preliminary project of the standard minimal scope and methods of testing acute toxicity of industrial chemical substances.

The standard minimal scope of experimental toxicity evaluation of industrial chemicals has been proposed. On the basis of literature and own experience the authors propose that the minimal scope of toxicity testing should include determination of lethal doses and evaluation of morphological alterations of inner organs in acute experiments, as well as assessment of eye and skin irritation and contact sensitization. The main lines of uniform procedures are presented.

[Lipid changes in the blood serum and arterial wall in rabbits chronically exposed to CS2].

In the studies carried out lipids content in blood serum and aorta wall as well as morphological changes in coronary vessels of CS2 exposed rats have been evaluated. The 10-month-exposure to CS2 at a concentration of 0,8--0,9 mg/l has been found to result in: (1) increased concentration of total and free cholesterol, cholesterol esters, triglycerides and phospholipids in blood serum; (2) increase in total cholesterol and significant rise in the level of cholesterol esters in the aorta wall; (3) a relative increase in serum VLDL, LDL and decrease in HDL fraction. Histological estimation has demonstrated in serial sections of hearts of the CS2 exposed animals thickened walls of left coronary artery branches with no lipid deposits.

[Biological and histological changes induced by cement dust].

In animal experiments pneumoconiogenic properties of metallurgic and Portland cement dust, produced in Poland, were investigated. Experimental pneumoconiosis was developed by intratracheal single administration, to white rats, of 50 mg of dust suspended in 0.6 ml of NaCl physiological solution.

Experimental studies on the chronic toxic effects of vinyl chloride in rats.

Male rats were exposed to vinyl chloride at the concentrations of 50, 500, and 20 000 ppm, 5 hours daily, 5 days a week for 10 months. Morphological lesions in the liver and the testes detected by light and electron microscope and depression in body weight increase intensified with the duration of exposure. Increased relative weights of some organs and slight hematological and biochemical changes in blood during the course of the experiment were also observed.

[Evaluation of acute toxic effect of 3-cyanopyridine].

General acute toxicity, irritating, and allergic effects of 3-cyanpyridine were studied. LD50 after oral administration amounts to 1185 mg/kg of body weight, 3-cyanpyridine is absorbed through the intact skin: administration of 3-cyanpyridine solution into rabbit skin caused death of animals. Histopathologic studies showed reversible liver and kidney injuries after single administration of lethal and sublethal doses.

[Experimental silicosis. I. Fibrogenic effect of synthetic amorphous silica].

Fibrogenic properties of two dusts of synthetic hydrated amorphous silicas, Ze-O-Sil (French production) and Arsil (Polish production) were studied. Experimental silicosis was induced by intratracheal administration to rats of a single dust dose (50 mg in 0.6 ml NaCl).

[Experimental silicosis. Evaluation of the silicogenic properties of apatites and phosphorites].

White rats were intratracheally injected with 50 mg of apatite or phosphorite dust. The animals were killed 3, 6 and 10 months after the injection. Fibrogenic properties were evaluated on the basis of biochemical and histopathological studies.

[Experimental silicosis. II. Fibrogenic effect of natural amorphous silica].

Fibrogenic effect of two natural amorphous silica dusts-diatomite from deposits near Leszczawka (Poland) and silica earth (from the USA) was tested on the rats. Pneumoconiosis was produced by intratracheal introduction of 50 mg dust, at a single dose. Fibrogenic effect was assessed after 3, 6 and 9 months after introduction of dust.