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Biomedical subjects

J Kolakowski

Publications and source records attributed to J Kolakowski.

6 recordsLinked to original sources
PubMed1984

Stimulation of lipid peroxidation and heme oxygenase activity with inhibition of cytochrome P-450 monooxygenase in the liver of rats repeatedly exposed to cadmium.

Exposure of rats to 0.1 and 0.5 mg Cd/kg subcutaneously (s.c.) thrice weekly for 5 weeks resulted in an accumulation of cadmium in the liver in concentrations of 40 and 95 micrograms/g tissue, respectively, and a microsomal burden of Cd amounting to approx. 2-3% of the retained cadmium. The cytoplasm contained about 80% of the cadmium. At an exposure dose of 0.1 mg Cd/kg, stimulation of lipid peroxidation by 22% and inhibition of ALA synthetase by 16% in the liver were observed. The higher exposure of 0.5 mg Cd/kg caused an inhibition of microsomal monooxygenase with depression of cytochrome P-450 and cytochrome b5 by 20% (over 2-fold prolongation of hexobarbital sleeping time and statistically significant decrease of activity of aniline p-hydroxylase). The loss of cytochrome P-450 probably was due to an intensified lipid peroxidation and induction of heme oxygenase (30% and 60% over control, respectively). Sequestration of cadmium by cytoplasm (metallothionein) does not protect microsomes against cadmium accumulation and specific biochemical disturbances.

5-Aminolevulinate Synthetase↗
PubMed1983

Effect of long-term inhalation exposure to cadmium oxide fumes on cardiac muscle ultrastructure in rats.

The ultrastructure of the cardiac muscle of rats exposed 5 h daily, 5 days a week to cadmium oxide (CdO) fumes at a concentration of 0.16 mg Cd/m3 for 3 and 6 months and at a concentration of 1 mg Cd/m3 for 3 and 4 months has been evaluated. The structure of muscle cells, arterioles and capillaries remained unchanged. There were distinct alterations of the intercalated disc structure dependent upon the level and time of exposure. The damage to intercalated discs varied from the enlargement of the fissure between membranes (within unspecialized segments) to disruption of the complex junctions.

Animals↗
PubMed1982

Effect of different conditions of acute exposure to carbon monoxide on the cerebral high-energy phosphates and ultrastructure of brain mitochondria in rats.

Rats were exposed to carbon monoxide (CO) in different conditions: 4 min at 1.3% CO, 40 min at 0.5% CO or 12 h at 0.13--0.15% CO. After 4 min exposure to 1.3% CO the brain content of ATP and PC was substantially reduced; after 40 min exposure to 0.5% CO the cerebral ATP level was slightly increased, whereas the content of both ATP and PC in the brain of rats exposed to CO for 12 h was significantly higher than in the controls. The decrease in the brain level of ATP and PC after 4 min exposure to 1.3% CO was accompanied by ultrastructural changes of mitochondria. No evident differences in the level of cerebral high-energy phosphates were found between rats intoxicated with CO and rats subjected to experimental hypoxemia.

Adenosine Diphosphate↗
PubMed1980

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. Some toxic effects including morphological liver injuries arose at the smallest exposure level, i. e., 50 ppm. Assuming 50 ppm as the threshold concentration for rats, the 5 ppm level has been estimated as the safe exposure limit in industry in relation to systemic effects of vinyl chloride.

Alanine Transaminase↗