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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    International archives of occupational and environmental health 37 (1976), S. 35-46 
    ISSN: 1432-1246
    Keywords: Carbon disulphide ; Alcohol ingestion ; Ethanol elimination ; Acetaldehyde production ; CS2-alcohol reaction (antabuse syndrome) ; Workplace hazards
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Exposure of rats to 20 ppm CS2 (the current MAC in various countries) for 8 h was followed by i.p. administration of 2 g/kg ethanol (blood level: 3-1‰) and another up to 4-h exposure to the same concentration of CS2. During the second exposure the acetaldehyde concentration increased significantly, the rise representing one third of the control values. Inhalation of 400 ppm CS2 for the same period, or 8-h exposures at 400 ppm CS2 on 5 consecutive days produced only a slight additional increase in acetaldehyde. The increased appearance of acetaldehyde in blood is considered to be due to inhibition of aldehyde dehydrogenase by CS2. This conclusion was derived from the significant lag in the clearance rate of acetaldehyde given i.v. (1 mmol/kg) after exposure at 400 ppm CS2/8 h, involving an increase of the excretion half-life of acetaldehyde (1 min, 45 s in the controls) to 2 min, 24 s. The finding thus obtained could be reproduced in man (adult males). At a blood alcohol concentration of approximately 0.75‰, maintained at this level for 8 h, the blood acetaldehyde concentration was found to be approximately 6 × 10−3‰; it rose significantly by about 50% during simultaneous 8-h exposure of the test subjects to a nonfluctuating, analytically defined concentration of 20 ppm CS2. When increasing the dose Of CS2 to 40 ppm and 80 ppm for 8 h, only a slight additional increase was noted. Administration of ethanol (ca. 0./5‰) for 8 h, instituted at 16 h after 8-h inhalation of 20 ppm CS2, produced a rise in blood acetaldehyde to slightly more than twice the control value. An approximately identical quantitative effect was observed after exposure to 20 ppm on 5 consecutive days at the same time of the day (8.00 a.m. - 4.00 p.m.). Under the conditions employed, there was no evidence of any subjective or objective signs of alcohol intolerance in terms of an “antabuse syndrome” in the experiments. Inhalation of CS2 vapor failed to exert a significant effect on the pharmacokinetic behavior of ethanol in with a blood alcohol content up to 0.8%., contact with CS2 is not likely to give rise to a CS2-alcohol reaction, provided the concentrations of CS2 encountered in the work environment are within the range of the MAC.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    International archives of occupational and environmental health 34 (1975), S. 269-282 
    ISSN: 1432-1246
    Keywords: Carbon Disulphide ; Liver Function ; Organic-Chemical Liver Cell Constituents ; Energy Metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In adult female rats 8-hr exposure to 400 ppm CS2 did not produce a change in conventional liver function tests (SGOT, SGPT, and SLDH activities; BSP clearance in the bile). This would seem to imply that the severe inhibition of the hepatic mixed-function oxidases observed in earlier experiments after the same dose of CS2 is not attributable to generalized cell damage, but should rather be taken to represent a selective lesion. Eight-hr exposures of the experimental animals to graded CS2 concentrations ranging from 20 to 400 ppm triggered a rapidly reversible substantial depletion of the hepatic glycogen. A concurrent increase of the lactate and inorganic phosphate levels and also of the oxygen consumption was demonstrated, in conjunction with an increased respiratory uptake of oxygen by the exposed animals, a fall in body temperature, and a decrease of the serum potassium and calcium levels. These changes may be interpreted as an extensive defect in the energy supply in the liver cell. The concomitant slight decrease of the liver weight is largely explained by the disappearance of glycogen; a possible reduction of the water content could be excluded. The small increase in total liver protein, which was another finding, is attributable to a nonspecific stimulation of protein synthesis. The observed quantitative changes in the liver substance required balancing of the food ingested: following 8-hr inhalation of 100 or 400 ppm there was a marked reduction in body weight, intake of standard food and water, and fecal excretion, whereas slight increases were observed after 20 ppm over 8 hrs. These alterations are probably due to a disturbance of the diencephalic controlling mechanisms.
    Type of Medium: Electronic Resource
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