Energy potential and hepatic function in rats under acute exposure to carbon disulphide

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.Presented in part at the 10th Spring Meeting of the Deutsche Pharmakologische Gesellschaft, Mainz, March 16 – 19, 1969.