Evaluation of blood lipid peroxidation parameters in carbon tetrachloride (CCl4) toxicity in sheep.
Seven female, 2-year-old, nonpregnant, Merino ewes were treated with a nonlethal dose of 0.3 ml/kg body mass carbon tetrachloride (CCl4) in 1:1 v/v dilution with paraffin oil via a stomach tube into the rumen. Blood samples were collected one day before and on the first, second, third, seventh and tenth day after toxin exposure to study the changes of the lipid peroxidation (LP) status of red blood cell haemolyzate (RBC-haem). The severity of liver damage was monitored by determination of aspartate aminotransferase (AST) activity and bilirubin concentration in the blood plasma. Twenty-four h after CCl4 exposure all animals became lethargic and anorexic, their heart rate and respiratory rate increased. On the subsequent two days these signs became more severe, but by the 10th day the symptoms disappeared. On the 1st and 2nd day following CCl4 exposure the concentration of malondialdehyde (MDA)--an end product of LP--in RBC-haem significantly increased. A slight decrease was found on the 3rd, 7th and 10th day, but MDA values remained significantly higher than the basal ones. The activity of glutathione peroxidase (GPX) in RBC-haem increased slowly on the 1st and 2nd day, then it rose intensively on the third day. GPX activity remained elevated until the 7th day, but on the 10th day it dropped again. Catalase (Cat) activity in RBC-haem did not show any significant changes during the experiment. AST activity in blood plasma showed a two-fold increase in the first three days; later on the high values decreased. Total and direct plasma bilirubin concentration slightly increased on the 3rd day, then both decreased. LP effects in CCl4-induced hepatocellular injury were significant in sheep, in line with the results of experiments on other species such as rats. The LP effects were demonstrated by the elevated MDA concentration and GPX activity.
Vajdovich
P
P
Department of Internal Medicine, University of Veterinary Science, Budapest, Hungary.
Szilágyi
A
A
Gaál
T
T
D000818:Animals; D001219:Aspartate Aminotransferases / Q000032:analysis; D002251:Carbon Tetrachloride / Q000633:toxicity*; D002374:Catalase / Q000032:analysis; D004912:Erythrocytes / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D005979:Glutathione Peroxidase / Q000032:analysis; D050356:Lipid Metabolism; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology*; D008055:Lipids / Q000032:analysis; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000502:physiology; D008315:Malondialdehyde / Q000494:pharmacology; D012756:Sheep / Q000097:blood* / Q000378:metabolism / Q000502:physiology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D008055:Lipids; D017392:Thiobarbituric Acid Reactive Substances; D008315:Malondialdehyde; D002251:Carbon Tetrachloride; D002374:Catalase; D005979:Glutathione Peroxidase; D001219:Aspartate Aminotransferases