US EPA

5204948 

Journal Article 

Rat liver lipolytic activity after carbon tetrachloride poisoning 

Ugazio MV GTorrielli 

1969 

1 

Life Sciences
ISSN: 0024-3205
EISSN: 1879-0631 

3 

HAPAB Rat liver lipolytic activity was estimated after both carbon tetrachloride (CC14)-poisoning and in vitro treatment with CC14 metabolites or lipoperoxides. Twenty male Wistar rats were administered, after an 18 hr fast, mineral oil ( 0.25 ml/100 g ) or 0.25 ml CC14 with an equal volume of mineral oil. Animals were sacrificed 4 hr later. The lipolytic activity, expressed as micromoles of fatty acids ( palmitic acid ) released into the medium by 1 g of liver 9 wet weight ) in 60 min, was calculated as the amount of the fatty acids liberated between the 15th and the 30th min of incubation. Lipolytic activity decreased by about 60%. Starved Wistar rats were used as liver donors for in vitro treatment with CC14. Aliquots of the liver homogenate ( 3.5 ml ) were added to 5 mcl of freshly distilled CC14 and then incubated for 15 or 30 min. Lipolytic activity was inhibited here also. The reported inactivation on aging was confirmed in the case of 30 min incubation. In further series of experiments, the enzymatic activity of fresh homogenate was lowered to about one- third that of the control when it was mixed with liver homogenate previously incubated under CC14 vapors. It seems that the preincubated homogenate, when mixed with substrate, contains only CC14 metabolites which act on lipase. The small traces of CC14 possibly trapped and transferred in the preincubated homogenate seem to exert no action on the lipid-protein complexes or the lipase substrate. Propyl gallate produced a protective effect on the inhibition in an in vitro experiment. While lipoperoxides impaired lipolytic activity in vitro, it seems likely they are less effective than CC14 metabolites in the lipase inactivation. Zymosan ( 4 mg/100 g ) was injected into male Wistar rats for five days and produced a remarkable decrease in liver lipolytic activity but no change in the triclyceride splitting rate. The enlarged liver weight caused by zymosan administration seems to provide the decrease in lipolytic activity. Zymosan added in vitro at twice the in vivo dosage failed to affect lipolytic activity. The results could be interpreted as evidence for a peroxidative mechanism of the inhibition. In addition, it seems possible that the described enzyme impairment could be contributing to the triglyceride accumulation in CC14-induced fatty liver. TOXICOLOGY AND PHARMACOLOGY 69/07/00, 225 1969