A mixture of carbon tetrachloride (CCl4) and 1,2-dibromoethane (DBE) results in a significant increase in relative liver weight (RLW) when compared with the effect of each substance individually. At the same time, the liver triglyceride levels of rats treated with the mixture are lower than in those treated with CCl4 alone. This increase in RLW is not caused by simple tissue oedema. Lipoprotein secretion and the concentration of circulating non esterified fatty acids (NEFA) are not involved in the DBE-induced reduction of steatosis provoked by CCl4. The synthesis of triglycerides is significantly depressed in animals treated with the mixture. These findings provide further evidence of the previously observed enhancement of liver toxicity caused by the simultaneous presence of both agents, since the apparent protection against steatosis is due to greater damage to the liver cell, which is no longer able to counter the steatogenic action of CCl4 through a sufficient synthesis of triglycerides.

In vivo studies on halogen compound interactions. II. Effects of carbon tetrachloride plus 1,2-dibromoethane on relative liver weight and hepatic steatosis.

ARAGNO, Manuela;DANNI, Oliviero;
1989-01-01

Abstract

A mixture of carbon tetrachloride (CCl4) and 1,2-dibromoethane (DBE) results in a significant increase in relative liver weight (RLW) when compared with the effect of each substance individually. At the same time, the liver triglyceride levels of rats treated with the mixture are lower than in those treated with CCl4 alone. This increase in RLW is not caused by simple tissue oedema. Lipoprotein secretion and the concentration of circulating non esterified fatty acids (NEFA) are not involved in the DBE-induced reduction of steatosis provoked by CCl4. The synthesis of triglycerides is significantly depressed in animals treated with the mixture. These findings provide further evidence of the previously observed enhancement of liver toxicity caused by the simultaneous presence of both agents, since the apparent protection against steatosis is due to greater damage to the liver cell, which is no longer able to counter the steatogenic action of CCl4 through a sufficient synthesis of triglycerides.
1989
66
105
116
ARAGNO M ;DANNI O ;UGAZIO G
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/31089
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