Disease relevance of Carbon Tetrachloride Poisoning

• Effect of CO2-induced hyperventilation on carbon tetrachloride (CCl4) levels following acute CCl4 poisoning [1].

High impact information on Carbon Tetrachloride Poisoning

• Because the mechanism of CCl4 hepatotoxicity is thought to be the same in the rat and in humans, hyperbaric O2 therapy is recommended for treatment of CCl4 poisoning in humans [2].
• Plasma and urinary levels of malondialdehyde-like products (MDA) and isoprostanes were identified as markers of in vivo lipid peroxidation in an animal model of CCl4 poisoning [3].
• Concerning the potential relevance of these findings, we consider that if similar interactions to those here reported occurred during CCl4 poisoning, the activity of enzymes having tyrosine in their active center might result in impairment [4].
• Alpha-fetoprotein was detected in the serum and urine of 2- to 9-mth-old rats subjected to protracted CCl4 poisoning [5].
• In CCl4 poisoning it is suggested to start UDCA treatment as early as possible and to continue it for some more days after improvement of serum bilirubin concentration [6].

Chemical compound and disease context of Carbon Tetrachloride Poisoning

• To find out whether cicloxilic acid was effective in maintaining a normal lipoprotein secretion after CCl4 poisoning, experiments were carried out with Triton WR-1339 [7].
• The authors studied the effect of realimentation after several days' isolated glucose or fructose intake on DNA synthesis in liver regenerating after partial hepatectomy (PH) (65-70%) or after carbon tetrachloride (CCl4) poisoning 1.5 ml/kg [8].
• Incorporation of acetate into triglycerides, phospholipids and cholesterol increases in CCl4 poisoning and this was not affected by EPL [9].

Biological context of Carbon Tetrachloride Poisoning

• Modulations in rat hepatic microsomal UDP-glucuronyl transferase activity have been observed during carbon tetrachloride (CCl4) poisoning, with a large decrease in the enzyme cooperatively and increase in the membrane fluidity, occurring 30 min after administration [10].

Anatomical context of Carbon Tetrachloride Poisoning

• Effects of CCl4 poisoning on metabolism of dolichol in rat liver microsomes and Golgi apparatus [11].

Gene context of Carbon Tetrachloride Poisoning

• Subcellular calmodulin distribution in rat liver after CCl4 poisoning [12].
• Attempts to localize glutamine synthetase mRNA within the liver acinus by selective destruction of the pericentral zone failed because of generally low levels of liver mRNAs after CCl4 poisoning [13].

References