Carbon tetrachloride liver damage

Carbon tetrachloride - liver damage Diethyl ether - flammable Benzene - suspect carcinogen... 

Acute Liver Damage Several compounds (e.g., dimethyl iiitrosoamine, carbon tetrachloride, and thioacetamide) cause necrosis of hepatocytes by inhibiting pro tein syndiesis at the translational level, i.e., by inhibiting the addition of new amino adds into the protein chain being sjTithetized. This is not, however, the only mechanism. Ethioiiine is a compound which inhibits protein synthesis bur doe not induce... 

A number of early in vitro studies demonstrated a considerable role of free radicals in liver injury (see, for example, Proceedings of International Meeting on Free Radicals in Liver Injury [341]). Later on, it was shown that chronic inflammation in the liver-induced oxidative DNA damage stimulated chronic active hepatitis and increased the risk of hepatocarcinogenesis [342,343]. Farinati et al. [344] showed that 8-OHdG content increased in circulating leukocytes of patients with chronic hepatitis C virus (HCV) infection. DNA oxidative damage is supposedly an early event of HCV-related hepatitis. The formation of isoprostanes in the liver of carbon tetrachloride-treated rats can be suppressed by the administration of vitamin E [345],... 

Its effects on the body are widespread. Inhalation of the vapor is the most common mode of entry, and when the chemical is inhaled in sufficient concentration, it has an immediate effect on the brain (hence the high that Harry was partial to) and ultimately, over longer periods, it causes damage to the liver and kidneys. Now it so happened, that although Harry had been working for five years with concentrations of carbon tetrachloride above the recommended limit, any obvious damage to his brain, liver, and kidneys at that time was no more than he would have derived from knocking back a six pack of beer several times a week. So what was the trouble ... 

Toxicology. Carbon tetrachloride causes central nervous system depression and severe damage to the liver and kidneys it is carcinogenic in experimental animals and has been classified as a potential human carcinogen. 

A number of substances including ethanol, isopropyl alcohol, polybrominated biphenyls, phenobarbital, and benzo( )pyrene have been shown to synergistically affect carbon tetrachloride toxicity." Alcohol has been a concomitant factor in many of the human cases of poisoning, especially in cases in which severe liver and kidney damage have occurred. Some substances such as chlordecone greatly potentiate the toxicity of carbon tetrachloride at... 

Liver or kidney damage Toluene, and carbon tetrachloride, 1,1,2-2-tetrachloroethane, chloroform... 

The liver is especially sensitive to carbon tetrachloride. In mild cases, the liver becomes swollen and tender, and fat builds up inside the organ. In severe cases, liver cells may be damaged or destroyed, leading to a decrease in liver function. Such effects are usually reversible if exposure is not too high or too long. 

Cardiovascular Effects. Inhalation and oral studies in humans and animals have not revealed any treatment-related histopathological lesions of heart tissue, or impairment of cardiac functions, even at dose levels causing severe liver and kidney damage (Adams et al. 1952 Stewart et al. 1961 Umiker and Pearce 1953). It is possible that high-level carbon tetrachloride exposure may produce cardiac arrhythmias by sensitization of the heart to catecholamines (Reinhardt et al. 1971). Accordingly, there is some concern for cardiovascular toxicity following substantial exposure to carbon tetrachloride. 

Haloalkanes. Certain haloalkanes and haloalkane-containing mixtures have been demonstrated to potentiate carbon tetrachloride hepatotoxicity. Pretreatment of rats with trichloroethylene (TCE) enhanced carbon tetrachloride-induced hepatotoxicity, and a mixture of nontoxic doses of TCE and carbon tetrachloride elicited moderate to severe liver injury (Pessayre et al. 1982). The researchers believed that the interaction was mediated by TCE itself rather than its metabolites. TCE can also potentiate hepatic damage produced by low (10 ppm) concentrations of carbon tetrachloride in ethanol pretreated rats (Ikatsu and Nakajima 1992). Acetone was a more potent potentiator of carbon tetrachloride hepatotoxicity than was TCE, and acetone pretreatment also enhanced the hepatotoxic response of rats to a TCE-carbon tetrachloride mixture (Charbonneau et al. 1986). The potentiating action of acetone may involve not only increased metabolic activation of TCE and/or carbon tetrachloride, but also possible alteration of the integrity of organelle membranes. Carbon tetrachloride-induced liver necrosis and lipid peroxidation in the rat has been reported to be potentiated by 1,2- dichloroethane in an interaction that does not involve depletion of reduced liver glutathione, and that is prevented by vitamin E (Aragno et al. 1992). 

Administration of hyperbaric oxygen following exposure to carbon tetrachloride improved survival from 31 to 96% in rats (Ellenhorn and Barceloux 1988). Hyperbaric oxygen has also been used in treating overdoses of carbon tetrachloride in humans and may correct regional tissue hypoxia and damage, as well as inhibit the P-450-dependent reductive dehalogentation of carbon tetrachloride to the metabolically active acute trichloromethyl radical in the liver. However, the effectiveness of this method has not been established in humans (Burkhart et al. 1991 Ellenhorn and Barceloux 1988). 

Use of three-dimensional magnetic resonance imaging (MRI) to observe progression and regression of carbon tetrachloride-induced liver damage in living animals. 

Ala-Kokko L, Stenback F, Ryhanen L. 1987. Preventive effect of malotilate on carbon tetrachloride-induced liver damage and collagen accumulation in the rat. Biochem J 246 503-509. 

Brondeau MT, Coulais C, de Ceaurriz J. 1991. Difference in liver and serum malathion carboxylesterase and glucose-6-phosphatase in detecting carbon tetrachloride-induced liver damage in rats. J AppI Toxicol 11 433-435. 

Chandler AC, Chopra RN. 1926. Effects of the administration of sugar, magnesium sulfate, sodium citrate and dilute acid on the liver damage done by carbon tetrachloride. Ind J Med Res 14 219- 226. 

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