Liver Carbon tetrachloride intoxication

Ochi Y, Yumori Y, Morioka A, et al. 1990. Effect of a-blockade on liver regeneration after carbon tetrachloride intoxication in the rat. Biochem Pharmacol 39 2065-2066. 

Bishayee, A., A. Sarkar, and M. Ghaterjee. Hepatoprotective activity of carrot (Daucus carota L.) against carbon tetrachloride intoxication in mouse liver. J Ethnopharmacol 1995 47(2) 69-74. 

Human health effects from longer-term human exposures to carbon tetrachloride generally resemble acute effects of liver and kidney damage. Consumption of alcohol and poorly controlled diabetes may increase the risk of harmful effects associated with carbon tetrachloride intoxication. The US EPA classifies carbon tetrachloride as a group B2, probable human carcinogen. 

Kawashima R, Mochida S, Matsui A, YouLuTu ZY, Ishikawa K, Toshima K, Yamanobe F, Inao M, Ikeda H, Ohno A, Nagoshi S, Uede T, Fujiwara K (1999) Expression of osteopontin in Rupffer cells and hepatic macrophages and Stellate cells in rat liver after carbon tetrachloride intoxication a possible factor for macrophage migration into hepatic necrotic areas. Biochem Biophys Res Commun 256(3) 527-531. doi 10.1006/bbrc. 1999.0372... 

Okita M, Watanabe A, Tsuji T. 1988. Effect of branched-chain amino acid on 15N incorporation into liver and skeletal muscle proteins following [15N]-ammonium chloride administration to carbon tetrachloride-intoxicated rats. J Nutr Sci Vitaminol 34(1) 85-96. 

K42 Kocher, Z., Habermannova, S., Cerhova, M. and Suva, J. The influence of orotic acid on liver parenchyma. IV. Changes in serum and liver lipids due to chronic carbon tetrachloride intoxication. Acta Vitaminol., 6, 269-275 (1964)... 

Kumaravelu P, Dakshinamoorthy DP, Subramaniam S, DevaraJ H, DevaraJ NS (1995) Effect of eugenol on drug-metabolizing CTzymes of carbon tetrachloride-intoxicated rat liver. Biochem Pharmacol 49 1703-1707... 

Two studies were located that reported the occurrence of liver cancer in humans exposed to carbon tetrachloride fumes, both acutely (Tracey and Sherlock 1968) and for longer periods (Johnstone 1948). In the former case, a male died of hepatocellular carcinoma 7 years after acute intoxication with carbon tetrachloride at an age of 59, although he had a history of moderate alcohol consumption (without demonstrable liver cirrhosis). In the second case, a 30- year-old female died of "liver cancer" after 2-3 years of occupational exposure to carbon tetrachloride that was sufficient to produce signs of intoxication. However, this evidence is much too sparse to establish a cause-and-effect relationship. 

Reversibility of Noncarcinogenic Systemic Effects. Most case reports of humans intoxicated with carbon tetrachloride indicate that, if death can be averted, clinical signs of renal and hepatic dysfunction diminish within 1-2 weeks, and recovery often appears to be complete. This is primarily because both liver and kidney have excellent regenerative capacity and can repair injured cells or replace dead cells (Dragiani et al. 1986 Norwood et al. 1950). However, high doses or repeated exposure can lead to fibrosis or cirrhosis that may not be reversible. The depressant effects of carbon tetrachloride on the central nervous system do appear to be reversible, although any neural cell death that occurs (Cohen 1957) is presumably permanent. 

Bertelli A, Giovannini L, Bertelli AA, et al. 1986. Tissue concentrations of coenzyme Q in liver of rats intoxicated by carbon tetrachloride. Int J Tissue React 8 343-346. 

Teschke R, Vierke W, Goldermann L. 1983. Carbon tetrachloride (CCH) levels and serum activities of liver enzymes following activities CCh intoxication. Toxicol Lett 17 175-180. 

Barone C, Cittadini A, Galeotti T, et al. 1973. The effect of intoxication induced in rat liver by carbon tetrachloride, ethionine, and white phosphorus on the level of microsomal cytochromes b5 and P450. Experientia 29 73-74. 

Lighter fuels, benzene, toluene, cleaning fluids (carbon tetrachloride), petrol, paraffin, and even the fluorocarbon propellants found in various household sprays and medications have all been used, particularly by children, to produce changes in consciousness. They are all inhaled, often with the aid of a plastic bag, and, since they are lipid-soluble, they are readily concentrated in brain tissue. As with many anesthetics there is an early period of hyperactivity, excitement, and intoxication, followed by sedation and confusion. Prolonged or regular use can cause serious toxicity, with bone-marrow depression, cardiac dysrhythmias, peripheral neuropathy, cerebral damage, and liver and kidney disorders (1). 

De Simplicio, R 1982. Glutathione and glutathione S-transferase in rat liver and plasma after carbon tetrachloride and thioacetamide intoxication. Pharmacology Research... 

Azri and coworkers (1990) have investigated carbon tetrachloride-induced hepato-toxicity in rat liver slices. Liver slices from male rats were incubated and exposed to carbon tetrachloride vapors, and the degree of injury to cellular tissue was determined. Covalent binding of CCU radical to proteins and lipid molecules in a slice caused the cellular injury. The toxicity depended on the vapor concentration and the time of exposure. Azri and coworkers reported further that rats pretreated with phenobarbital were more rapidly intoxicated even at a lower concentration of carbon tetrachloride vapors. On the other hand, pretreatment with allyliso-propylacetamide inhibited the toxicity of carbon tetrachloride. 

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