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Carbon tetrachloride liver toxicity

Ko, K.M., M.K.T. Poon, S.P. Ip, K. Wu, and R. Ko. 2002. Protection against carbon tetrachloride liver toxicity by enantiomers of schisandrin B associated with differential changes in hepatic glutathione antioxidant system in mice. Pharm. Biol. 40(4) 298-301. [Pg.797]

Bruckner JV, Luthra R, Kyle GM, et al. 1984. Influence of time of exposure to carbon tetrachloride on toxic liver injury. Ann Rev Chronopharmacol 1 373- 376. [Pg.151]

Carbon tetrachloride is toxic through both inhalation and ingestion. Toxic symptoms from inhalation tend to be associated with nervous system, whereas those from ingestion often involve the gastrointestinal tract and liver. Both the liver and kidney may be substantially damaged by carbon tetrachloride. [Pg.344]

Fennel oil displayed an anti-inflammatory, central analgesic, and antioxidant effect in experimental animals. The oil also had a hepatoprotective effect against carbon tetrachloride-induced toxicity in a liver injury model in rats. ... [Pg.284]

Hepatic Hepatic means "pertaining to the liver." For example, hepatitis is inflammation of the liver. Liver disorders are sometimes marked by jaundice, a yellowish coloration to the whites of the eyes and skin. Certain chemicals are hepatotoxins (toxic to the liver), usually as a result of chronic exposure. One example is carbon tetrachloride (CCI4). [Pg.531]

Yellow phosphorus was the first identified liver toxin. It causes accumulation of lipids in the liver. Several liver toxins such as chloroform, carbon tetrachloride, and bromobenzene have since been identified. I he forms of acute liver toxicity are accumulation of lipids in the liver, hepartxiellular necrosis, iii-trahepatic cholestasis, and a disease state that resembles viral hepatitis. The types of chrome hepatotoxicity are cirrhosis and liver cancer. [Pg.298]

Le Page, KN., Cheeseman, K.H., Osman, N. and Slater, T.F. (1988). Lipid peroxidation in purified plasma membrane fractions of rat liver in relation to the toxicity of carbon tetrachloride. Cell Biochem. Function 6, 87-99. [Pg.244]

Chlordane interacts with other chemicals to produce additive or more-than-additive toxicity. For example, chlordane increased hepatotoxic effects of carbon tetrachloride in the rat (USEPA 1980 WHO 1984), and in combination with dimethylnitrosamine acts more than additively in producing liver neoplasms in mice (Williams and Numoto 1984). Chlordane in combination with either endrin, methoxychlor, or aldrin is additive or more-than-additive in toxicity to mice (Klaassen et al. 1986). Protein deficiency doubles the acute toxicity of chlordane to rats (WHO 1984). In contrast, chlordane exerts a protective effect against several organophosphorus and carbamate insecticides (WHO 1984), protects mouse embryos against influenza virus infection, and mouse newborns against oxazolone delayed hypersensitivity response (Barnett et al. 1985). More research seems warranted on interactions of chlordane with other agricultural chemicals. [Pg.869]

No other studies of interactions of hexachloroethane with other chemicals were identified in the published literature. However, the primary metabolites of hexachloroethane (tetrachloroethene and pentachloroethane) are themselves toxic and would be expected to exacerbate hexachloroethane toxicity if they were present in a mixture with hexachloroethane. Concurrent carbon tetrachloride exposure would also be expected to exacerbate hexachloroethane toxicity. Both hexachloroethane and carbon tetrachloride are processed by microsomes to generate free radicals, and carbon tetrachloride also forms endogenous hexachloroethane in the liver (Fowler 1969a). [Pg.99]

Nachtomi E, Alumot E. 1972. Comparison of ethylene dibromide and carbon tetrachloride toxicity in rats and chicks Blood and liver levels lipid peroxidation. Exp Mol Pathol 16 71-78. [Pg.126]

Because 1,4-dichlorobenzene is a liver toxin, it probably can interact with other chemicals that are liver toxicants. These toxicants are many, and include ethanol, halogenated hydrocarbons (chloroform, carbon tetrachloride, etc ), benzene, and other haloalkanes and haloalkenes. In addition, 1,4-dichlorobenzene toxicity may also be exacerbated by concurrent exposure with acetaminophen, heavy metals (copper, iron, arsenic), aflatoxins, pyrrolizidine alkaloids (from some types of plants), high levels of vitamin A, and hepatitis viruses. Such interactions could either be additive or S5mergistic effects. [Pg.152]

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... [Pg.127]

When absorbed, isopropyl alcohol is oxidized in the liver at the hydroxyl moiety and converted to acetone." Occupational exposure to isopropyl alcohol can be biomonitored by means of urinalysis for acetone after exposures as low as 70ppm." The acetone metabolite may also be responsible for the enhanced toxicity of carbon tetrachloride following pretreatment of animals with isopropyl alcohol. Extra caution is in order when isopropyl alcohol is... [Pg.414]

Cardiovascular Effects. Most studies of humans exposed to carbon tetrachloride by inhalation have not detected significant evidence of cardiovascular injury, even at exposure levels sufficient to markedly injure the liver and/or kidney. Changes in blood pressure, heart rate, or right- sided cardiac dilation have sometimes, but not always, been observed (Ashe and Sailer 1942 Guild et al. 1958 Kittleson and Borden 1956 Stewart et al. 1961 Umiker and Pearce 1953), and are probably secondary either to fluid and electrolyte retention resulting from renal toxicity, or to central nervous system effects on the heart or blood vessels. Carbon tetrachloride also may have the potential to induce cardiac arrhythmias by sensitizing the heart to epinephrine, as has been reported for various chlorinated hydrocarbon propellants (Reinhardt et al. 1971). [Pg.30]


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