Liver injury carbon tetrachloride induce

Galati, E.M. et al., Opuntia jicus indica (L.) Mill fruit juice protects liver from carbon tetrachloride-induced injury, Phytother. Res., 19, 796, 2005. 

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],... 

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). 

Bhathal PS, Rose NR, Mackay IR, et al. 1983. Strain differences in mice in carbon tetrachloride-induced liver injury. Br J Exp Pathol 64 524-533. 

Biesel KW, Ehrinpreis MN, Bhathal PS, etal. 1984. Genetics of carbon tetrachloride-induced liver injury in mice. II. Multigenic regulation. Br J Exp Pathol 65 125-131. 

Towner RA, Reinke LA, Janzen EG, et al. 1991. Enhancement of carbon tetrachloride-induced liver injury by a single dose of ethanol proton magnetic resonance imaging (MRI) studies In vivo. Acta Biochem Biophys 1096 222- 230. 

Singh, N., Kamath, V., Narasimhamurthy, K., Rajini, P. S. (2008). Protective effect of potato peel extracts against carbon tetrachloride-induced liver injury in rats. Environ. Toxicol. Pharmacol, 26(2), 241-246. 

Czaja, M.J., Xu, J. Alt, E. (1995) Prevention of carbon tetrachloride-induced rat liver injury by soluble tumor necrosis factor receptor. Gastroenterology, 108. 1849-1854... 

ElSisi, A.E., Hall, P, Sim, W.-L. W, Earnest, D.L. Sipes, I.G. (1993c) Characterization of vitamin A potentiation of carbon tetrachloride-induced liver injury. Toxicol, appl. Pharmacol., 119, 280-288... 

The hepatotoxicity produced by acute carbon tetrachloride-induced liver injury was found to be inhibited by essential oil from fennel, as evidenced by decreased levels of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and bilirubin (Ozbek et al., 2003). 

Carbon tetrachloride-induced liver injury is another animal model for studying free-radical injury to tissues. Animals maintained on high zinc regimen are resistant to this type of biochemical injury, thus suggesting that zinc may be protective against free-radical injury. More recent studies have shown that zinc also inhibits the analogous metro-midazole-dependent, free-radical sequence. 

Figure 4. Dose-response curve for carbon tetrachloride-induced liver injury in male rats. The carbon tetrachloride was dissolved in corn oil and doses of 0 (controls), l, 10, and 33 mg/kg b.w. were administered 5 dayslweek for 12 weeks. Severe liver injury was observed in all animals at the highest dose, but only relatively mild changes (increased liver weights) were seen at 10 mg/kg b.w. No differences of any type were observed between the control and low dose animals. The dose of 1 mg/kg b.w. is thus a NOEL for this species and this period of dosing. Data were reported by J.V. Bruckner and co-workers in 1986 in Fundamental and Applied Toxicology, Vol. 6 (No. 1), pages 16—34.

Fujisawa K, Yabuuchi C, Izawa T, Kuwamura M, Takasu N, Torii M, Yamate J (2013) Expression patterns of heat shock protein 25 in carbon tetrachloride-induced rat liver injury. Exp Toxicol Pathol 65(5) 469-476. doi 10.1016/j.etp.2012.02.001... 

Wang, D., Verney, E., and Sidransky, H., Protective effect of tryptophan and cysteine against carbon tetrachloride-induced liver injury, Exp. Mol. Pathol., 43, 364, 1985. 

Ohta, Y., Kongo, M., Sasaki, E., Nishida, K., and Ishiguro, I., Therapeutic effect of melatonin on carbon tetrachloride-induced acute liver injury in rats, J. Pineal... 

Raiford, D. S., and Thigpen, M. C. (1994). Kupffer cell stimulation with Corynebacterium parvum reduces some cytochrome P450-dependent activities and diminishes acetaminophen and carbon tetrachloride-induced liver injury in the rat. Toxicol. Appl. Pharmacol. 129, 36-45. 

Cytokines have also been shown to play protective roles in several liver injury models, including viral hepatitis, carbon tetrachloride (CCl4)-induced liver injury, concanavalin A-induced liver injury, 1/R injury, partial hepatectomy, and AILI, where they exert their hepatoprotective effects by downregulating inflammatirm and promoting liver regeneration (Diehl 2000 Gao 2005 James et al. 2005b Lacour et al. 2005 Liu and Kaplowitz 2006). 

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. 

Mitcheva, M., Astroug, H., Drenska, D., Popov, A., and Kassarova, M. 1993. Biochemical and morphological studies on anthocyans and vitamin E on carbon tetrachloride induced liver injury. Cell Mol Biol 39, 443-448. 

B2 (59) has been noted to exhibit activity which promotes restoration of hepatocyte function against carbon tetrachloride induced liver cell injury in rat (206). 

Eukao, T., Hosono, T., Misawa, S. Seki, T., and Ariga, T. 2004. Chemoprotective effect of diallyl trisulfide from garlic against carbon tetrachloride-induced acute liver injury of rats. BioFactors 21 171-174. 

Enhanced Therapeutic Benefit of QuercetinPhospholipid Complex in Carbon Tetrachloride-Induced Acute Liver Injury in Rats A Comparative Study. Iranian Journal of Pharmacology and Therapeutics (IJPT). 

Loki, A. L., Rajamohan, T. (2003). Hepatoprotective and antioxidant effect of tender coconut water on carbon tetrachloride induced liver injury in rats. 

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. ... 

Iwai, S., Karim, R., Kitano, M., Sukata, T., Min, W., Morimura, K., Wanibuchi, H., Seki, S., and Fukushima, S. (2002). Role of oxidative DNA damage caused by carbon tetrachloride-induced liver injury- enhancement of MelQ-induced glutathione S-transferase placental form-positive foci in rats. Cancer Lett. 179,15-24. 

Bai C-L, Canfield PJ, Stacey NH. 1992. Individual serum bile acids as early indicators of carbon tetrachloride- and chloroform-induced liver injury. Toxicol 75(3) 221-234. 

Lee, C.H. et al. (2007) Protective mechanism of glycyrrhizin on acute liver injury induced by carbon tetrachloride in mice. Biological ei Pharmaceutical Bulletin, 30 (10), 1898-1904. 

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