Carbon tetrachloride induced

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

Panduro, A., et al., Transcriptional switch from albumin to alpha-fetoprotein and changes in transcription of other genes during carbon tetrachloride induced liver regeneration, Biochemistry, 25, 1986. 

Young RA, Mehendale HM. 1986. Effect of endrin and endrin derivatives on hepatobiliary function and carbon tetrachloride-induced hepatotoxicity in male and female rats. Food Chem Toxicol 24 863-868. 

Agarwal AK, Mehendale HM. 1986. Effect of chlordecone on carbon tetrachloride-induced increase in calcium uptake in isolated perfused rat liver. Toxicol Appl Pharmacol 83 342-348. Cited in text... 

Kodayanti PR S, Kodavanti UP, Mehendale HM. 1991. Carbon tetrachloride-induced alterations of hepatic calmodulin and free calcium levels in rats pretreated with chlordecone. Hepatology (Baltimore) 13(2) 230-238. 

Sensitivity to carbon tetrachloride-induced neoplasms varied widely among five strains of rats receiving twice-weekly subcutaneous injections of 2080mg/kg as a 50% solution in corn oil. ... 

Dermal/Ocular Effects. Very few reports mention any effect of carbon tetrachloride inhalation on the skin. Inhalation exposure to carbon tetrachloride for several days in the workplace caused a blotchy, macular rash in one man (but not in six others) (McGuire 1932). Similarly, a hemorrhagic rash occurred in a woman exposed to carbon tetrachloride fumes for several days in the workplace (Gordon 1944), and black and blue marks were seen in a patient exposed intermittently to carbon tetrachloride vapors for several years (Straus 1954). Because observations of dermal effects are so sporadic, it is difficult to judge whether these effects are related to carbon tetrachloride exposure, or are incidental. Conceivably, they may have been secondary to reduced synthesis of blood coagulation factors resulting from carbon tetrachloride-induced hepatotoxicity. No studies were located regarding ocular effects in humans or animals after inhalation exposure to carbon tetrachloride. 

Dermal/Ocular Effects. Skin rashes have been infrequently reported in humans after inhalation exposure (Gordon 1944 McGuire 1932). No data were available on effects by oral exposure or dermal contact. Because the effects were sporadic, no firm conclusions can be made regarding the potential effects of carbon tetrachloride on the skin in humans. No reports are available on the effects of carbon tetrachloride on the eyes. In mice, selective localization of bound radioactivity was observed in the conjunctival epithelium after intravenous injection (Brittebo et al. 1990). However, in the absence of carbon tetrachloride-induced lesions in the conjunctiva, the significance of this metabolism and molecular binding is not clear. 

Immunological Effects. The effects of carbon tetrachloride on the immune system have not been evaluated in humans. Immune responses were not affected in rats orally exposed to carbon tetrachloride (Smialowicz et al. 1991). Parenteral exposure of animals to carbon tetrachloride has been reported to impair the immune system (Kaminski et al. 1989 Muro et al. 1990 Tajima et al. 1985), and oral exposure caused depletion of lymphocytes, hemorrhage, and hemosiderin deposition in the pancreaticoduodenal lymph node (Doi et al. 1991). These findings are supported by in vitro studies in which the IgM antibody formation response of isolated mouse splenocytes to sheep erythrocytes was inhibited in a dose-dependent manner when the splenocytes were exposed to carbon tetrachloride for 1-3 hours in the presence of cocultured hepatocytes (Kaminski and Stevens 1992). No effects were observed in the absence of cocultured hepatocytes. Mice appear to be more sensitive than rats to carbon tetrachloride-induced immunosuppression, but the biological significance to humans of these reported effects are yet ascertainable from the available data. 

Ethanol. Alcohol (ethanol) ingestion has repeatedly been associated with potentiation of carbon tetrachloride-induced hepatic and renal injury in humans. In two cases in which men cleaned furniture and draperies with carbon tetrachloride, one man, a heavy drinker, became ill and died (Smetana 1939). His coworker, a nondrinker, suffered a headache and nausea but recovered quickly after breathing fresh air. Both men were subjected to the same carbon tetrachloride exposure, as they had been working in the same room for the same amount of time. In 19 cases of acute renal failure due to carbon tetrachloride inhalation or ingestion, 17 of 19 patients had been drinking alcoholic beverages at about the time of their carbon tetrachloride exposure (New et al. 

Many other cases of carbon tetrachloride-induced hepatic and/or renal injury associated with ethanol ingestion have been described in the medical literature (Durden and Chipman 1967 Guild et al. 1958 Jennings 1955 Lamson et al. 1928 Markham 1967 Tracey and Sherlock 1968). These clinical reports establish that occasional or frequent ingestion of alcoholic beverages can increase the danger from relatively moderate carbon tetrachloride exposure. As ethanol is known to induce microsomal mixed-function oxidase activity in man (Rubin and Lieber 1968), the mechanism of potentiation may involve ethanol-induced enhancement of the metabolic activation of 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). 

A variety of conditions may predispose certain segments of the population to carbon tetrachloride toxicity. Persons with alcoholic cirrhosis, or other liver diseases which have significantly diminished the functional reserve of the liver, have a reduced capacity to tolerate carbon tetrachloride-induced hepatotoxicity. The same is true for carbon tetrachloride-induced nephrotoxicity in people with significant renal dysfunction from other causes. Diabetics may be particularly susceptible to carbon... 

There are a number of clinical and biochemical tests available that can detect early signs of hepatic and renal injury in humans. However, these tests are not specific for carbon tetrachloride- induced effects. For this reason, studies to identify and measure effects more diagnostic of carbon tetrachloride-specific injury would be helpful. Also, improvements in the sensitivity of these tests would be valuable in evaluating the health status of any individuals who have been exposed to low levels of carbon tetrachloride. 

Relative importance of covalent binding and lipid peroxidation in carbon tetrachloride-induced liver toxicity role of cell calcuim, protein and phospholipid degradation development of treatments/ antidotes. 

Role of phospholipase A-2 in carbon tetrachloride induced hepatotoxicity influence of elevated cell calcium, and... 

Concentration and time dependence of carbon tetrachloride-induced injury to proximal tubule mechanism of action role of metabolism in renal toxicity of carbon tetrachloride. 

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

Role of human cytochrome P450IIG1 and potentiation of carbon tetrachloride-induced hepatoxicity. 

Influence of oxidant stress mechanism carbon tetrachloride-induced hepatic necrosi s. 

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. 

Ariosto F, Riggio 0, Cantafora A, et al. 1989. Carbon tetrachloride-induced experimental cirrhosis in the rat A reappraisal of the model. Eur Surg Res 21 280-286. 

Bengtsson F, Bugge M, Vagianos C, et al. 1987. Brain serotonin metabolism and behavior in rats with carbon tetrachloride-induced liver cirrhosis. Res Exp Med 187 429-438. 

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