Liver intoxication with

Of particular interest in brevetoxin research are the diagnosis of intoxication and identification of brevetoxins and their metabolites in biological fluids. We are investigating the distribution and fate of radiolabeled PbTx-3 in rats. Three model systems were used to study the toxicokinetics and metabolism of PbTx-3 1) rats injected intravenously with a bolus dose of toxin, 2) isolated rat livers perfused with toxin, and 3) isolated rat hepatocytes exposed to the toxin in vitro. 

Giurgea R, Baba I, Haller J, et al. 1989. Modifications in the liver and thymus of Wistar rats intoxicated with lead. Revue Romaine de Biologie Serie Biologie Animale 34 113-115. 

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. 

Curcumin (9) is an arylheptanoid isolated from turmeric, the rhizome of Curcuma longa L. Turmeric has been used as a remedy for inflammatory in Asia for centuries. There are a number of reports supporting an anti-inflammatory effect of curcumin. Its hepatoprotective activity against inflammatory liver injury was also demonstrated in a recent study [105], where pretreatment with curcumin (50 mg/kg, p.o.) significantly inhibited the elevation of serum transaminase activities after intoxication with D-GalN and LPS in mice. The hepatoprotective effect is presumably... 

A variety of pathological changes of the liver occur with repeated exposures of rats, rabbits,guinea pigs and dogs to PCE. Hepatotoxicity is increased in rats pretreated with aroclor or phenobarbital. This observation as well as the urinary excretion of chlorinated metabolites points to the liver as a probable oxidation site (ref. 67). In man, acute intoxication has generally resulted from industrial degreasing operations. 

N-acetylcysteine is believed to promote the supply of oxygen to the tissues. (72) As a result, this substance, which is free from side effects, was also recommended for cases of CCI4 intoxication (52) and is even considered helpful in acute liver failure with a different aetiology. 

Buko, V., Artsukevich, A., Maltsev, A., Nikitin, V., Ignatenko, V., Gun-dermann, K.-J., Schumacher, R. Effect of polyunsaturated phosphatidylcholine on lipid structure and camp-dependent signal transduction in the liver of rats chronically intoxicated with ethanol. Exp. Toxic. Pathol. 1994 46 375-382... 

Acute intoxication with phenylbutazone is dominated by metabolic acidosis, which can progress to coma, seizures, hypotension, shock, and oliguria. Kidney and liver reactions, acute bone marrow depression, and acute perforation of peptic ulcer have all been described (5,11,35). 

Szarek J, Fabczak J, Zasadowski A, et al. 1995. Pathomorphological pattern of the liver and kidney in rats exposed to mixed intoxication with selenium and diazinon. Pathol Res Pract 191(7-8) 790. 

Wronska-Nofer T, Tarkowski S, Gomy R, et al. 1972. Accelerated turnover rate of nicotinamide-adenine dinucleotides in the liver of rats intoxicated with carbon disulfide. Biochem Pharmacol 21 2945-1950. 

Figure 2 summarizes the localization of the egasyn-pG complex and dissociation and release of PG from liver microsomes into plasma. When animals a.s well as humans arc intoxicated with OP, the OP is incorporated into the liver microsomes and metabolized to form the corresponding oxon. In order to study the release of PO from the liver to plasma, rats and hamsters were treated with bis-p-nitrophenylphosphaie, which is a specific CarbE inhibitor, and plasma pG activities were determined. As shown in Table 2, plasma pG activities... 

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