Liver chloroform

A sex-related difference in chloroform metabolism was observed in mice (Taylor et al. 1974). Chloroform accumulated and metabolized in the renal cortex of males to a greater extent than in females, while liver chloroform concentrations were greater in females than in males the results may have been influenced by testosterone levels. This effect was not observed in any other species and may explain why male mice were more susceptible to the lethal and renal effects of chloroform than were females (Deringer et al. 

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. 

Liver cancer can also be a consequence of exposure to hepatotoxic chemicals. Natural hepatocarcinogens include fungal aflatoxins. Synthetic hepato-carcinogens include nitrosoamines, certain chlorinated hydrocarbons, polychlorinated biphenyls (PCBs), chloroform, carbon tetrachloride, dimethyl-benzanthracene, and vinyl chloride.Table 5.15 lists the chemical compounds that induce liver cancer or cirrhosis in experimental animals or... 

One type of fatty liver that has been smdied extensively in rats is due to a deficiency of choline, which has therefore been called a lipotropic factor. The antibiotic puromycin, ethionine (a-amino-y-mercaptobu-tyric acid), carbon tetrachloride, chloroform, phosphorus, lead, and arsenic all cause fatty liver and a marked reduction in concentration of VLDL in rats. Choline will not protect the organism against these agents but appears to aid in recovery. The action of carbon tetrachloride probably involves formation of free radicals... 

Unconjugated hyperbilirubinemia can result from toxin-induced liver dysfunction such as that caused by chloroform, arsphenamines, carbon tetrachloride, acetaminophen, hepatitis virus, cirrhosis, and Amanita... 

The most critical decision to be made is the choice of the best solvent to facilitate extraction of the drug residue while minimizing interference. A review of available solubility, logP, and pK /pKb data for the marker residue can become an important first step in the selection of the best extraction solvents to try. A selected list of solvents from the literature methods include individual solvents (n-hexane, " dichloromethane, ethyl acetate, acetone, acetonitrile, methanol, and water ) mixtures of solvents (dichloromethane-methanol-acetic acid, isooctane-ethyl acetate, methanol-water, and acetonitrile-water ), and aqueous buffer solutions (phosphate and sodium sulfate ). Hexane is a very nonpolar solvent and could be chosen as an extraction solvent if the analyte is also very nonpolar. For example, Serrano et al used n-hexane to extract the very nonpolar polychlorinated biphenyls (PCBs) from fat, liver, and kidney of whale. One advantage of using n-hexane as an extraction solvent for fat tissue is that the fat itself will be completely dissolved, but this will necessitate an additional cleanup step to remove the substantial fat matrix. The choice of chlorinated hydrocarbons such as methylene chloride, chloroform, and carbon tetrachloride should be avoided owing to safety and environmental concerns with these solvents. Diethyl ether and ethyl acetate are other relatively nonpolar solvents that are appropriate for extraction of nonpolar analytes. Diethyl ether or ethyl acetate may also be combined with hexane (or other hydrocarbon solvent) to create an extraction solvent that has a polarity intermediate between the two solvents. For example, Gerhardt et a/. used a combination of isooctane and ethyl acetate for the extraction of several ionophores from various animal tissues. 

Normal phase silica column Chloroform-methanol-ammonia solution (86.8 12.5 0.7) 254 nm Assay of primaquine and hepatic targeting neoglycoalbumin-primaquine in whole blood and liver of mouse by reversed-phase HPLC. [105]... 

Extraction of nalidixic acid with chloroform from utine has also been reported.(40) Another fluorimetric method for chicken liver and muscle containing not less than 100 ppb nalidixic acid was reported by Browning(9) using an ethyl-acetate extraction and alumina column to retain the nalidixic acid. The fluorescence was measured at 325/408 nm. 

Since arylazoamidoximes release nitric oxide when incubated in rat liver microso-mial fraction [172], 3-arylazo-l,2,4-oxadiazol-5-ones 136 have been prepared from the corresponding arylazoamidoximes 134 as their potential pro-drugs [172]. Reaction with chloroformate afforded compounds 135 which underwent cyclisation to 136 in alkaline medium (Scheme 6.26). 

Mansuy, D., Beaune, P., Crestell, T., Lange, M., and Leroux, M. 1977. Evidence for phosgene formation during liver microsomal oxidation of chloroform. Biochem. Biophys. Res. Comm. 79 513-517. 

Pohl, L.R., Martin, J.L., and George, J.W. 1980a. Mechanism of metabolic activation of chloroform by rat liver microsomes. Biochem. Pharmacol. 29 3271—3276. 

Thibaut et al. [14] published a procedure for determination of NP and NP transformation products in snails, duckweed and trout liver and viscera. Samples were homogenised in MeOH, and either directly chromatographed on HPLC (liver, duckweed), or subjected to a further clean-up using L/L partitioning with methanol, chloroform and acetonitrile/isooctane, successively. 

Hewitt LA, Palmason C, Masson S, et al. 1990. Evidence for the involvement of organelles in the mechanism of Kepone-potentiated chloroform-induced hepatotoxicity. Liver 10(1) 35-48. 

A drin and Dieldrin Metabolism.— The in vivo metabolism of the chlorinated alicyclic insecticides, aldrin and dieldrin, has been measured. Fish were exposed to l c-labelled aldrin or dieldrin for 6 hours. The metabolism of each compound was monitored by thin layer chromatography of hexane and chloroform-methanol extracts of liver homogenates, followed by liquid scintillation counting of the spots (5,15,16). 

Chloroform can enter your body if you breathe air, eat food, or drink water that contains chloroform. Chloroform easily enters your body through the skin. Therefore, chloroform may also enter your body if you take a bath or shower in water containing chloroform. In addition, you can breathe in chloroform if the shower water is hot enough for chloroform to evaporate. Studies in people and in animals show that after you breathe air or eat food that has chloroform in it, the chloroform can quickly enter your bloodstream from your lungs or intestines. Inside your body, chloroform is carried by the blood to all parts of your body, such as the fat, liver, and kidneys. Chloroform usually collects in body fat however, its volatility ensures that it will eventually be removed once the exposure has been removed. Some of the chloroform that enters your body leaves unchanged in the air that you breathe out, and some chloroform in your body is broken down into other chemicals. These chemicals are known as breakdown products or metabolites, and some of them can attach to other chemicals inside the cells of your body and may cause harmful effects if they collect in high enough amounts in your body. Some of the metabolites also leave the body in the air you breathe out. Only a small amount of the breakdown products leaves the body in the urine and stool. 

Although we can measure the amount of chloroform in the air that you breathe out, and in blood, urine, and body tissues, we have no reliable test to determine how much chloroform you have been exposed to or whether you will experience any harmful health effects. The measurement of chloroform in body fluids and tissues may help to determine if you have come into contact with large amounts of chloroform. However, these tests are useful only a short time after you are exposed to chloroform because it leaves the body quickly. Because it is a breakdown product of other chemicals (chlorinated hydrocarbons), chloroform in your body might also indicate that you have come into contact with those other chemicals. Therefore, small amounts of chloroform in the body may indicate exposure to these other chemicals and may not indicate low chloroform levels in the environment. From blood tests to determine the amount of liver enzymes, we can tell whether the liver has been damaged, but we cannot tell whether the liver damage was caused by chloroform. 

Larson et al. (1996) investigated the ability of acute chloroform vapor exposure to produce toxicity and regenerative cell proliferation in the liver of female B6C3F, mice. Groups of 5 animals were exposed to 0, 0.3, 2, 10, 30, or 90 ppm chloroform via inhalation for 6 hours a day for 4 consecutive days. Animals were administered BrdU via an implanted osmotic pump, and cell proliferation was quantitated as the percentage of cells in S-phase (LI) measured by immunohistochemical detection of BrdU-labeled nuclei. 

At necropsy, livers were removed, weighed, examined macroscopically, and prepared for microscopic evaluation. Exposure to 90 ppm chloroform resulted in increased relative liver weights. Female mice exposed to chloroform for 4 days experienced a dose-dependent mild response of uniform hepatocyte lipid vacuolization. Scattered individual hepatocyte necrosis also occurred in a dose-dependent manner. 

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