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PubMed1983

Allergic contact dermatitis due to highly reactive halogenated compounds.

10 cases of dermatitis in a fine organic chemicals plant are reported. These cases were all due to exposure to chemical compounds with reactive bromine or chlorine atoms. This type of chemical is always extremely irritant, but evidence is put forward to suggest that these cases were the result of allergic sensitization. Chemicals with reactive halogen atoms should always be handled with extreme care and patch testing should be approached with caution.

Adult↗
PubMed1990

[Volatile organic halogen compounds in food].

Volatile halocarbons have been found in raw water, chlorinated tap water, in blood of healthy individuals and patients, in milk, urine, solutions and laboratory suspensions manufactured by the Medical Industry. Tap water is also used in the food industry and therefore it is reasonable that they also could be analysed in food.

Animals↗
PubMed1985

Model studies in cytochrome P-450-mediated toxicity of halogenated compounds: radical processes involving iron porphyrins.

Haloalkane toxicity originates from attack on biological targets by reactive intermediates derived from haloalkane metabolism by a hemoprotein, cytochrome P-450. Carbon-centered radicals and their peroxyl derivatives are most likely involved. The reactions of iron porphyrin--a model for cytochrome P-450--with various carbon-centered and peroxyl radicals generated by pulse radiolysis are examined. Competition between iron porphyrin and unsaturated fatty acids for attack by peroxyl radicals is pointed out. These kinetic data are used to derive a model for toxicity of haloalkanes with particular attention to carbon tetrachloride and halothane. The importance of local oxygen concentration and structural arrangement of fatty acids around cytochrome P-450 is emphasized.

Animals↗
PubMed1990

Impact of halogenated compounds on calcium homeostasis in hepatocytes.

Halocarbons (CCl4, 1,1-dichlorethylene) cause a wide spectrum of effects and injury in hepatocytes. One early effect of these compounds is the inhibition and destruction of the endoplasmic reticulum (ER) calcium pump. Subsequent to inhibition of this pump, the ER calcium pool is depleted and cytosolic levels of calcium are increased for a prolonged period of time. This effect of halocarbons has been characterized and is similar in vivo and in vitro. The importance of this redistribution of cell calcium in expression of halocarbon injury of hepatocytes has not been fully resolved. Several degradative enzymes (phospholipases, proteases) have been implicated as calcium-dependent mediators in toxicity. Our preliminary studies of the effect of calcium redistribution suggest that activation of a calcium-sensitive endonuclease in liver does not play a central role in initiating the lethal effect of halocarbons on hepatocytes.

Animals↗
PubMed1983

Toxic activity of seventeen industrial solvents and halogenated compounds on human lymphocytes cultured in vitro.

Seventeen chemicals (solvents, insecticides and intermediates in the production of textiles and resins) were tested in a short-term in vitro system with human lymphocytes to determine their toxic action. The parameters studied were the tritiated thymidine uptake and cell viability in cultures grown with or without a rat liver metabolizing system (S-9 mix). Data obtained showed that 1,3-dichlorobenzene, 1,2-dichlorobenzene, hexane, 1,2-diiodoethane, 1,4-dichlorobenzene, tetrachloroethylene, 2,3-dibromopropanol, chloromethyl methyl ether, 1,2- and 1,3-dibromopropane, in order, exerted the more toxic effects; ethyl acetate, cyclohexane, cyclohexanone and benzene showed lower toxic activity. The chemicals lost their toxic power in the presence of the metabolizing system with the exception of 1,2- and 1,3-dichlorobenzene which maintained in some degree their toxicity even in the presence of the S-9 mix. Only chloromethyl methyl ether elicited unscheduled DNA synthesis acting as DNA damaging agent.

Adult↗
PubMed1989

Damage to protein synthesis concurrent with lipid peroxidation in rat liver slices: effect of halogenated compounds, peroxides, and vitamin E1.

Protein synthesis and lipid peroxidation were evaluated in rat liver slices incubated in the presence of oxidants and protein synthesis inhibitors. Protein synthesis by rat liver slices was evaluated by [3H]leucine incorporation into the trichloroacetic acid (TCA)-insoluble material, and lipid peroxidation was evaluated by thiobarbituric acid-reactive substances (TBARS) released into the incubation medium. Protein synthesis inhibition by bromotrichloromethane (BrCCl3) or t-butyl hydroperoxide (t-BOOH) depended on the incubation time and oxidant concentration. [3H]Leucine incorporation was decreased to 20 and 47% of control values and TBARS were enhanced from the control value of 16.9 to 45.3 and 62.5 nmol/g of liver by incubation for 1 h with 1 mM BrCCl3 and t-BOOH, respectively. Following incubation, both protein synthesis damage and lipid peroxidation were decreased in control and oxidant-treated slices prepared from rats injected with 200 mg of DL-alpha-tocopherol/kg of body wt. Release of lactate dehydrogenase was not enhanced by oxidant treatment. Protein synthesis inhibitors reversibly decreased [3H]leucine incorporation, but the effect of oxidants on protein synthesis was irreversible. Cumene hydroperoxide and methyl ethyl ketone peroxide, but not hydrogen peroxide, damaged protein synthesis and induced lipid peroxidation. The ability of carbon tetrabromide, benzyl chloride, bromoform, bromobenzene, carbon tetrachloride, chloroform, dichloromethane, and bromochloromethane to inhibit protein synthesis was correlated with their ability to induce lipid peroxidation, and with their LD50. The results suggest that oxidant-induced lipid peroxidation and protein synthesis damage occurred concurrently, and that protein synthesis inhibition may be involved in cell injury or death mediated by free radicals.

Animals↗
PubMed1979

Studies on biologically active halogenated compounds. 1. Synthesis and central nervous system depressant activity of 2-(fluoromethyl)-3-aryl-4(3H)-quinazolinone derivatives.

Some 2-(fluoromethyl) analogues of 2-methyl-3-aryl-4-(3H)-quinazolinones have been synthesized and screened for CNS activities. It was shown that the 2-(fluoromethyl) analogues possess in general more potent CNS depressant activities and less toxicities than their parent compounds. Of particular interest were the 2-(fluoromethyl) analogues (22, 24, and 31) of methaqualone and 6-aminomethaqualone. Compound 24 was more potent in CNS depressant activity and less toxic than methaqualone. Compound 31 exhbited potent central muscle relaxing activity and markedly reduced toxicity as compared with 6-aminomethaqualone.

Animals↗
PubMed1976

[Diagnostic tests for hypersensitivity to halogen compounds].

The authors present a critical analysis of immunological tests used by some authors to establish the diagnosis of halothane-induced hepatitis. These tests include the lymphocyte transformation test (LTT), the leukocyte migration inhibition test (LMIT) and detection of auto-antibodies. It has not been possible for all investigators to reproduce the results of these tests. The inhibition of these tests is not specific for halothane since it is also observed after infectious and serum viral hepatitis.

Autoantibodies↗
PubMed1992

In vivo studies on halogen compound interactions. III. Effect of carbon tetrachloride plus 1,2-dichloroethane on liver necrosis and fatty accumulation.

The effect of a single dose of carbon tetrachloride (CT), 1,2-dichloroethane (DCE) and the mixture on liver toxicity was investigated. The co-presence of both toxins exerts a more than additive effect on liver necrosis and on TBA-reactive substances produced by liver homogenates incubated at 37 degrees C. Both these effects are prevented in animals treated with vitamin E. The liver GSH is not involved in the synergistic action. The liver triglyceride levels of rats treated with the mixture are lower than in those treated with CT alone. This finding cannot be explained either by an improvement in the lipoprotein secretion or by the fact that the liver receives less NEFA. It is thus likely that the apparent protection against liver steatosis is the sign of more severe damage to the liver cell that partially blocks triglyceride synthesis. The mixture composed of CT+DCE exerts a potentiating action on liver toxicity with CT+DCE having the same characteristics as those, as previously reported, exerted by the co-presence of CT+DBE.

Alanine Transaminase↗