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Human tissue burdens of halogenated aromatic chemicals in Michigan.

A cross section of the population of Michigan was studied in 1978 to evaluate residual burdens of polybrominated biphenyls (PBBs), a flame-retardant chemical that had contaminated the state's food supply five years earlier. Levels of PBB were measured in serum specimens in 1,681 people and in adipose samples in 844. Ninety-seven percent of the adipose samples had detectable PBB concentrations. Levels of PBB were highest in that part of the state where meat and dairy products had been most contaminated and were lowest in the upper peninsula, farthest from the source. Levels for the rest of the state were in between. Polychlorinated biphenyls (PCB) and 2,2'-bis(p-chlorophenyl)-1, 1-dichloroethylene (p,p'-DDE), a dichlorodiphenyltrichloroethane (DDT) residue, were also measured, and variations of PBB, PCB, and p,p'-DDE levels with age and sex were investigated.

Accidents↗

[Cysteine activity in the poisoning of animals by various aliphatic series halogenated hydrocarbons].

In poisoning animals with various aliphatic series haloid-hydrocarbons (LK99 and LD99) free cysteine was found to be a group antidote in rats poisoned with monohaloid-hydrocarbons. It was established that the therapeutic activity of cystein depends not on the nature of haloid and double bonds, but on the number of the haloid atoms in a molecule, the length, ramification and nature of the radical. A good durative action are shown by such cystein derivatives as acetyl-cysteine, glutathione and cystein salts. In poisoning with haloid-alkyls dithiol antidotes (unithiol, mecaptide, BAL) and other drugs proved ineffective.

Acetylcysteine↗

Improved staining characteristics of serum lipids after halogenation and esterification of thin-layer chromatograms.

We describe a procedure for treatment of thin-layer chromatographic serum lipid patterns so that they may be stained by dyes for evaluation by densitometry. After development of the chromatogram [Clin. Chem. 18, 384 (1972)] the plates are dried and sprayed with butyryl chloride. This esterifies the free cholesterol. After drying, the plate is treated with iodine monobromide, to add iodline to the double bonds. The triacylglycerols (triglycerides), cholesterol esters, free cholesterol, and phospholipids are now all in the form of esters with no unsaturated double bonds. The free fatty acids are also now saturated. The chromatogram is now stained with basic fuchsine in acetate buffer (0.1 mol/liter, pH 5.0). Excess stain is removed with a buffered solution of guanidine hydrochloride. Erythrosine B may also be used. With basic fuchsine the background will be a uniform pink. With erythrosine B the background is white, but the stain tends to be washed out of the free fatty acids. The chromatograms are evaluated by densitometry, with use of a 540-nm filter for basic fuchsine and a 520-nm filter for erythrosine B. The stained chromatograms and densitometric scans accurately represent the relative concentration of the various lipid fractions as compared to that of an internal standard, and correlate with the nature of the disease being explored.

Adult↗

Halogenated methanes: metabolism and toxicity.

Dihalomethanes are metabolized to carbon monoxide (CO) both in vivo and in vitro. The reaction is catalyzed by the hepatic microsomal cytochrome P-450 dependent mixed function oxidase system. Reaction mechanism studies suggest an initial oxygen insertion reaction followed by rearrangement to a formyl halide intermediate, which in turn decomposes to yield CO. In vitro studies show that [14C]dichloromethane becomes covalently bound to both microsomal protein and lipid. The similar characteristics of metabolism to CO and covalent suggest that a common intermediate, perhaps the formyl halide, may be involved. Dihalomethanes are also metabolized for formaldehyde, formic acid, and inorganic halide. A glutathione transferase located in hepatic cytosol fractions appears to be involved. Reaction mechanism studies suggest that a S-hydroxymethyl glutathione intermediate may yield formaldehyde or be diverted via formaldehyde dehydrogenase/S-formyl glutathione hydrolase to yield formic acid. Haloforms are also metabolized to carbon monoxide both in vivo and in vitro by a hepatic microsomal cytochrome P-450 dependent mixed function oxidase system. In vitro, this reaction is markedly stimulated by sulfhydryl compounds. Reaction mechanism studies suggest an initial oxygen insertion reaction followed by rearrangement to a dihalocarbonyl intermediate, which in turn reacts with sulfhydryl reagents to yield a thiol-S-formyl halide. Subsequent attack by other sulfhydryl compounds would result in the formation of CO and a disulfide.

Biotransformation↗