Bromobenzene

Abstract: Treatment of rats with phenobarbital, which stimulates the activity of the drug-metabolizing enzymes in the liver, potentiates hepatic necrosis elicited by bromobenzene and a number of other chemically inert halogenated aromatic hydrocarbons. Radioautographic studies indicate that [14C]bromobenzene is covalently bound at the sites of necrosis. From these results, it is inferred that the hepatotoxic effects of the halogenated aromatic hydrocarbons are mediated by chemically active metabolites formed in hepatocytes. In accord with this view, a number of aromatic halogenated hydrocarbons are converted by microsomes in vitro to active intermediates which form covalent complexes with glutathione (GSH).

Abstract: [Pd]-exchanged NaY zeolites have been prepared, characterized, and applied for the first time for catalytic carbon-carbon coupling reactions. The catalysts exhibit a high activity and selectivity toward the Heck reaction of aryl bromides with olefins for small palladium concentrations (< or =0.1 mol % of Pd). The catalysts can easily be separated from the reaction mixture and reused after washing without loss in activity. No limitation to the diffusion of adducts in the zeolite cages was observed (for linear alkenes). The electronic nature of the aryl bromides and the olefins has a dominating effect on the reaction yield and selectivity. The heterogeneous catalysts quantitatively convert all types of all aryl bromide (complete conversion of bromobenzene within 30 min) and activated aryl chlorides under standard reaction conditions. Product form selectivity is observed in the Heck reaction with cyclic olefins.

Abstract: The mechanisms of bromobenzene toxicity in extrahepatic tissues of mice were studied. Kidney, lung, heart and brain were examined. As observed in this as well as in a previous report for the liver, bromobenzene intoxication caused a progressive decrease in the glutathione content of all the tissues examined. Cellular damage (as assessed by both biochemical determinations and histologic observations) appeared after 6 hours in the case of the kidney and the heart and after 15 hours in the case of the lung. Lipid peroxidation (as assessed by the tissue content of malonic dialdehyde, a parameter correlating with both the diene conjugation absorption and the amount of carbonyl functions in cellular phospholipids) was found to occur at the same times at which cellular damage was observed or even before. As in the case of bromobenzene-induced liver injury, when the individual values for cell damage obtained at 15-20 hours were plotted against the corresponding glutathione contents, a severe cellular damage was generally observed when the glutathione levels reached a threshold value (3.0-0.5 nmol/mg protein). Such a glutathione threshold was also observed for the onset of lipid peroxidation. Glutathione depletion and lipid peroxidation are therefore general phenomena occurring not only in the liver but in all the tissues as a consequence of bromobenzene poisoning. The possibility that lipid peroxidation is the cause of bromobenzene-induced damage to liver and extrahepatic tissues is discussed.