Lipid peroxidation induced by some halomethanes as measured by in vivo pentane production in the rat
Sagai, M.; Tappel, A.L.
Toxicology and Applied Pharmacology 49(2): 283-291
1979
ISSN/ISBN: 0041-008X PMID: 494281 Document Number: 147890
Pentane production in vivo in rats was used as an index to support the concept that lipid peroxidation is involved in the toxicity of some halomethanes. Time-response relationships showed that the rats had maximum pentane production by 15-30 min following i.p. administration of carbon tetrachloride (CCl4), bromotrichloromethane (BrCCl3) and chloroform (CHCl3). BrCCl3 and CCl4 caused the production of the greatest amounts of pentane, CHCl3 induced a smaller amount of pentane production, and dichloromethane (CH2Cl2) did not increase pentane production over that caused by injection of the mineral oil carrier. There was a good relationship (r = 0.987; P < 0.001) between the amount of pentane produced and the bond dissociation energies of BeCCl3, CCl4, and CHCl3. Trichloromethyl radicals (.cntdot.CCl3) produced by homolytic cleavage of halomethanes evidently induce lipid peroxidation. Conjugated dienes in liver, kidney, intestine, spleen, lung and heart were measured following administration of CCl4 and BrCCl3. There was a good correlation (r = 0.96; P < 0.01) between pentane production in vivo and conjugated diene formation in the liver. The liver accounted for 85 and 94% of the total conjugated dienes measured after administration of CCl4 and BrCCl3, respectively. The amount of pentane produced during a 30-min period following injection of 1 mmol of CCl4 corresponded to .apprx. 0.2% of the lipid peroxides, measured as conjugated dienes, in the liver following the same time period. Pentane production occurs principally in the liver.