Metabolism of haloforms to carbon monoxide. II. In vivo studies.
Administration of haloforms (trihalomethanes) to rats led to substantial elevations in blood carbon monoxide levels. The administration of 13C-bromoform led to the formation of similarly enriched 13CO. A dose-dependent relationship between bromoform dose and CO production was observed. It was found that phenobarbital, but not 3-methylcholanthrene, treatment increased the blood CO levels seen after the administration of bromoform as compared to saline-treated controls. Lower blood CO levels were found in rats given 2H-bromoform as compared to rats given bromoform. Furthermore, SKF 525-A significantly inhibited the in vivo metabolism of bromoform to CO. Administration of either diethyl maleate or D-penicillamine did not alter the blood CO levels produced in response to bromoform administration. The in vivo metabolism of haloforms to CO followed the halide order; thus, administration of iodoform yielded the highest blood CO levels, whereas chloroform yielded the lowest levels.
D000818:Animals; D002248:Carbon Monoxide / Q000096:biosynthesis* / Q000097:blood; D002263:Carboxyhemoglobin / Q000378:metabolism; D006846:Hydrocarbons, Halogenated / Q000378:metabolism*; D008297:Male; D008697:Methane / Q000031:analogs & derivatives* / Q000378:metabolism; D051381:Rats; D013329:Structure-Activity Relationship
D006846:Hydrocarbons, Halogenated; D002248:Carbon Monoxide; D002263:Carboxyhemoglobin; D008697:Methane