RT Journal Article
SR Electronic
T1 Metabolism of haloforms to carbon monoxide. II. In vivo studies.
JF Drug Metabolism and Disposition
JO Drug Metab Dispos
FD American Society for Pharmacology and Experimental Therapeutics
SP 556
OP 560
VO 6
IS 5
A1 Anders, M W
A1 Stevens, J L
A1 Sprague, R W
A1 Shaath, Z
A1 Ahmed, A E
YR 1978
UL http://dmd.aspetjournals.org/content/6/5/556.abstract
AB 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.