. Author manuscript; available in PMC: 2010 Apr 23.

Published in final edited form as: Toxicol Appl Pharmacol. 2008 Dec 9;235(2):143–152. doi: 10.1016/j.taap.2008.11.017

Table 5.

The effects of the FMO inhibitor (methimazole, 500 μM) and CYP inhibitor (ketoconazole, 500 μM) on the biotransformation of fenthion in microsomal fractions isolated from liver from freshwater- and hypersaline-acclimated rainbow trout (Oncorhynchus mykiss)

Exposure	Metabolite	NADPH+ fenthion	NADPH+ methimazole+ fenthion	NADPH+ ketoconazole+ fenthion
Freshwater
	Fenoxon	20.5±2.2	23.0±1.9	6.9±1.3^**
	S-Fenthion sulfoxide	59.6±4.5	42.8±1.7^*	33.7±2.7^*
	R-Fenthion sulfoxide	27.6±2.5	20.5±1.1^*	16.7±1.7^**
	MMTP (NADPH-independent)	7.4±2.9	6.9±2.3	5.3±2.1
	MMTP (NADPH-dependent)	132.2±10.3	132.1±2.3	121.2±15.3
Hypersaline
	Fenoxon	42.2±4.1	47.0±3.7	16.8±2.4^**
	S-Fenthion sulfoxide	298.1±22.4	214.1±8.5^*	168.4±13.2^*
	R-Fenthion sulfoxide	138.3±12.4	72.5±5.4^**	83.4±8.4^**
	MMTP (NADPH-independent)	6.4±2.3	10.1±2.9	4.5±1.1
	MMTP (NADPH-dependent)	21.1±10.5	18.3±2.8	13.2±4.5

Data are presented as pmol/min/mg protein and as mean±SD (n=4 individuals with 3 reaplicated for each one). Significant differences with respect to freshwater-acclimated rainbow trout indicated by ^* (P<0.05; Student’s t-test) and ^** (P<0.01; Student’s t-test).

MMTP: 3-methyl-4-(methylthio)-phenol.

bdl: below detection limit (<0.3 pmol/min/mg protein).