Cytochrome P450 enzymes - 2E1
Inhibitors
-
tioconazole K(i), 0.4 microM) = high affinity
- chlormethiazole
-
diallyl sulfide (in garlic)
-
disulfiram
-
A number of phytochemicals; eg isothiocyanates in cruciferous vegetables [sulforaphane and phenethylisothiocyanate]
Substrates
-
Ethyl alcohol
-
chlorzoxazone, 6-hydroxylation (marker)
-
Sodium salicylate and acetylsalicylic acid
-
paracetamol (acetaminophen)
-
valproic acid
-
pro carcinogens, and low molecular weight solvents (inc. alcohols)
-
fatty acids and ketone bodies
Inducers
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colchicine
-
nicotine
-
isoniazid
-
cigarette smoke
-
Ethyl alcohol
Genetic polymorphism
Probably polymorphic; ? functional consequences
In view of the potential role of CYP2E1 in alcohol-induced oxidative stress and liver injury, the potentiation of CYP2E1-dependent toxicity and the elevation of CYP2E1 levels by salicylate may be of clinical significance; caution in the use of salicylates with some other drugs may be appropriate. Alcohol can contribute to oxidative stress through its microsomal metabolism via cytochrome 2E1
Paracetamol (acetaminophen), CYP2E1 accounts for the formation of NAPQI in humans; the contribution of other cytochrome P450s appears to be negligible.