Cyp2g1 is a cytochrome P450 monooxygenase uniquely expressed in the olfactory mucosa (OM) [1,2,3,4,5,6,7]. It functions as a steroid hydroxylase, metabolizing testosterone and progesterone [3]. The gene is involved in the metabolic activation of xenobiotic compounds like coumarin, acetaminophen (AP), and 2,6-dichlorobenzonitrile (DCBN) [1,5]. Mouse models have been crucial in studying Cyp2g1's function.

In Cyp2g1 -null mice, OM microsomes showed significantly lower activities in testosterone, progesterone metabolism, and coumarin activation [1]. Unexpectedly, Cyp2a5 expression was reduced in the liver, lateral nasal gland (LNG), and kidney [1]. Although systemic clearance and hepatotoxicity of AP were unaffected, the LNG was protected from AP toxicity in Cyp2g1 -null mice [1]. Also, CYP2A5 and CYP2G1 were found to play major roles in mouse OM microsomal metabolic activation of DCBN and AP, with CYP2A5 potentially more important in AP metabolism in OM microsomes and the roles in DCBN metabolism being dose -dependent [5].

In conclusion, Cyp2g1 plays a key role in the metabolism of steroids and xenobiotic compounds in the olfactory mucosa. The use of Cyp2g1 -null mouse models has provided insights into its function, especially in relation to the toxicity of compounds like AP in specific tissues such as the LNG. This contributes to our understanding of the role of Cyp2g1 in maintaining olfactory mucosal health and the potential implications for chemical -induced olfactory system damage [1,5].