Sult1d1 is a sulfotransferase gene, a member of the large superfamily of detoxification enzymes. It plays a crucial role in inactivating endogenous dopamine-derived compounds, especially catecholamines, and is involved in pathways related to stress response and metabolic regulation. Genetic models, such as knockout mouse models, are valuable tools for studying its functions [1].

In mice, Sult1d1 knockout led to a 99% decrease in renal activation of the genotoxicant 1-hydroxymethylpyrene, verifying its role in the metabolic activation of this compound in the kidney [2]. In another study, knocking out Sult1d1 along with Sult1a1 almost totally eliminated the gender gap in bladder susceptibility to the human carcinogen 4-aminobiphenyl (ABP) in mice, suggesting Sult1d1's role in promoting ABP-DNA adduct formation in hepatic cells [3]. However, the Sult1d1 knockout did not influence the formation of hemoglobin adducts of furfuryl alcohol [4].

In conclusion, Sult1d1 is essential for the inactivation of catecholamines and plays a role in the metabolic activation of certain genotoxicants and carcinogens. Gene knockout mouse models have been instrumental in revealing its functions in specific biological processes related to chemical activation and carcinogen-induced tissue susceptibility.