Under normal physiological conditions, glucuronidation generally terminates the biological activities of steroids and leads to their elimination in the bile and urine. This process is postulated to play a role in homeostasis by regulating the intracellular steady-state levels of these effector ligands. Indeed, the duration of response to specific steroid signals may be partly determined by the capacity of the cell or tissue to eliminate the steroids as unreactive glucuronides. Under pathophysiological conditions or during steroid therapies, glucuronidation may sometimes result in the formation of more biologically active or toxic metabolites as exemplified by the steroid D ring glucuronides. The degree of toxicity or biological effect in the cell exposed to these steroids will also depend on its complement of UTTs. To investigate these processes in more detail, the steroid specificities and distribution of individual UGTs in various target organs require elucidation. In this review, our current knowlege of the steroid specificities of various rat and human UGTs is described and preliminary investigations on the mechanisms governing tissue specificity are presented.
|Journal||Journal of Endocrinology|
|Issue number||SUPPL. 3|
|Publication status||Published - Sep 1996|