Glucuronide is a substance produced by attaching glucuronic acid to another substance with glycosidic bonds.
Toxic substances can be removed from the body in this manner - glucuronic acid is introduced into the body, the acid forms a glycosidic bond with the toxic substance and neutralises it, and the resulting glucuronide is eventually excreted.
Glucuronidation plays many roles in the body, not just that of binding estrogen, thus one may have low or normal levels of glucaronic acid along with low, normal or high levels of estrogen.
This, glucuronidation represents a major means of converting most drugs, steroids, and many toxic and endogenous substances to metabolites that can then be excreted into the urine or bile.
Many of these toxic and otherwise therapeutic substances (xenobiotics, drugs) disrupt the glucuronidation by impairing it, stopping it, or causing the binds to be rupture, separating the bound molecules from its inert transport.
TAM glucuronide conjugates have been identified in the serum of TAM-treated patients [25,27], and it has been suggested that glucuronidation within target tissues such as the adipose tissue of the breast may also be important in terms of TAM metabolism and overall TAM activity [28].
As controls, glucuronidation assays were regularly performed using human liver microsomes (as a positive control for glucuronidation activity) and untransfected HK293 cell homogenate protein (as a negative control for glucuronidation activity) as previously described [34,38].
Single glucuronide peaks were observed in assays with either substrate (Figure 3a,b), with these peaks corresponding to the retention times of peaks 5 and 7 in glucuronidation assays with human liver microsomes (see Figure 1).