Glucuronidation is a major inactivating pathway for a huge variety of exogenous and endogenous molecules, including drugs, polluants, bilirubin, androgens, estrogens, mineralocorticoids, glucocorticoids, fatty acid derivatives, retinoids and bile acids. Image File history File links Glucuronidation. ... Image File history File links Glucuronidation. ... Image File history File links Glucus. ... Image File history File links Glucus. ...
Acyl glucuronidation is an important metabolic pathway for fluoroquinoloneantibiotics. Santorio Santorio (1561-1636) in his steelyard balance, from Ars de statica medecina, first published 1614 Metabolism (from μεÏαβολιÏÎ¼Î¿Ï (metabolismos), the Greek word for change, or overthrow (Etymonline)), is the biochemical modification of chemical compounds in living organisms and cells. ... Quinolones and fluoroquinolones form a group of broad-spectrum antibiotics. ... An antibiotic is a drug that kills or slows the growth of bacteria. ...
N-glucuronidation
External links
Species Differences in N-Glucuronidation
N-glucuronidation of nicotine and cotinine by human liver microsomes...
N-glucuronidation of trans-3'-hydroxycotinine by human liver microsomes
Ethnic differences in N-glucuronidation of nicotine and cotinine
General references
Mannfred A Hollinger, Introduction to Pharmacology
Glucuronidation in physiology
Chang, K. M.; McManus, K.; Greene, J.; Byrd, G. D.; DeBethizy, J. D. Glucuronidation as a metabolic pathway for nicotine metabolism. 1991
Coffman B.L., King C.D., Rios G.R. and Tephly T.R. The glucuronidation of opioids, other xenobiotics, and androgens by human
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).