Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • HUMAN UDP-GLUCURONOSYLTRANSFERASES  (1)
  • NONSTEROIDAL ANTIINFLAMMATORY DRUGS  (1)
  • 1
    Keywords: HUMAN LIVER-MICROSOMES ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; glutathione-S-transferase ; HUMAN UDP-GLUCURONOSYLTRANSFERASES ; HUMAN GASTROINTESTINAL-TRACT ; HUMAN CYTOCHROME-P450 1A2 ; TUMOR-SPECIFIC EXPRESSION ; HUMAN CYP2C SUBFAMILY ; HUMAN-FETAL LIVERS ; UGT1 GENE-COMPLEX
    Abstract: In humans, the liver is generally considered to be the major organ contributing to drug metabolism, but studies during the last years have suggested an important role of the extra-hepatic drug metabolism. The gastrointestinal tract (GI-tract) is the major path of entry for a wide variety of compounds including food, and orally administered drugs, but also compounds - with neither nutrient nor other functional value - such as carcinogens. These compounds are metabolized by a large number of enzymes, including the cytochrome P450 (CYP), the glutathione S-transferase (GST) family, the uridine 5'-diphospho- glucuronosyltransferase (UDP-glucuronosyltransferase - UGT) superfamily, alcohol-metabolizing enzymes, sulfotransferases, etc. These enzymes can either inactivate carcinogens or, in some cases, generate reactive species with higher reactivity compared to the original compound. Most data in this field of research originate from animal or in vitro studies, wherein human studies are limited. Here, we review the human studies, in particular the studies on the phenotypic expression of these enzymes in the colon and rectum to get an impression of the actual enzyme levels in this primary organ of exposure. The aim of this review is to give a summary of currently available data on the relation between the CYP, the GST and the UGT biotransformation system and colorectal cancer obtained from clinical and epidemiological studies in humans.
    Type of Publication: Journal article published
    PubMed ID: 25686853
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...