These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Microsomal metabolism of the carcinogen, N-2-fluorenyl-acetamide, by the mammary gland and liver of female rats. II. Glucuronidation of ring- and N-hydroxylated metabolites of N-2-fluorenylacetamide.
    Author: Malejka-Giganti D, Ryzewski CN.
    Journal: Carcinogenesis; 1985 May; 6(5):687-92. PubMed ID: 3924428.
    Abstract:
    We determined UDP-glucuronyltransferase (UDP-GT) activities of hepatic and mammary gland microsomes of female rats with p-nitrophenol and the ring- and N-hydroxylated metabolites of N-2-fluorenylacetamide (2-FAA) and the effects of hepatic inducers of UDP-GT's on these glucuronidations. Pre-treatment of non-lactating (NL) and lactating (L) rats with beta-naphthoflavone (beta-NF) significantly increased glucuronidations, of p-nitrophenol, the phenolic metabolites of 2-FAA, especially of 5-hydroxy-2-FAA, and also of N-hydroxy-2-FAA by hepatic microsomes. Pre-treatment of L rats with beta-NF or 3-methyl-cholanthrene (3-MC) significantly increased glucuronidations of these compounds by mammary gland microsomes suggesting that both liver and mammary gland of L rats possess similar UDP-GT activities. In NL rats, UDP-GT activities of mammary microsomes toward phenols were greater than in L rats, and except for that of 5- and 7-hydroxy-2-FAA, were not inducible with beta-NF. The data obtained with L rats, the greater magnitude of stimulation of the hepatic UDP-GT of NL rats by beta-NF than by phenobarbital, and the lack of effect of the latter on UDP-GT of mammary microsomes suggested that the phenolic metabolites of 2-FAA and N-hydroxy-2-FAA share chiefly the characteristics of substrates for group 1 UDP-GT activities (i.e., those inducible with beta-NF or 3-MC). Neither inducer increased glucuronidation of 9-hydroxy-2-FAA, a relatively poor substrate for UDP-GT of mammary or hepatic microsomes. In contrast to hepatic microsomes which formed considerable amounts of the glucuronide of N-hydroxy-2-FAA, mammary gland microsomes glucuronidated this substrate to a minor extent only. This suggested that glucuronide of N-hydroxy-2-FAA may play a role in systemic, but not in local mammary tumorigenesis by N-hydroxy-2-FAA.
    [Abstract] [Full Text] [Related] [New Search]