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Vol. 298, Issue 1, 49-56, July 2001
Institute of Experimental Physiology, School of Biochemical and
Pharmaceutical Sciences, Rosario, Argentina (M.G.L., V.A.C., E.J.S.P.,
L.M.V., J.M.P., A.D.M.); Graduate Center for Toxicology, University of
Kentucky, Lexington, Kentucky (T.H., M.V.); and Department of Life
Science, Faculty of Science, Himeji Institute of Technology, Harima
Science Garden City, Hyogo, Japan (S.I., Y.E., T.I.)
The molecular basis of perinatal changes occurring in major
UDP-glucuronosyltransferase (UGT) family 1 isoforms and in UGT2B1, a
relevant isoform belonging to family 2, was analyzed in rat liver.
Nonpregnant, pregnant (19-20 days of pregnancy), and two groups of
postpartum animals corresponding to early and middle stages of
lactation (2-4 and 10-12 days after delivery, respectively) were
studied. UGT activity determined in
UDP-N-acetylglucosamine-activated microsomes revealed
that bilirubin, p-nitrophenol, and ethynylestradiol (17
-OH and 3-OH) but not androsterone and estrone glucuronidation rates, were decreased in pregnant rats. Decreased enzyme activities returned to control values after delivery.
p-Nitrophenol, androsterone, and estrone conjugation
rate increased in postpartum rats. Western blot analysis performed with
anti-peptide-specific (anti-1A1, 1A5, 1A6, and 2B1) antibodies revealed
decreased levels of all family 1 isoforms and UGT2B1 during pregnancy.
In postpartum animals, protein level recovered (1A5 and 2B1) or even
increased (1A1 and 1A6) with respect to control rats. Northern blot
analysis suggested that expression of UGT proteins is down-regulated at
a post-translational level during pregnancy and that increased levels
of 1A1 and 1A6 observed in postpartum rats were associated to increased
mRNA. To establish whether prolactin is involved in up-regulation of UGT1A1 and 1A6 postpartum, ovariectomized rats were treated with 300 µg of ovine prolactin per day for 7 days. The data indicated that
prolactin was able to increase expression of UGT1A6 (protein and mRNA)
but not 1A1. Thus, prolactin is the likely mediator of the increased
expression of UGT1A6 observed in maternal liver postpartum.
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