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Research ArticleABSORPTION, DISTRIBUTION, METABOLISM, AND EXCRETION

Molecular Basis of Perinatal Changes in UDP-Glucuronosyltransferase Activity in Maternal Rat Liver

Marcelo G. Luquita, Viviana A. Catania, Enrique J. Sánchez Pozzi, Luis M. Veggi, Tim Hoffman, José M. Pellegrino, Shin-ichi Ikushiro, Yoshikazu Emi, Takashi Iyanagi, Mary Vore and Aldo D. Mottino
Journal of Pharmacology and Experimental Therapeutics July 2001, 298 (1) 49-56;
Marcelo G. Luquita
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Viviana A. Catania
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Enrique J. Sánchez Pozzi
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Luis M. Veggi
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Tim Hoffman
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José M. Pellegrino
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Shin-ichi Ikushiro
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Yoshikazu Emi
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Takashi Iyanagi
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Mary Vore
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Aldo D. Mottino
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Abstract

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 (17β-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.

Footnotes

  • This work was supported by Research Grants from Consejo Nacional de Investigaciones Cientı́ficas y Técnicas, Universidad Nacional de Rosario, and Subsecretarı́a de Investigación y Tecnologı́a, Ministerio de Salud de la Nación, Argentina; and by U.S. Public Health Service Grants GM55343 and NS31220.

  • Abbreviations:
    UGT
    UDP-glucuronosyltransferase
    UDPGA
    UDP-glucuronic acid
    UDP-N-AG
    UDP-N-acetylglucosamine
    pp
    postpartum
    SSC
    standard saline citrate
    ntcp
    Na+-taurocholate cotransport polypeptide
    Mrp
    multidrug-resistant protein
    • Received January 17, 2001.
    • Accepted March 13, 2001.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 298 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 298, Issue 1
1 Jul 2001
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Research ArticleABSORPTION, DISTRIBUTION, METABOLISM, AND EXCRETION

Molecular Basis of Perinatal Changes in UDP-Glucuronosyltransferase Activity in Maternal Rat Liver

Marcelo G. Luquita, Viviana A. Catania, Enrique J. Sánchez Pozzi, Luis M. Veggi, Tim Hoffman, José M. Pellegrino, Shin-ichi Ikushiro, Yoshikazu Emi, Takashi Iyanagi, Mary Vore and Aldo D. Mottino
Journal of Pharmacology and Experimental Therapeutics July 1, 2001, 298 (1) 49-56;

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Research ArticleABSORPTION, DISTRIBUTION, METABOLISM, AND EXCRETION

Molecular Basis of Perinatal Changes in UDP-Glucuronosyltransferase Activity in Maternal Rat Liver

Marcelo G. Luquita, Viviana A. Catania, Enrique J. Sánchez Pozzi, Luis M. Veggi, Tim Hoffman, José M. Pellegrino, Shin-ichi Ikushiro, Yoshikazu Emi, Takashi Iyanagi, Mary Vore and Aldo D. Mottino
Journal of Pharmacology and Experimental Therapeutics July 1, 2001, 298 (1) 49-56;
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