Liu L, Klaassen C D
Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City 66160, USA.
Mol Pharmacol. 1996 Sep;50(3):565-72.
The developmental and hormonal regulation of three male-dominant rat hepatic sulfotransferases (STs) was studied in male and female rats. ST1A1 (phenol ST) mRNA levels increased gradually in both male and female rats after birth until puberty and then declined to a greater extent in female than in male rats. In adult rats, hepatic ST1A1 mRNA levels were approximately 2-3-fold higher in males than in females. However, ST1C1 and ST1E2 mRNAs (corresponding to N-hydroxy-2-acetylaminofluorene ST and estrogen ST, respectively) increased dramatically at puberty in male rats but remained low in female rats. ST1C1 and ST1E2 expression is > 10-fold higher in adult male than in adult female rats. Estradiol, progesterone, and testosterone administration to hypophysectomized rats did not have marked effects on hepatic ST expression. Hypophysectomy decreased ST1A1 gene expression in rat liver, but neither intermittent growth hormone (GH) injection (male pattern) nor continuous GH infusion (female pattern) restored ST1A1 mRNA levels. ST1C1 gene expression was abolished by hypophysectomy and reversed by GH injection. Hypophysectomy did not dramatically decrease hepatic ST1E2 mRNA in male rats but markedly increased ST1E2 expression in female rats. GH infusion (female pattern) in hypophysectomized male and female rats decreased ST1E2 mRNA levels. Prolactin increased hepatic ST1C1 mRNA levels, which is similar to the effect of GH. It is concluded that the three male-dominant rat hepatic STs are regulated differently because the developmental pattern of ST1A1 is markedly different from that for ST1C1 and ST1E2. The high expression of ST1C1 in adult males is determined by male GH secretory pattern, whereas male dominance of ST1E2 is due to the suppressive effect of female GH secretory pattern in adult female rats.
研究了雄性和雌性大鼠中三种雄性优势大鼠肝脏磺基转移酶(STs)的发育和激素调节。ST1A1(苯酚ST)mRNA水平在出生后的雄性和雌性大鼠中均逐渐升高,直至青春期,然后在雌性大鼠中比雄性大鼠下降幅度更大。在成年大鼠中,肝脏ST1A1 mRNA水平在雄性中比雌性高约2 - 3倍。然而,ST1C1和ST1E2 mRNA(分别对应于N - 羟基 - 2 - 乙酰氨基芴ST和雌激素ST)在雄性大鼠青春期时急剧增加,而在雌性大鼠中保持低水平。成年雄性大鼠中ST1C1和ST1E2的表达比成年雌性大鼠高10倍以上。对垂体切除的大鼠给予雌二醇、孕酮和睾酮对肝脏ST表达没有显著影响。垂体切除降低了大鼠肝脏中ST1A1基因的表达,但无论是间歇性生长激素(GH)注射(雄性模式)还是持续GH输注(雌性模式)都不能恢复ST1A1 mRNA水平。垂体切除消除了ST1C1基因的表达,而GH注射使其恢复。垂体切除并没有显著降低雄性大鼠肝脏中ST1E2 mRNA水平,但显著增加了雌性大鼠中ST1E2的表达。对垂体切除的雄性和雌性大鼠进行GH输注(雌性模式)降低了ST1E2 mRNA水平。催乳素增加了肝脏ST1C1 mRNA水平,这与GH的作用相似。得出结论,三种雄性优势大鼠肝脏STs的调节方式不同,因为ST1A1的发育模式与ST1C1和ST1E2明显不同。成年雄性中ST1C1的高表达由雄性GH分泌模式决定,而ST1E2的雄性优势是由于成年雌性大鼠中雌性GH分泌模式的抑制作用。