Ontogeny and hormonal basis of male-dominant rat hepatic sulfotransferases.
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.
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Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City 66160, USA.
Klaassen
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D000375:Aging / Q000378:metabolism*; D000818:Animals; D015239:Arylsulfotransferase / Q000096:biosynthesis; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D018507:Gene Expression Regulation, Developmental; D015971:Gene Expression Regulation, Enzymologic; D013006:Growth Hormone / Q000494:pharmacology; D007016:Hypophysectomy; D008099:Liver / Q000201:enzymology* / Q000254:growth & development; D008297:Male; D011374:Progesterone / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012727:Sex Characteristics; D012741:Sexual Maturation; D015238:Sulfotransferases / Q000096:biosynthesis*; D013739:Testosterone / Q000494:pharmacology; D014158:Transcription, Genetic
D012333:RNA, Messenger; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D013006:Growth Hormone; C084221:St1C1 N-hydroxyarylamine sulfotransferase; D015238:Sulfotransferases; D015239:Arylsulfotransferase; C020122:estrone sulfotransferase