Kane R E, Chen L J, Herbst J J, Thaler M M
Department of Pediatrics, University of Utah Medical Center, Salt Lake City 84132.
Pediatr Res. 1988 Aug;24(2):247-53. doi: 10.1203/00006450-198808000-00022.
The mature female rat has three times the hepatic bile salt sulfotransferase (BSS) activity compared with male rats. This study examined the changes in two hepatic BSS isoenzyme activities during sexual maturation, and the role of estrogen in development of sex differences in BSS activities in mature rats. DEAE-Sephadex A-50 chromatography of hepatic cytosol from prepubescent pups revealed that more than 90% of total BSS activity was due to BSS I activity relative to BSS II, similar to postpubertal females. Sex differences in total BSS activities and the isoenzyme patterns developed after the onset of puberty at 30-35 days of age. BSS I was still the predominant isoenzyme in the adolescent female, similar to the prepubescent pup and mature female. In contrast, BSS I activity declined in adolescent males, which appeared to explain the fall in total BSS activity to only one-third of that of the female by maturity. BSS II activity was similar in both sexes at any age. Estrogen treatment of postpubertal male rats rapidly increased hepatic BSS capacity by enhancing BSS I activity producing an isoenzyme pattern similar to the mature female. This rapid enhancement of BSS I by estrogen was blocked by actinomycin D and puromycin. We concluded that 1) sex differences in BSS activities that develop during adolescence were in part due estrogen-maintaining BSS I activity in females and 2) estrogen regulates the synthesis of BSS I at a translational (or pretranslational) level.
成熟雌性大鼠的肝脏胆汁盐磺基转移酶(BSS)活性是雄性大鼠的三倍。本研究检测了性成熟过程中两种肝脏BSS同工酶活性的变化,以及雌激素在成熟大鼠BSS活性性别差异形成中的作用。对青春期前幼鼠肝脏胞质溶胶进行二乙氨基乙基葡聚糖A - 50层析分析发现,相对于BSS II,超过90%的总BSS活性归因于BSS I活性,这与青春期后雌性大鼠相似。在30 - 35日龄青春期开始后,总BSS活性和同工酶模式出现了性别差异。BSS I仍然是青春期雌性大鼠中的主要同工酶,与青春期前幼鼠和成熟雌性大鼠相似。相比之下,青春期雄性大鼠的BSS I活性下降,这似乎解释了到成熟时总BSS活性降至雌性大鼠的三分之一的原因。在任何年龄,两性的BSS II活性相似。对青春期后雄性大鼠进行雌激素处理,通过增强BSS I活性迅速增加了肝脏BSS能力,产生了与成熟雌性大鼠相似的同工酶模式。雌激素对BSS I的这种快速增强作用被放线菌素D和嘌呤霉素阻断。我们得出结论:1)青春期出现的BSS活性性别差异部分归因于雌激素维持雌性大鼠的BSS I活性;2)雌激素在翻译(或翻译前)水平调节BSS I的合成。