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Xenobiotica
the fate of foreign compounds in biological systems
Volume 41, 2011 - Issue 3
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General Xenobiochemistry

Mechanisms of gender-specific regulation of mouse sulfotransferases (Sults)

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Pages 187-197 | Received 19 Aug 2010, Accepted 26 Oct 2010, Published online: 23 Nov 2010
 

Abstract

  1. Marked gender differences in the expression of sulfotransferases (Sults) are known to exist in several species including rats, mice and hamsters. However, the mechanism for this gender difference is not known. Therefore, in the present study, it was determined whether sex and/or growth hormone (GH) are responsible for the gender difference in the expression of Sults using gonadectomized (GNX), hypophysectomized (HX) and GH-releasing hormone receptor-deficient little (lit/lit) mouse models.

  2. Sult1a1 and Papss2 in liver and kidney, and Sult1d1 in liver are female-predominant in mice because of suppressive effects of both androgens and male-pattern GH secretion. Sult2a1/a2 is the most markedly female-predominant Sult in mouse liver due to suppressive effects of androgens and male-pattern GH secretion, as well as stimulatory effects by estrogens and female-pattern GH secretion. Sult3a1 is female-predominant in mouse liver due to suppressive effects of androgens as well as stimulatory effects of estrogens and female-pattern GH secretion. Sult1c1 expression is male-predominant in mouse liver and kidney because of stimulatory effects of androgens in males. Sult4a1 expression is female-predominant in mouse brain due to stimulatory effects of estrogens.

  3. In conclusion, gender-divergent Sults are mostly female-predominant and Sult1c1 is the only male-dominant Sult. The gender differences in expression of various mouse Sults are influenced by various mechanisms involving sex and/or GHs.

Acknowledgements

The authors would like to thank David Buckly, Peizhen Song, Xiaohong Lei, and Drs. Chuan Chen and Hong Lu for technical assistance.

Declaration of interest

This work was supported by NIH grants ES-09649, ES-09716, ES013714 and COBRE grant P20-RR-021940.

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