title: Identification and endocrine control of sex steroid binding sites in the lacrimal gland.
abstract: Previous research has indicated that the lacrimal gland may be a target organ for sex steroids and that androgen effects on this tissue may be inhibited by pituitary deficiency or diabetes. To extend these findings, the objectives of the current investigation were 3-fold: [a] to determine whether specific and high-affinity binding sites for androgens and estrogens exist in rat lacrimal tissue; [b] to assess whether the number and affinity of androgen binding sites in the lacrimal gland may be influenced by hypophysectomy or acute diabetes; and [c] to examine whether androgen receptor mRNA may be detected in lacrimal tissues of a variety of species. Following the collection of lacrimal gland samples, tissues were processed for the conduct of equilibrium binding methods or molecular biological techniques. Our results demonstrated that a single class of saturable, high-affinity and stereochemically selective binding sites for androgens exist in lacrimal tissues of male and female rats. These sites possessed a dissociation constant of approximately 1 nM and were also present in isolated acinar epithelial cells. In contrast, we were unable to find any evidence for the presence of specific or high-affinity receptors for estrogens in the rat lacrimal gland. With regard to changes in the endocrine environment, hypophysectomy led to an increase in the number and affinity of androgen binding sites in rat lacrimal tissue cytosol, whereas diabetes reduced the total quantity of these sites. Of interest, androgen receptor mRNA was detected in lacrimal glands of mice, rats, hamsters, guinea pigs, rabbits and humans. Overall, our findings show that the lacrimal gland is a target organ for androgens and that androgen action in this tissue may be mediated through an interaction with specific and high-affinity binding sites.
authors.affiliation: Schepens Eye Research Institute, Boston, MA 02114, USA.
authors.forename: D A
authors.initials: DA
authors.lastname: Sullivan
authors.forename: J A
authors.initials: JA
authors.lastname: Edwards
authors.forename: L A
authors.initials: LA
authors.lastname: Wickham
authors.forename: J D
authors.initials: JD
authors.lastname: Pena
authors.forename: J
authors.initials: J
authors.lastname: Gao
authors.forename: M
authors.initials: M
authors.lastname: Ono
authors.forename: R S
authors.initials: RS
authors.lastname: Kelleher
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000728:Androgens / Q000378:metabolism*; D000818:Animals; D001483:Base Sequence; D001665:Binding Sites; D002369:Castration; D002469:Cell Separation; D002478:Cells, Cultured; D006224:Cricetinae; D017931:DNA Primers / Q000737:chemistry; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D004702:Endocrine Glands / Q000502:physiology; D004967:Estrogens / Q000378:metabolism*; D005260:Female; D006168:Guinea Pigs; D006801:Humans; D007016:Hypophysectomy; D007765:Lacrimal Apparatus / Q000166:cytology / Q000378:metabolism*; D008297:Male; D008647:Mesocricetus; D051379:Mice; D008807:Mice, Inbred BALB C; D008969:Molecular Sequence Data; D010902:Pituitary Gland / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D017207:Rats, Sprague-Dawley; D011944:Receptors, Androgen / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism*
chemical_list: D000728:Androgens; D017931:DNA Primers; D004967:Estrogens; D012333:RNA, Messenger; D011944:Receptors, Androgen; D011960:Receptors, Estrogen