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Dietary Zinc Deficiency Alters 5-Reduction and Aromatization of Testosterone and Androgen and Estrogen Receptors in Rat Liver¹

Department of Food and Nutrition, College of Home Economics, Hanyang University, Seuol, Korea ^* Department of Anatomical Sciences, University of Oklahoma College of Medicine, Oklahoma City, OK 73104

We studied the effects of zinc deficiency on hepatic androgen metabolism and aromatization, androgen and estrogen receptor binding, and circulating levels of reproductive hormones in freely fed, pair-fed and zinc-deflcient rats. Hepatic conversion of testosterone to dihydrotestosterone was significantly less, but formation of estradiol from testosterone was significantly greater in rates fed the zinc-deficient diet compared with freely fed and pair-fed control rats. There were significantly lower serum concentrations of luteinizing hormone, estradiol and testosterone in rats fed the zinc-deficient diet. No difference in the concentration of serum follicle-stimulating hormone was observed between the zinc-deficient group and either control group. Scatchard analyses of the receptor binding data showed a significantly higher level of estrogen receptor in zinc-deficient rats (36.6 ± 3.4 fmol/mg protein) than in pair-fed controls (23.3 ± 2.2 fmol/mg protein) and a significantly lower level of androgen binding sites in rats fed the zinc-deficient diet (6.7 ± 0.7 fmol/mg protein) than in pair-fed control rats (11.3 ± 1.2 fmol/mg protein). There were no differences in hepatic androgen and estrogen receptor levels between freely fed and pair-fed controls. These findings indicate that zinc deficiency reduces circulating luteinizing hormone and testosterone concentrations, alters hepatic sterold metabolism, and modifles sex steroid hormone receptor levels, thereby contributing to the pathogenesis of male reproductive dysfunction.

KEY WORDS: • rats • zinc deficiency • trace elements • sex hormones • receptors

¹ The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

² Current address: Department of Anatomical Sciences, University of Oklahoma College of Medicine, Oklahoma City, OK 73104.

³ To whom correspondence and reprint requests should be addressed.

Manuscript received 3 July 1995. Revision accepted 2 January 1996.