Abstract
Testicular feminization syndrome, an X-linked recessive disorder in humans, is caused by the insensitivity of target organs such as testes to the stimulation of androgens. Two animal models are available, the tfm mouse and the tfm rat. In tfm rats abnormal androgen receptor binding and/or defective processing of testosterone occurs. Zinc has been reported to affect dihydrotestosterone-receptor binding in vitro. Our study reports an abnormal testicular zinc level in tfm rats. Copper and zinc concentrations in liver, kidney, adrenals, testes and plasma from tfm and control pairs were determined. Metal contents of the various tissues and plasma of tfm and normal control rats were comparable except testicular zinc which is lower in tfm testes. Testicular zinc content is primarily under the influence of luteinizing hormone (LH) whose concentration is higher in tfm rats. The present results support the proposed metal carrier role of steroid-receptor complex and suggest the LH effect on zinc metabolism may be mediated through this complex. These data also suggest that the action of zinc and androgens on normal testicular development is interrelated.
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