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. 2000 Jan-Feb;72(1-2):61-9.
doi: 10.1016/s0960-0760(99)00150-8.

Effect of prenatal melatonin on the gonadotropin and prolactin response to the feedback effect of testosterone in male offspring

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Effect of prenatal melatonin on the gonadotropin and prolactin response to the feedback effect of testosterone in male offspring

E Díaz et al. J Steroid Biochem Mol Biol. 2000 Jan-Feb.

Abstract

The purpose of this study was to investigate the effects of prenatal melatonin administration on the sensitivity of the androgens negative feedback effect on gonadotropin and prolactin secretion in male offspring. Male offspring of control (control-offspring) and melatonin treated (MEL-treated) (150 microg/100 g BW) mother rats during pregnancy (MEL-offspring), at infantile, prepubertal, and pubertal periods were studied. LH secretion in response to testosterone propionate (TP) in control-offspring showed the classical negative feedback effect at all ages studied. In MEL-offspring a negative response after TP was also observed in all ages studied although the magnitude of this response was altered in this group as compared to controls. FSH values were significantly lower at most ages and time points studied in MEL-offspring than in control-offspring. FSH secretion in MEL-offspring showed a delayed negative feedback action of TP injection as compared to control-offspring. This response was observed at 21 days of age in control-offspring and delayed until day 30 of life in MEL-offspring. Parallely it remain at later age in MEL-offspring than in control-offspring. Prolactin secretion in control-offspring showed increased values after TP injections from infantile to pubertal periods. This increase was blunted in MEL-offspring at 17 and 35 days of age showing significantly reduced (p<0.01; p<0.05) plasma prolactin levels. During pubertal period a prolactin positive response to TP administration was observed in MEL-offspring but with significantly lower magnitude than in control-offspring. These results indicate that prenatal melatonin exposure induced changes in the sensitivity of gonadotropin and prolactin feedback response to testosterone, indicating a delayed sexual maturation of the neuroendocrine-reproductive axis in male offspring.

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