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      Spontaneous and Melatonin-Induced Testicular Regression in Male Golden Hamsters: Augmented Sensitivity of the Old Male to Melatonin Inhibition


      S. Karger AG

      Aging, Melatonin, Testes, Accessory sex organs, LH, Prolactin

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          Effects of aging and melatonin on testicular function of golden male hamsters were investigated. Young (3–4 months) and old (22–26 months) male hamsters were maintained on a long photoperiod (14 h light, 10 h dark) and injected with graded doses of 10, 25, 50 µg melatonin or injection vehicle, at 17:00 h (3 h before lights off) for a period of 6 weeks. Old male hamsters had significantly decreased testicular weights as compared with the young counterparts, but accessory sex organ (seminal vesicles and accessory glands) weights did not differ between young and old male hamsters. All doses of melatonin suppressed testicular and accessory sex organ weights in the young as well as in the old animals. The percent decrease in testicular weight in response to melatonin treatment was significantly greater (p < 0.01) in the old than in the young hamsters. Basal plasma prolactin concentration did not differ between young and old male hamsters. Melatonin significantly decreased plasma prolactin concentrations in both age-groups. Young hamsters had greater mean plasma luteinizing hormone concentrations than old hamsters, and melatonin suppressed luteinizing hormone equally in both groups. These results indicate that the testes of the male hamster spontaneously regress during the aging process, and this may be independent of prolactin, since there was no difference in serum prolactin concentrations between young and old hamsters. The finding that melatonin injections brought about a greater percent decrease in testicular weight in the old than in the young hamsters suggests that there is an increased sensitivity of the reproductive system to melatonin inhibition in the old male hamster.

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          Author and article information

          S. Karger AG
          26 March 2008
          : 33
          : 1
          : 43-46
          Division of Neurobiology, Barrow Neurological Institute, Phoenix, Ariz., USA
          123198 Neuroendocrinology 1981;33:43–46
          © 1981 S. Karger AG, Basel

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          Pages: 4
          Original Paper


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