Abstract
Abstract A mouse model for cyclophosphamideinduced testicular damage has been created which produces severe damage to both spermatogonia and maturing spermatocytes. Pretreatment and continued administration of [D-leu 6 ]-des-Gly-NH 2 10 pro-ethylamide GnRH, a synthetic analogue of gonadotropin-releasing hormone, produces striking protection from the histologically detectable cyclophosphamide-induced damage. These results suggest that temporary interruption of the pituitarygonadal axis may ameliorate the gonadal toxicity of systemic chemotherapy.
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