Protection against cytotoxic-induced testis damage--experimental approaches.
In animal models the possibility has been explored that pharmacological inhibition of cell division in the spermatogenic epithelium during cytotoxic treatment for cancer would preserve fertility. Recent animal models are reviewed. In the rat, gonadotrophin releasing hormone (GnRH) analogues or a combination of a progestogen and an androgen will protect spermatogenesis from the cytotoxic and mutagenic effects of procarbazine and radiation. Cyclophosphamide toxicity is not alleviated by GnRH treatment. In the mouse, a GnRH analogue was ineffective against cisplatin testicular toxicity. Complete suppression of the spermatogenic process does not seem to be important for a successful outcome. These experiments serve to illustrate the inconsistency between different laboratories. However, it is argued that once the correct pharmacological approach and the mechanisms have been established in animal models, only then will it be possible to predict the efficacy of these adjuvant treatments to preserve fertility in men being treated for cancer.
Morris
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ID
Molecular Pharmacology and Toxicology, Physiological Sciences, University of Manchester, UK.
D000818:Animals; D000970:Antineoplastic Agents / Q000633:toxicity*; D004195:Disease Models, Animal; D006801:Humans; D007248:Infertility, Male / Q000139:chemically induced / Q000209:etiology* / Q000517:prevention & control; D008297:Male; D011344:Procarbazine / Q000633:toxicity; D011833:Radiation Injuries, Experimental / Q000517:prevention & control; D013091:Spermatogenesis / Q000187:drug effects* / Q000528:radiation effects*
D000970:Antineoplastic Agents; D011344:Procarbazine