[A study on spermatogenic damage induced by ethane dimethanesulphonate (EDS) in the rat: protective effects of hCG injection].
When ethane dimethanesulphonate (EDS) is administered to rats, Leydig cells are destroyed, and damage to the seminiferous tubules is caused due to lack of testosterone (T), but administration of hCG can prevent this damage. In this paper, in order to study in detail this action of hCG, we conducted the following experiment. Eleven-week-old male Sprague-Dawley rats were used and we set up a control group, an EDS group and hCG + EDS groups (in addition to EDS, hCG was administered at various concentrations and for various periods). The experimental period was 28 days, and EDS was administered on the 8th day, and the animals were sacrificed on the 28th day. Then we evaluated the degree of testicular damage by determining the diameter of the seminiferous tubules, testicular weight, accessory reproductive organ weight, serum LH and FSH concentrations, and serum and seminiferous tubule T concentrations. Our results show that in comparison with the control group in the EDS group the T level in the seminiferous tubule decreased and the siminiferous tubules had atrophied, but in the hCG administration groups the T level in the seminiferous tubules was to some extent maintained, and atrophy of the seminiferous tubules was slight. These phenomena were to a certain extent dependent on the concentration of hCG, and in the groups administered hCG in advance EDS administration, these effects appeared at lower concentrations. In the groups, in which hCG administration started at the same time as EDS, high concentrations of hCG were observed to produce a partial prophylactic action. Given the above, in rats by advance administration of hCG it is thought that following EDS administration T is maintained and it is possible to prevent damage to the seminiferous tubules. Also, it is thought that in treating seminiferous tubules already damaged by EDS, administration of high doses of hCG can promote recovery.
Department of Urology, Okayama University Medical School.
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Oeda
D000818:Animals; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D007985:Leydig Cells / Q000187:drug effects* / Q000473:pathology; D008297:Male; D008698:Mesylates / Q000633:toxicity*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012671:Seminiferous Tubules / Q000187:drug effects / Q000473:pathology; D013091:Spermatogenesis / Q000187:drug effects*
D006063:Chorionic Gonadotropin; D008698:Mesylates