JRI 

Haleh Atrian Corresponding Author
- Department of Biology, Islamic Azad University, Kazeroun, Iran
Saeed Khatamsaz
- Department of Biology, Islamic Azad University, Kazeroun, Iran
Mokhtar Mokhtari
- Department of Biology, Islamic Azad University, Kazeroun, Iran

Received: 7/1/2007 Accepted: 7/1/2007 - Publisher : Avicenna Research Institute

Related Articles

 

Other Format

 


Abstract

Introduction: Finasteride, a synthetic 4-azasteroid compound, is a competitive and specific inhibi-tor of type II 5--reductase, an intracellular enzyme that converts testosterone into dihydrotestos-terone (DHT). Finasteride is prescribed for nearly all disturbances related to DHT concentration such as benign prostatic hyperplasia, male-pattern androgenetic alopecia, hirsutism, acne and seborrhea. Since finasteride is frequently prescribed in men, the effects of different doses of finas-teride on the number of spermatogonia, Sertoli and Leydig cells have been investigated in the present study. Materials & Methods: Forty mature male Sprague-Dawley rats were divided into five groups of eight. The first group was kept as the control group and received nothing. The second or the sham group, only received distilled water orally, but the last three experimental groups respectively received 25, 50 and 100mg/kg of BW/d doses of finasteride orally for a 32-day period. Then photo-micrographs of testis tissues were studied and the results of the five groups were statistically analyzed by ANOVA, t, Tukey and Duncan tests. P<0.05 was considered significant. results: administration of 50 and 100mg g per bw doses of finasteride significantly decreased the number of spermatogonia and 50mg g doses reduced the number of primary spermatocytes (p0.05). the number of sertoli cells had no significant difference in the experimental groups in comparison with the control group but there was a significant increase in the number of leydig cells in all of the experimental groups (p0.05). this drug did not have any significant effects on the density of different kinds of cells, and nuclear or cytoplasmic staining properties of spermato-gonia. conclusion: finasteride causes a significant decrease in the number of spermatogonia and primary spermatocytes. it also causes a significant increase in the number of leydig cells but it does not have any significant histological effects on the testis or any effects on spermatogenesis. therefore, it seems that short-term uses of the medication may not have harmful effects on male fertility.< pan>


Keywords: Finasteride, Testosterone, Testis, Dihydrotestosterone, Sertoli cell, Leydig cell, Spermatogonia, Primary spermatocyte, Spermatogenesis, Male fertility, 5-a-reductase, Germ cells


To cite this article:


References

  1. McLachlan RI, O’Donnell L, Meachem SJ, Stanton tification of specific sites of hormonal regulation in spermatogenesis in rats, monkeys, and man. Recent Prog Horm Res. 2002;57:149-79.   [PubMed]
  2. O’Donnell L, Stanton PG, Wreford NG, Robertson DM, McLachlan RI. Inhibition of 5 alpha-reductase activity impairs the testosterone-dependent restoration of spermiogenesis in adult rats. Endocrinology. 1996; 137:2703-10.   [PubMed]
  3. Rittmaster RS. Finasteride. N Engl J Med. 1994;330 (2);120-5. Review.   [PubMed]
  4. Ovrerstreet JW, Fuh VL, Gould J, Howards SS, Lieber MM, Hellstrom J, et al. Chronic treatment with finas-teride daily dose not affect spermatogenesis or semen production in young men. J Urol. 1999;162(4): 1295-300.   [PubMed]
  5. Jin Y, Penning TM. Steroid 5-reductase and 3-hydroxysteroid dehydrogenases: Key enzymes in androgen metabolism. Best Pract Res Clin Endocrinol Metab. 2001;15:79-94.   [PubMed]
  6. Ou XM, Storring JM, Kushwaha N, Albert PR. Heterodimerization of mineralocorticoid and glucocor-ticoid receptors at a novel negative response element of the 5-HT1 A receptor gene. J Biol Chem. 2001;276 (17):14299-307.   [PubMed]
  7. Kennel PF, Pallen CT, Bars RG. Evaluation of the rodent Hershberger assay using three refrence endo-crine disrupters (androgen and antiandrogens). Reprod Toxicol. 2004;18(1):63-73.   [PubMed]
  8. Bowman CJ, Barlow NJ, Turner Kj, Wallace DG, Foster PMD. Effects of in utero exposure to finasteride on androgen-dependent reproductive development in the male rat. Toxicol Sci. 2003;74(2):393-406.   [PubMed]
  9. Kaufman KD, Olsen EA, Whiting D, Savin R, Devillez R, Bergfeld W, et al. Finasteride in the treatment of men With undrogenetic alopecia. Finasteride Male Pattern Hair Loss Study Group. J Am Acad Dermatol. 2000;42(5):848-9.   [PubMed]
  10. Kolasa A, Marchlewicz M, wenda-Różewicka L, Wiszniewska B. Morphology of the testis and the epididymis in rats with dihydrotestosterone(DHT) deficiency. Ann Acad Med Bial. 2004;49(1):117-9.   [PubMed]
  11. Huynh H. Induction of apoptosis in rat ventral prostate by finasteride is associated with alteration in MAP kinase pathways and Bc1-2 related family of proteins. Int J Oncol. 2002;20:1297-303.   [PubMed]
  12. Huynh H, seyam RM, Brock GB. Reduction of ventral prostate weight by finasteride is associated with suppression of insulin-like growth factor I (IGF-I) and IGF-I receptor genes and with an increase in IGF binding protein 3. Cancer Res. 1998;58(2):215-8.   [PubMed]
  13. Rittmaster RS, Norman RW, Thomas LN, Rowden G. Evidence for atrophy and apoptosis in the prostates of men given finasteride. J Clin Endocrinol Metab. 1996; 1:814-9.   [PubMed]
  14. Tobin VA, Canny BJ. The regulation of gonado-tropin releasing hormone induced calcium signals in male rat gonadotrophs by testosterone is mediated by dihydro testosterone. Endocrinology. 1998;139(3): 1038-45.   [PubMed]
  15. Frieidlin V, Ko HS, Wilkin JK, Chronic treatment with finasteride daily does not effect spermatogenesis or semen production in young men. J Urol. 2000;164 (4):1319-20.   [PubMed]
  16. Wang LG, Liu XM, Kreis W, Budman DR. Down-regulation of prostate-specific antigen expression by finasteride through inhibition of complex formation between androgen receptor and steroid receptor-binding consensus in the promoter of the PSA gene in LNCaP cells. Cancer Res. 1997;57(4):714-9.   [PubMed]
  17. Khisti RT, VanDoren MJ, O’Buckley T, Morrow AL. Neuroactive steroid 3-hydroxy-5-pregnan-20-one modulates ethanol-induced loss of rigthing reflex in rats. Brain Res. 2003;980(2):255-65.   [PubMed]
  18. Disney A, Calford MB. Neurosteroids mediate habi-tuation and tonic inhibition in the auditory midbrain. J Neurophysiol. 2001;86(2):1052-56.   [PubMed]
  19. McNeilly AS, Sharpe RM, Davidson DW, Fraser HM. Inhibition of gonadotropin seretion by induced hyperprolactinemia in the male rat. J Endocrinol. 1978; 79;59-68.   [PubMed]
  20. Matzkin H, Chen J, Lewyshon O, Ayalon D, Braf Z. Effects of long term treatment with finasteride (MK-906), a 5-alpha reductase in hibitor, on circulating LH, FSH, Prolactin and estradiol. Horm Metab Res. 1992; 24(10):498-9.   [PubMed]
  21. George FW, Johnson L, Wilson JD. The Effect of a 5 alpha-reductase inhibitor on androgen physiology in the immature male rat. Endocrinology. 1989;125:2434-8.   [PubMed]
  22. Rhoden EL, Gobbi D, Menti E, Rhoden C, Telöken C. Effects of the chronic use of finasteride on testicular weight and spermatogenesis in wistar rats. BJU Int. 2002;89(9):961-3.   [PubMed]
  23. Killian J, Pratis K, Clifton RJ, Stanton PG, Robertson DM, O’Donnell L. 5 alpha- reductase isoenzymes 1 and 2 in the rat testis during postnatal development. Biol Reprod. 2003;68:1711-8.   [PubMed]
  24. Pratis K, O’Donnell L, Ooi GT, McLachlan RI, Ro-bertson DM. Enzyme assay for 5 alpha-reductase type 2 activity in the presence of 5 alpha-reductase type 1 activity in rat testis. J Steroid Biochem Mol Biol. 2000; 75:75-82.   [PubMed]

COPE
SID
NLM
AJMB
IJBMLE
IJBMLE

Home | About Us | Current Issue | Past Issues | Submit a Manuscript | Instructions for Authors | Subscribe | Search | Contact Us

"Journal of Reproduction & Infertility" is owned, published, and managed by Avicenna Research Institute .
Creative Commons License

This work is licensed under a Creative Commons Attribution –NonCommercial 4.0 International License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.

Journal of Reproductoin and Infertility (JRI) is a member of COMMITTEE ON PUBLICATION ETHICS . Verify here .

©2024 - eISSN : 2251-676X, ISSN : 2228-5482, For any comments and questions please contact us.