Investigation on the effect of chronic ethanol consumption on IGF-I receptors in rat testes during puberty period by immunohistochemical method

Yagci A., Yakisik M., Altunbas K., Zik B.

REVUE DE MEDECINE VETERINAIRE, cilt.160, sa.3, ss.127-132, 2009 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 160 Sayı: 3
  • Basım Tarihi: 2009
  • Dergi Adı: REVUE DE MEDECINE VETERINAIRE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.127-132
  • Anahtar Kelimeler: IGF-IR, chronic alcoholism, testes, immunohistochemistry, GROWTH-FACTOR-I, SIGNAL-TRANSDUCTION, CELL-PROLIFERATION, SERTOLI-CELLS, INSULIN, APOPTOSIS, LOCALIZATION, INHIBITION, BINDING, LEYDIG
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

While the ethanol is a gonadal toxin, insulin-like growth factor-I (IGF-I) has an important role in regulation of spermatogenesis and its signal is predominantly mediated by the IGF-I receptor (IGF-IR). In this study it was aimed to investigate the effect of chronic ethanol consumption on IGF-IR in the rat testes. The rats were divided into two groups: sucrose and alcohol group. The experiment was started on 25(th) day of postnatal period. Water including 15 percent of ethanol was fed up with the alcohol group. The applications were finished on 35(th), 41(th), 50(th) and 70(th) day of experiment according to puberty periods of rats. Testes were fixed in Bouin's solution and embedded in paraffin. The paraffin-embedded sections were processed for standard immunohistochemistry by the labelled streptavidin-biotin technique. During the experimental period, the ethanol exposed group consumed ethanol approximately 12g/kg/d. The immunoreactivity of IGF-IR wits significantly (p lower than 0.05) depressed on 41(th), 50(th) and 70(th) day in spermatids, and 50(th) day in Leydig cells in ethanol exposed group in contrary to that of sucrose group. As a result, it was concluded that the degradation in IGF-IR caused by ethanol affected the paracrine and autocrine mechanism of IGF-I in testicular cells and thus resulting in the corruption in spermatogenesis and delay in sexual maturation.