Chronic cadmium toxicity induces midkine and galectin-3 production in rat testis


Kocak M. K., YAZIHAN N., Akcil E., Erdem O., Sayal A., Guven C., ...Daha Fazla

TRACE ELEMENTS AND ELECTROLYTES, cilt.30, sa.1, ss.7-13, 2013 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 30 Sayı: 1
  • Basım Tarihi: 2013
  • Doi Numarası: 10.5414/tex01253
  • Dergi Adı: TRACE ELEMENTS AND ELECTROLYTES
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.7-13
  • Anahtar Kelimeler: cadmium, testis, TNF-alpha, galectin-3, midkine, apoptosis, MICE, EXPRESSION, EXPOSURE, STRESS, INJURY, DAMAGE, LIVER, HEART, SEMEN, ACID
  • Ankara Üniversitesi Adresli: Evet

Özet

Background: Cadmium (Cd) is known as a wide spread environmental toxin and it exerts toxic effects on multiple organs, including the testes. Aim: The present study was focused to evaluate involvement of TNF-alpha, midkine and galectin-3 levels in Cd toxicity. Methods: Male Wistar rats were exposed to Cd (15 ppm) in their drinking water for 8 weeks. Histopathological examination of testis was carried out by light microscopy. Testis tissue caspase-3 level was used to identify apoptosis. Tissue TNF-alpha, midkine and galectin-3 levels were evaluated by ELISA. Results: A significant increase in galectin-3, midkine tissue levels was seen after Cd toxicity (p < 0.001), this was accompanied by a significant increase in the TNF-alpha levels (p < 0.001). A combination of ongoing necrosis, apoptosis of germinal cells and dysregulation of seminiferous tubules were found in histological examination. Caspase-3 levels increased in Cd toxicity group (p < 0.001). Conclusion: Chronic Cd administration induces inflammation, apoptosis and degeneration in rat testis. Cd increased midkine and galectin-3 production in rat testis tissue. The formation of TNF-alpha due to Cd exposure induced inflammation might likely trigger this mechanism. Further studies are needed to evaluate the underlying pathophysiological mechanism of increased midkine and galectin-3 expressions in Cd toxicity group.