Effects of selenium on altered mechanical and electrical cardiac activities of diabetic rat

Ayaz M., Ozdemir S., UĞUR M., Vassort G., TURAN B.

Archives of Biochemistry and Biophysics, cilt.426, sa.1, ss.83-90, 2004 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 426 Sayı: 1
  • Basım Tarihi: 2004
  • Doi Numarası: 10.1016/j.abb.2004.03.030
  • Dergi Adı: Archives of Biochemistry and Biophysics
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.83-90
  • Anahtar Kelimeler: action potential, contraction, sodium selenite, K+ currents, glutathione metabolism, VENTRICULAR MYOCYTES, K+ CURRENTS, POTASSIUM CURRENTS, SODIUM SELENATE, INSULIN, GLUTATHIONE, CARDIOMYOPATHY, TISSUE, HEART, REVERSIBILITY
  • Lokman Hekim Üniversitesi Adresli: Hayır

Özet

Since selenium compounds can restore some metabolic parameters and structural alterations of diabetic rat heart, we were tempted to investigate whether these beneficial effects extend to the diabetic rat cardiac dysfunctions. Diabetes was induced by streptozotocin (50mg/kg body weight) and rats were then treated with sodium selenite (5μmol/kg body weight/day) for four weeks. Electrically stimulated isometric contraction and intracellular action potential in isolated papillary muscle strips and transient (I to) and steady state (Iss) outward K+ currents in isolated cardiomyocytes were recorded. Sodium selenite treatment could reverse the prolongation in both action potential duration and twitch duration of the diabetic rats, and also cause significant increases in the diminished amplitudes of the two K+ currents. Treatment of rats with sodium selenite also markedly increased the depressed acid-soluble sulfhydryl levels of the hearts. Our data suggest that the beneficial effects of sodium selenite treatment on the mechanical and electrical activities of the diabetic rat heart appear to be due to the restoration of the diminished K+ currents, partially, related to the restoration of the cell glutathione redox cycle. © 2004 Elsevier Inc. All rights reserved.