Expression of Glucose-6-Phosphate Dehydrogenase and 6-Phosphogluconate Dehydrogenase in Oxidative Stress Induced by Long- Term Iron Toxicity in Rat Liver

BUDAK H., CEYLAN H., Kocpinar E. F., Gonul N., ERDOĞAN O.

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, sa.5, ss.217-223, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1002/jbt.21556
  • Dergi Adı: JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.217-223
  • Anahtar Kelimeler: G6PD, 6PGD, Iron Toxicity, Expression, Enzyme Activity, GLUTATHIONE SYSTEM, METAL-IONS, CADMIUM, DEFICIENCY, MECHANISMS, EXPOSURE, ERYTHROCYTES, DISEASES, DRUGS
  • Atatürk Üniversitesi Adresli: Evet

Özet

Reactive oxygen species (ROS) are highly reactive and oxygen-containing molecules that are derived by metabolic activities or from environmental sources. Toxicity of heavy metals including iron has the ability to generate ROS in all living organisms. The pentose phosphate pathway enzymes, which are glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase, produce nicotinamide adenine dinucleotide phosphate (NADPH) that enables cells to counterbalance the oxidative stress via the action of the glutathione system. The results presented herehaveshown that toxic and nontoxic levels of iron have a strong effect on the expression of both genes. While toxic levels of iron exhibited significant changes in enzyme activity, nontoxic levels had no effect on enzymes in rat liver. Our results are the first evidence to elucidate how oxidative stress induced by long-term iron toxicity affects both enzymes at the enzymatic and molecular level and also to determine any possible correlation between the enzymatic and molecular levels.