Protective effect of alpha-tocopherol on oxidative stress in experimental pulmonary fibrosis in rats


Deger Y., Yur F., Ertekin A., Mert N., Dede S., Mert H.

CELL BIOCHEMISTRY AND FUNCTION, cilt.25, sa.6, ss.633-637, 2007 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 25 Sayı: 6
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1002/cbf.1362
  • Dergi Adı: CELL BIOCHEMISTRY AND FUNCTION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.633-637
  • Anahtar Kelimeler: oxidative stress, vitamin E, pulmonary fibrosis, antioxidant, free radical, INDUCED LUNG FIBROSIS, VITAMIN-E SUPPLEMENTATION, BLEOMYCIN, GLUTATHIONE, DAMAGE, ACID, INHIBITOR, MELATONIN, TOXICITY
  • Van Yüzüncü Yıl Üniversitesi Adresli: Evet

Özet

The study was undertaken to investigate the influence of alpha-tocopherol (vitamin E) on malondialdehyde (MDA) and glutathione (GSH) levels and catalase (CAT) activity in lung of rats with bleomycin-induced pulmonary fibrosis (PF). Fourteen Wistar-albino rats were randomly divided into two groups of seven animals each. The first group was treated intra-tracheally with bleomycin hydrochloride (BM group); the second group was also instilled with BM but received injections of alpha-tocopherol twice a week (BM + E group). The third group was treated in the same manner with saline solution only, acting as controls (C). There were decreases in GSH level and CAT activity while an increase in MDA level in BM group was found compared to the control group (p < 0.05). Vitamin E had a regulator effect on these parameters. After administration of (alpha-tocopherol, the increase in GSH level and CAT activity and the decrease in MDA level were seen in BM + E group compared to BM group (p < 0.05). Distinct histopathological changes were found in the BM group compared to the untreated rats. Less severe fibrotic lesions were also observed in the BM + E group. The results show that vitamin E is effective on the prevention of BM-induced PF, as indicated by differences in the lung levels of oxidants and antioxidants. Copyright (C) 2006 John Wiley & Sons, Ltd.