Oxidative stress and gene expression of antioxidant enzymes in the streptozotocin-induced diabetic rats under hyperbaric oxygen exposure.

نویسندگان

  • Tokio Matsunami
  • Yukita Sato
  • Takuya Sato
  • Satomi Ariga
  • Toshiko Shimomura
  • Masayoshi Yukawa
چکیده

Diabetes mellitus (DM) causes not only hyperglycemia but oxidative stress, resulting mainly enhanced production of mitochondrial reactive oxygen species (ROS). Hyperbaric oxygen (HBO) treatments are applied various diseases including diabetic patients with unhealing foot ulcers, however, and also increases the formation of ROS. Recently, it has been reported that oxidative stress worsens many pathological conditions including DM and obesity suggesting possible changes in regulation of genes associated with the oxidative stress, however, effects of HBO which could induce ROS on the gene expressions of oxidative stress parameters in DM animals are unknown. The purpose of this study is to investigate the effect of HBO exposure on the gene expression of three important antioxidant enzymes, cytosolic superoxide dismutase (Cu-Zn SOD), cytosolic glutathione peroxidase (GPx-1), and catalase (CAT) in DM rats, respectively. We used streptozotocin-induced DM model rats and examined both mRNA expressions and the activities of these antioxidant enzymes in the liver, skeletal muscle, and pancreas. The mRNA expressions of Cu-Zn SOD and CAT decreased significantly (p < 0.001), and GPx increased significantly (p < 0.001) in all the studied organs of DM rats under HBO exposure compared to those from DM-induced rats not exposed to HBO. Similarly, activities of these three enzymes changed in accordance with the mRNA levels. These results suggested that DM induction and HBO exposure might synergistically affect antioxidant enzymes, resulting increase of oxidative stress state. Thus, HBO exposure seems to be an excellent model system for investigating oxidative stress.

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عنوان ژورنال:
  • International journal of clinical and experimental pathology

دوره 3 2  شماره 

صفحات  -

تاریخ انتشار 2009