Oxidative stress is produced under diabetic con-ditions and possibly causes various forms of tis-sue damage in patients with diabetes. The aim of the study was to investigate the effect of ginger on the occurrence of oxidative stress in the small intestine of diabetic rats. Materials and Methods: Twenty-four male Wis-tar rats were divided into three groups: control group, nontreated diabetic group, and diabetic group treated with ginger powder as 5% of their daily food. After 6 weeks, lipid peroxidation, protein oxidation, superoxide dismutase (SOD), and catalase levels of the small intestine were measured. Results: Diabetes caused significant increase of small intestine lipid peroxidation, protein oxida-tion, and SOD levels and decrease of catalase ac-tivity. Lipid peroxidation and protein oxidation were attenuated after consumption of ginger in the diabetic rats, and increased catalase activity. Conclusions: These findings indicate that ginger, as an oxidant, improves diabetes induced oxidative stress and its complications through prevention of lipid peroxidation and protein oxidation.

"/> Oxidative stress is produced under diabetic con-ditions and possibly causes various forms of tis-sue damage in patients with diabetes. The aim of the study was to investigate the effect of ginger on the occurrence of oxidative stress in the small intestine of diabetic rats. Materials and Methods: Twenty-four male Wis-tar rats were divided into three groups: control group, nontreated diabetic group, and diabetic group treated with ginger powder as 5% of their daily food. After 6 weeks, lipid peroxidation, protein oxidation, superoxide dismutase (SOD), and catalase levels of the small intestine were measured. Results: Diabetes caused significant increase of small intestine lipid peroxidation, protein oxida-tion, and SOD levels and decrease of catalase ac-tivity. Lipid peroxidation and protein oxidation were attenuated after consumption of ginger in the diabetic rats, and increased catalase activity. Conclusions: These findings indicate that ginger, as an oxidant, improves diabetes induced oxidative stress and its complications through prevention of lipid peroxidation and protein oxidation.

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The Effect of Ginger (Zingiber officinale) on Oxidative Stress Status in the Small Intestine of Diabetic Rats

AUTHORS

MH Khadem Ansari 1 , M Karimipour 1 , S Salami 1 , A Shirpoor 2 , *

1 Department of Biochemistry,Faculty of Medicine, Urmia University of Medical Sciences, IR.Iran

2 Department of Physiology,Faculty of Medicine, Urmia University of Medical Sciences, [email protected], IR.Iran

How to Cite: Khadem Ansari M, Karimipour M, Salami S, Shirpoor A. The Effect of Ginger (Zingiber officinale) on Oxidative Stress Status in the Small Intestine of Diabetic Rats, Int J Endocrinol Metab. Online ahead of Print ; 6(3):144-150.

ARTICLE INFORMATION

International Journal of Endocrinology and Metabolism: 6 (3); 144-150
Article Type: Original Article
Received: January 7, 2008
Accepted: August 28, 2008
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Abstract

Oxidative stress is produced under diabetic con-ditions and possibly causes various forms of tis-sue damage in patients with diabetes. The aim of the study was to investigate the effect of ginger on the occurrence of oxidative stress in the small intestine of diabetic rats. Materials and Methods: Twenty-four male Wis-tar rats were divided into three groups: control group, nontreated diabetic group, and diabetic group treated with ginger powder as 5% of their daily food. After 6 weeks, lipid peroxidation, protein oxidation, superoxide dismutase (SOD), and catalase levels of the small intestine were measured. Results: Diabetes caused significant increase of small intestine lipid peroxidation, protein oxida-tion, and SOD levels and decrease of catalase ac-tivity. Lipid peroxidation and protein oxidation were attenuated after consumption of ginger in the diabetic rats, and increased catalase activity. Conclusions: These findings indicate that ginger, as an oxidant, improves diabetes induced oxidative stress and its complications through prevention of lipid peroxidation and protein oxidation.

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