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Effects of simvastatin treatment on oxidant/antioxidant state and ultrastructure of streptozotocin‐diabetic rat lung
Author(s) -
Ozansoy Gülgün,
Güven Cengiz,
Ceylan Aslı,
Can Belgin,
Aktan Fügen,
Öz Eser,
Gönül Bilge
Publication year - 2005
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1168
Subject(s) - simvastatin , medicine , glutathione peroxidase , diabetes mellitus , endocrinology , malondialdehyde , streptozotocin , lipid peroxidation , antioxidant , nitric oxide , catalase , chemistry , oxidative stress , biochemistry
In the present study, we investigated the effects of simvastatin, a 3‐hydroxy‐3‐methyl‐glutaryl coenzyme A reductase inhibitor, on lipid metabolism, lipid peroxidation, antioxidant enzyme activities and ultrastructure of diabetic rat lung. Diabetes was induced by a single injection of streptozotocin (45 mg kg −1 , i.p.). After 8 weeks induction of diabetes, some control and diabetic rats were treated with simvastatin (10 mg kg −1  rat day −1 ; orally) for 4 weeks. Diabetes resulted in significantly high levels of blood glucose and plasma lipids. Malondialdehyde levels were unchanged after 12‐week‐old diabetic rats, whereas catalase activity significantly decreased in the lung. Glutathione peroxidase activity and nitric oxide level were significantly elevated in the diabetic lung. Histological analysis of the diabetic lung revealed some deterioration in the structure. Simvastatin treatment reduced plasma lipid levels and partially decreased the severity of hyperglycaemia. Catalase, glutathione peroxidase activities and nitric oxide levels were partially restored and accompanied by improved structure in diabetic lung by the simvastatin treatment. These results suggest that structural disturbances and alteration of antioxidative enzyme activities occurred in diabetic lung. Simvastatin treatment may provide some benefits in the maintenance of antioxidant status and structural organization of diabetes‐induced injury of lung. Copyright © 2004 John Wiley & Sons, Ltd.

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