Affiliations: University of Erciyes, Medical Faculty, Department of Physiology, 38039 Kayseri, Turkey
Note: [] Corresponding author: M. Betul Yerer, University of Erciyes, Medical Faculty, Department of Physiology, 38039 Kayseri, Turkey. Tel.: +90 352 437 4938 23310; Fax: +90 352 437 5269; E‐mail: eczbetul@yahoo.com.
Abstract: Reactive oxygen species avidly reacts with nitric oxide (NO) producing cytotoxic reactive nitrogen species capable of nitrating proteins and damaging other molecules which leads to the reduction of erythrocyte deformability. The aim of this investigation was to assess the importance of α‐tocopherol (Vit‐E) in the total antioxidant status of the erythrocytes in sodium nitroprusside (SNP), a nitric oxide donor, induced oxidative stress and its relation to erythrocyte deformability. Male Swiss Albino rats were used in 4 groups, comprising of 10 animals in each group. The first group was the control, and the other groups were administered SNP (10 mg/kg, i.p.), Vit‐E (10 mg/kg, i.p.) + SNP, and SNP + L‐NAME (10 mg/kg, i.p.), respectively. Relative filtration rate (RFR), relative filtration time (RFT) and relative resistance (Rrel) were determined as the indexes of erythrocyte deformability. In addition, malondialdehyde (MDA, as an index of lipid peroxidation) and nitric oxide levels and the antioxidant activities of glutathione peroxidase (GSH‐Px), superoxide dismutase (SOD) and catalase (CAT) were also determined in the red blood cells of all groups revealing the oxidant‐antioxidant activity. RFT and the Rrel of the erythrocytes of the SNP‐treated rats increased significantly (p<0.05) whereas the RFR of the erythrocytes decreased (p<0.05) in comparison to all groups reflecting the impaired deformability. This reduction in RFR was prevented with both L‐NAME or Vit‐E incubation. Vit‐E has also reduced the Rrel of the erythrocyte which reveals that it has improved the erythrocyte deformability. Lipid peroxidation was suppressed by Vit‐E and L‐NAME significantly, where the red blood cell deformability was improved. Furthermore, SOD and CAT activities were significantly stimulated with SNP treatment (p<0.05), where as GSH‐Px remained unchanged. In the contrary, GSH‐Px activity was triggered significantly by Vit‐E administration, whereas the SOD and CAT activities were reduced (p<0.05). As a result, these data reveal that Vit‐E improves the erythrocyte deformability in SNP‐induced oxidative stress by its antioxidant effects on the lipid peroxidation and antioxidant enzyme activities.
