Akademik Veri Yönetim Sistemi
JOURNAL OF RESEARCH IN PHARMACY, cilt.26, sa.3, ss.534-542, 2022 (ESCI)
Although there are many studies showing chronic hyperglycemia in diabetes increases oxidative stress, those examining the influence of acute glucose increase are limited. The aim of this study was to investigate the effect of acute hyperglycemia on oxidative stress markers in non-treated and vitamin E pretreated healthy rabbits. Acute hyperglycemia was induced by oral glucose administration (1g/kg). Before and at different time points up to 180 minutes following the administration, blood samples were collected to measure malondialdehyde and glutathione spectrophotometrically as oxidative stress and antioxidant capacity markers respectively. Same markers were also determined in kidney and liver homogenates. There was no difference in glucose tolerance between non-treated and vitamin E pre-treated groups (p=0.10). Plasma malondialdehyde levels were increased after glucose administration in both groups. There was a positive-correlation between blood glucose and plasma malondialdehyde in non-treated (r=+0.447; p=0.008) but not in vitamin E pre-treated group (r=0.076; p=0.361). Plasma glutathione levels were higher in vitamin E pre-treated group at all-time points compared to non-treated group (p<0.05). There was a negative-correlation between blood glucose and plasma glutathione levels in non-treated (r=- 0.357; p=0.033) hut not in vitamin E pre-treated group (r=0.007; p=0.485). According to our results acute hyperglycemia provokes oxidative stress which is partially prevented by vitamin E pretreatment.