Melatonin reduces lens oxidative stress level in STZ-induced diabetic rats through supporting glutathione peroxidase and reduced glutathione values
Hyperglycemia plays a critical role in the
development and progression of diabetic cataract oxidative injuries via the
increased reactive oxygen species (ROS) production. Melatonin
has been considered a potent strong antioxidant that detoxifies a
variety of ROS in many metabolic diseases. The present study was conducted to explore whether melatonin administration
protects against diabetic lens oxidative injuries through modulation of reduced
glutathione (GSH) and glutathione peroxidase (GPx) systems in streptozotocin
(STZ)-induced diabetic rats. Thirty two rats were
equally divided into four groups as control, STZ, melatonin and STZ and
melatonin. The third and fourth groups received intraperitoneal 10 mg/kg
melatonin for 2 weeks. For induction of diabetes in the second and fourth groups,
intraperitoneal STZ (45 mg/kg) was given.
Lipid peroxidation (MDA),
total oxidant status and intracellular ROS levels in the lens were increased in
STZ group although they were decreased by melatonin treatment. GPx activity,
GSH concentration and total antioxidant status (TAS) were lower in STZ group
than in control. However, the GSH concentration, GPx activity and TAS levels
were recovered by melatonin. TAS was also higher in melatonin group than in the
STZ and melatonin groups.
In conclusion, the present study shows that melatonin
induced protective effects against diabetes-induced lens oxidative injury
through up-regulation of the GSH and GPx values but down-regulation of
oxidative stress.
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- Yayın Aralığı: Yıllık
- Başlangıç: 2008
- Yayıncı: Hücresel Sinir Bilimleri ve Oksidatif Stres Derneği