Journal
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
Volume 122-123, Issue -, Pages 35-44Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2022.03.001
Keywords
Diabetes; Neurotransmitters; Oxidative stress; Nitrosative stress; Behaviour; S-nitrosoglutathione (GSNO)
Categories
Funding
- Council of Scientific and IndustrialResearch (CSIR) [37 (1447) /10/EMR-II, 09/135 (0608) /2010-EMR-I]
Ask authors/readers for more resources
This study evaluated the protective role of GSNO in preventing neurobehavioral deficits induced by hyperglycemia. GSNO supplementation ameliorated alterations in monoaminergic system and nitro-oxidative stress, restoring neurobehavioral functions.
The present study evaluated the protective role of S-nitrosoglutathione (GSNO) in preventing hyperglycemia induced nitro-oxidative stress and alterations in monoaminergic system associated with neurobehavioral deficits in mice. Mice were subjected to diabetes by intraperitoneal injection of streptozotocin (40 mg/kg body weight) for 5 days, whereas GSNO (100 mu g/kg body weight) was administered daily via oral route for 8 weeks. Diabetic mice showed deficits in neurobehavioral functions associated with memory, learning, anxiety and motor coordination. These neurobehavioral deficits observed in diabetic mice may be attributed to decrease in norepinephrine (NE), dopamine (DA), serotonin (5-HT) and increased monoamine oxidase (MAO) activity in cortex and hippocampus. Further, a significant increase in reactive oxygen species (ROS), protein carbonyls, nitrotyrosine (NT) and lipid peroxidation were observed in brain regions of diabetic animals suggesting increased nitro-oxidative stress. Hyperglycemia induced nitro-oxidative stress appears to involve reduction in redox ratio (GSH/GSSG) and enzymatic antioxidants; catalase (CAT) and superoxide dismutase (SOD) in cortex and hippocampus. However, GSNO supplementation was able to ameliorate alterations in monoaminergic system and nitro-oxidative stress in the brain regions thereby restoring neurobehavioural functions. These findings suggest GSNO as potential therapeutic molecule to prevent diabetic encephalopathy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available