Lutein and docosahexaenoic acid prevent cortex lipid peroxidation in streptozotocin-induced diabetic rat cerebral cortex.
The mechanisms underlying diabetic encephalopathy, are largely unknown. Here, we examined whether docosahexaenoic acid (DHA) and lutein could attenuate the oxidative changes of the diabetic cerebral cortex. The levels of malondialdehyde (MDA) were significantly increased and glutathione (GSH) and glutathione peroxidase activity (GPx) were decreased in diabetic rats. The number of 4-hydroxynonenal (4-HNE) positive cells was increased. Treatment with insulin, lutein or DHA and the combination of each antioxidant with insulin, significantly restored all markers concentrations mentioned above, and the increase in 4-HNE inmunofluorescence. We combined 4-HNE immunofluorescence with NeuN (Neuronal Nuclei) staining. The latter demonstrated extensive overlap with the 4-HNE staining in the cortex from diabetic rats. Our findings demonstrate a clear participation of glucose-induced oxidative stress in the diabetic encephalopathy, and that the cells suffering oxidative stress are neurons. Lowering oxidative stress through the administration of different antioxidants may be beneficial for the central nervous tissue in diabetes.
Arnal
E
E
Fundación Oftalmológica del Mediterráneo, Valencia, Spain.
Miranda
M
M
Barcia
J
J
Bosch-Morell
F
F
Romero
F J
FJ
D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D034961:Antigens, Nuclear / Q000032:analysis / Q000378:metabolism; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D001928:Brain Diseases, Metabolic / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D048909:Diabetes Complications / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications; D004195:Disease Models, Animal; D004281:Docosahexaenoic Acids / Q000378:metabolism / Q000494:pharmacology*; D004359:Drug Therapy, Combination; D005455:Fluorescent Antibody Technique; D005947:Glucose / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006943:Hyperglycemia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007328:Insulin / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects* / Q000502:physiology; D014975:Lutein / Q000378:metabolism / Q000494:pharmacology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000032:analysis / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D016896:Treatment Outcome
D000447:Aldehydes; D034961:Antigens, Nuclear; D000975:Antioxidants; D015415:Biomarkers; D007328:Insulin; D009419:Nerve Tissue Proteins; C546339:Rbfox3 protein, rat; D004281:Docosahexaenoic Acids; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D005978:Glutathione; D005947:Glucose; C027576:4-hydroxy-2-nonenal; D014975:Lutein