title: Beneficial effect of docosahexanoic acid and lutein on retinal structural, metabolic, and functional abnormalities in diabetic rats.
abstract: OBJECTIVE
  To assess the effect of docosahexanoic acid (DHA) and lutein (both compounds with anti-inflammatory and antioxidant properties) on experimental diabetic retinopathy.
  
  
  METHODS
  Male Wistar rats were studied: non-diabetic controls, untreated diabetic controls, and diabetic rats were treated with DHA and lutein or the combination of DHA + insulin and lutein + insulin for 12 weeks. Oxidative stress and inflammatory markers, apoptosis, and functional tests were studied to confirm biochemical and functional changes in the retina of diabetic rats. Malondialdehyde (MDA), glutathione concentrations (GSH), and glutathione peroxidase activity (GPx) were measured as oxidative stress markers. TUNEL assay and caspase-3 immunohistochemistry and electroretinogram were performed.
  
  
  RESULTS
  Diabetes increases oxidative stress, nitrotyrosine concentrations, and apoptosis in the retina. At 12 weeks after onset of diabetes, total thickness of retinas of diabetic rats was significantly less than that in control rats. Specifically, the thickness of the outer and inner nuclear layers was reduced significantly in diabetic rats and demonstrated a loss of cells in the GCL. These retinal changes were avoided by the administration of insulin and DHA and lutein alone or in combination with insulin. Impairment of the electroretinogram (b-wave amplitude and latency time) was observed in diabetic rats. DHA and lutein prevented all these changes even under hyperglycemic conditions.
  
  
  CONCLUSIONS
  Lutein and DHA are capable of normalizing all the diabetes-induced biochemical, histological, and functional modifications. Specifically, the cell death mechanisms involved deserve further studies to allow the proposal as potential adjuvant therapies to help prevent vision loss in diabetic patients.
authors: Ophthalmological Mediterranean Foundation, Valencia, Spain.
authors: Emma
authors: E
authors: Arnal
authors: Maria
authors: M
authors: Miranda
authors: Siv
authors: S
authors: Johnsen-Soriano
authors: Raquel
authors: R
authors: Alvarez-Nölting
authors: Manuel
authors: M
authors: Díaz-Llopis
authors: Javier
authors: J
authors: Araiz
authors: Enrique
authors: E
authors: Cervera
authors: Francisco
authors: F
authors: Bosch-Morell
authors: Francisco J
authors: FJ
authors: Romero
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D053148:Caspase 3 / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D003930:Diabetic Retinopathy / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D004359:Drug Therapy, Combination; D004596:Electroretinography; D004797:Enzyme-Linked Immunosorbent Assay; D019084:Fluorescent Antibody Technique, Indirect; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D007328:Insulin / Q000494:pharmacology; D014975:Lutein / Q000494:pharmacology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000187:drug effects* / Q000503:physiopathology*; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D015415:Biomarkers; D001786:Blood Glucose; D007328:Insulin; D004281:Docosahexaenoic Acids; C002744:3-nitrotyrosine; D014443:Tyrosine; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D053148:Caspase 3; D005978:Glutathione; D014975:Lutein