Dietary Virgin Olive Oil Reduces Oxidative Stress and Cellular Damage in Rat Brain Slices Subjected to Hypoxia-Reoxygenation

• Published in: Lipids 2007-10, Vol.42 (10), p.921-929
• Main Authors: González-Correa, J. A, Muñoz-Marín, J, Arrebola, M. M, Guerrero, A, Narbona, F, López-Villodres, J. A, Cruz, J. P. de la
• Format: Article
• Language: English
• Subjects: 6-ketoprostaglandin F1 alpha; Agglomeration; Animals; Brain; Brain - drug effects; Brain - metabolism; Brain damage; Brain injury; Brain slice preparation; Damage assessment; Dehydrogenase; Dehydrogenases; dietary fat; Dietary Fats, Unsaturated - administration & dosage; Dietary Fats, Unsaturated - pharmacology; Disease Models, Animal; Glutathione; Hypoxia; Hypoxia, Brain - metabolism; Ischemia; L-Lactate dehydrogenase; Lactate dehydrogenase; Lactic acid; Lipid peroxidation; Lipids; Male; nitrates; Nitric oxide; Nitric Oxide Synthase - metabolism; Nitric-oxide synthase; Nitrites; Olive Oil; Oxidative stress; Oxidative Stress - drug effects; Peroxidation; Plant Oils - administration & dosage; Plant Oils - pharmacology; Platelet aggregation; Platelets; Prostaglandin E2; prostaglandins; Rats; Rats, Wistar; thromboxanes
• ISSN: 0024-4201; 1558-9307
• DOI: 10.1007/s11745-007-3097-6

We investigated how virgin olive oil (VOO) affected platelet and hypoxic brain damage in rats. Rats were given VOO orally for 30 days at 0.25 or 0.5 mL kg-¹ per day (doses A and B, respectively). Platelet aggregation, thromboxane B₂, 6-keto-PGF₁α, and nitrites + nitrates were measured, and hypoxic damage was evaluated in a hypoxia-reoxygenation assay with fresh brain slices. Oxidative stress, prostaglandin E ₂, nitric oxide pathway activity and lactate dehydrogenase (LDH) activity were also measured. Dose A inhibited platelet aggregation by 36% and thromboxane B₂ by 19%; inhibition by dose B was 47 and 23%, respectively. Virgin olive oil inhibited the reoxygenation-induced increase in lipid peroxidation (57% in control rats vs. 2.5% (P < 0.05) in treated rats), and reduced the decrease in glutathione concentration from 67 to 24% (dose A) and 41% (dose B). Brain prostaglandin E ₂ after reoxygenation was 306% higher in control animals, but the increases in treated rats were only 53% (dose A) and 45% (dose B). The increases in nitric oxide production (213% in controls) and activity of the inducible isoform of nitric oxide synthase (175% in controls) were both smaller in animals given VOO (dose A 84%; dose B 12%). Lactate dehydrogenase activity was reduced by 17% (dose A) and 42% (dose B). In conclusion, VOO modified processes related to thrombogenesis and brain ischemia. It reduced oxidative stress and modulated the inducible isoform of nitric oxide synthase, diminishing platelet aggregation and protecting the brain from the effects of hypoxia-reoxygenation.