L‐NAME co‐treatment prevent oxidative damage in the lung of adult Wistar rats treated with vitamin A supplementation

Based on the fact that vitamin A in clinical doses is a potent pro‐oxidant agent to the lungs, we investigated here the role of nitric oxide (NO^?) in the disturbances affecting the lung redox environment in vitamin A‐treated rats (retinol palmitate, doses of 1000–9000 IU·kg^?1·day^?1) for 28 days. Lung mitochondrial function and redox parameters, such as lipid peroxidation, protein carbonylation and the level of 3‐nytrotyrosine, were quantified. We observed, for the first time, that vitamin A supplementation increases the levels of 3‐nytrotyrosine in rat lung mitochondria. To determine whether nitric oxide (NO ?) or its derivatives such as peroxynitrite (ONOO‐) was involved in this damage, animals were co‐treated with the nitric oxide synthase inhibitor L‐NAME (30 mg·kg^?1, four times a week), and we analysed if this treatment prevented (or minimized) the biochemical disturbances resulting from vitamin A supplementation. We observed that L‐NAME inhibited some effects caused by vitamin A supplementation. Nonetheless, L‐NAME was not able to reverse completely the negative effects triggered by vitamin A supplementation, indicating that other factors rather than only NO? or ONOO‐ exert a prominent role in mediating the redox effects in the lung of rats that received vitamin A supplementation. Copyright © 2011 John Wiley & Sons, Ltd.