IL1B and acute respiratory distress syndrome: Since the mechanism of action of CCl4 and its metabolites promote lipid peroxidation, mitochondrial dysfunction, oxidative and nitrosative stress, inflammation by activation of Tumor Necrosis Factor α, Interleukin (IL)−1, IL-6, IL-10 and the release of Nitric Oxide (NO) (Weber et al., 2003), features that are closely involved in the pathophysiology of ALI, we used this experimental model to characterize a plausible effect on Glu transporters and metabolism in liver, brain and cerebellum.