Manganese (Mn) is a required element for biological systems; however, its excessive exposure may lead to a neurological syndrome known as manganism. The aim of the present study was to assess the toxic effects of subacute exposure of Mn by measuring weight gain, motor performance, and biochemical parameters (complex I activity, lipid peroxides, and protein carbonyls) in brain mitochondria in rats. We also examined whether edaravone (EDA), a radical scavenger, exerts protective effects against Mn-induced neurotoxicity. In addition, we evaluated the accumulation of Mn in brain regions using magnetic resonance imaging. Mn-exposed rats revealed significantly impaired motor performance, weight loss, and Mn accumulation in particular brain area. Lipid peroxides and protein carbonyls were significantly increased in Mn-exposed rats, whereas complex I activity was found to be decreased. EDA treatment significantly prevented mitochondrial oxidative damage and improved motor performance. These findings suggested that EDA might serve as a clinically effective agent against Mn-induced neurotoxicity. (C) 2016 Wiley Periodicals, Inc.