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crosses easily cell membranes, including blood brain barrier (Costa et al. 1995), reaching all subcellular compartments and allowing it to be administered either orally or intravenously. Taking into account melatonin’s low toxicity and that patients treated with high doses of melatonin do not experience any harmful side effects (Seabra et al. 2000), its potential spectrum for improving medical treatment against CWAs seems to be wide. The toxic effects of organophosphates (OPs) compounds such as the nerve agents are not limited to acetylcholinesterase inhibition. Oxidative stress is a major mechanism in the pathophysiology of several toxins and diseases. In both acute and chronic OPs toxicity, changes in antioxidant enzymes occur, and lipid peroxidation increases in many organs, especially in the brain. Moreover, an important neuro-inflammation process occurs after OPs exposure (Collombet 2011). Recent insights and new therapeutic perspectives about melatonin’s anti-inflammatory properties and molecular aspects have been recently reviewed (Mauriz et al. 2012). However, it would be important to determine if the neuroprotective efficacy of melatonin against OPs could be effective as prophylactic and/or as post-exposure treatment, because some drugs exert higher protective activity when given under one set of conditions versus the other. Oxidative stress is a key element in the pathogenesis of blister agent toxicity. Some studies have suggested that oxidative stress due to reactive oxygen species (ROS) play an important role in the toxic mechanism of action of mustard gas action (Jafari 2007). However, the powerful nitrosating agent ONOO is involved in the initial detrimental effects of all mustards (Korkmaz et al. 2006). Nowadays, both melatonin and its metabolites have important advantages when compared to “classical antioxidants” including iNOS inhibition and ONOO scavenging properties against mustard’s induced acute toxicity (Sadir et al. 2007). In a recent Chemical Warfare Agents (CWAs) are substances that can kill, injure or incapacitate people because of its pathophysiological effects. Many CWAs are able to generate free radicals and derived reactants, excitotoxicity and inflammatory processes; as consequence, they can produce neurological symptoms and damage in different organs. Nowadays, total immediate decontamination after CWAs exposure is difficult to achieve, and there are no completely effective antidotes or treatments against these agents. In this complex scenario, we think that a broadspectrum multipotent molecule, such as melatonin, would be an interesting antidote and its use could provide a good strategy to counteract CWAs-induced injury. Melatonin (N-acetyl-5-methoxytryptamine), a versatile and pleiotropic molecule that modulates and controls oxidative stress by several mechanisms (Hengstler and Bolt 2007), is a well-known antioxidant and free radical scavenger (Tan et al. 1993; Reiter et al. 2001). Melatonin is also involved in several and important functions such as vasomotor control and adrenal function, possesses antiexcitatory actions, regulates immune function and energy metabolism, including anti-inflammatory properties (Hardeland et al. 2011). Melatonin is highly lipophilic and consequently

Melatonin as potential candidate to prevent the toxicity induced by chemical warfare agents