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These data suggest that protective mechanisms observed with AMIN involve decreased LTC(4)/D(4)/E(4) mediated pulmonary capillary permeability and attenuated lipid peroxidation

In vitro cytotoxicity studies confirm the absence of cellular toxicity at physiological and supraphysiological concentrations

Therefore, sufficient GSH supply and active glutathione peroxidase are main defence resources of neurons under pro-oxidative conditions 23,24,25

Another potential approach could involve combining GHK with an anti-inflammatory agent

They showed that doses above 400 mg/kg caused an almost complete exhaustion of GSH levels in the liver and a sharp rise in the amount of covalent binding (Figure6B)