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Considering the putative role of oxidative stress as a pathogenetic factor for the development of colitis and because the reductive metabolism of TNBS has been shown to generate ROS, this model of colitis was chosen to evalute the temporal relationship between the levels of GSH in mucosa and the appearance and extent of injury in vivo during the acute phase of colitis in TNBS+ethanol-treated rats and to determine the effect of NAC administration on mucosal GSH levels and extent of injury

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