Dietary intake of exogenous antioxidants has been shown to have only a modest impact on asthma inception and control. Our work has demonstrated that endogenous antioxidant enzyme concentrations are a far stronger predictor of asthma inception compared with dietary antioxidant intake and/or serum antioxidant concentrations. This is likely because we regulate oxidative stress to a greater extent, not by exogenous intake, but by antioxidant enzymes. The milk thistle plant extract, silymarin, has been shown to be an inducer of the endogenous antioxidant enzymes, superoxide dismutase and catalase. As reactive oxygen species have been implicated in the pathogenesis of asthma and, in atopic asthmatics, endogenous superoxide dismutase (SOD) enzyme levels are known to decrease, this supports that increasing SOD levels, either by induction of endogenous SOD or replacing a failed endogenous SOD enzyme system with a mimetic of the endogenous enzyme, would be beneficial and protective. We hypothesize that administration of silymarin, an inducer of antioxidant enzymes, to subjects with atopic asthma will increase antioxidant enzyme concentrations, decrease markers of oxidative stress, decrease indirect measures of airway inflammation that have been correlated with clinical outcomes (exhaled nitric oxide, eNO), and thus improve lung function and symptom scores in participants with asthma. To test this hypothesis we will conduct a randomized, double-masked, placebo-controlled cross-over pilot investigation of an inducer of endogenous antioxidant enzymes, silymarin, in asthma. No clinical trial has tested either silymarin, or any inducer of antioxidant enzymes in patients with asthma. We therefore aim to determine whether this novel treatment is effective, and if both inflammatory and clinical endpoints are improved with treatment.