Supplementation with the Antioxidant Sulforaphane Does Not Protect Airway Epithelium Against O3-Induced Injury In Vivo
Saturday, March 5, 2016
South Exhibit Hall H (Convention Center)
Michelle L. Hernandez, MD, Katherine Mills, BA, Allison J. Burbank, Matthew J Kesic, PhD, Charity Duran, PhD, David B. Peden, MD MS FAAAAI

Airway epithelial cell injury is the initial event in ozone (O3)-induced inflammatory responses. Oral supplementation with sulforaphane (SFN), an antioxidant compound derived from broccosprouts, upregulates expression of NRF2-regulated antioxidant enzymes in airway epithelial cells at baseline.  We hypothesized that antioxidant supplementation can decrease O3-induced inflammation by modulating epithelial cell antioxidant gene expression in vivo.


Thirteen healthy volunteers completed a double-blinded, placebo controlled crossover study where they consumed either SFN-rich broccosprout homogenate (BSH) vs. alfalfa sprout homogenate (placebo).  After 3 days of daily supplementation, they underwent a 2-hour 0.4 part per million O3 exposure. Plasma levels of SFN and its major metabolites, Sulforaphane-N-acetylcysteine (NAC) and Sulforaphane-Glutathione (GSH) were obtained. We assessed changes in nasal epithelial cell mRNA expression of NRF2 and the NRF2-regulated antioxidants (GSTM1, GSTP1, NQO1, and HO1) four hours after the O3 exposure. The effect of BSH v. placebo was compared by paired T-test.

Results: Three days of supplementation with BSH significantly increased levels of SFN (p=0.001) and its major metabolites, SFN-NAC (p=0.002) and SFN-GSH (p<0.001) compared to placebo.  Despite these increases in SFN and metabolite levels, we did not see a significant difference in post-O3 nasal epithelial cell mRNA expression of NRF2 or NRF2-regulated antioxidant genes between placebo v. BSH treatment.

Conclusions: BSH supplementation successfully increased peripheral blood levels of SFN and its major metabolites in healthy volunteers.  However, supplementation with BSH does not confer protection against O3 -induced changes in airway epithelial cell oxidative stress in vivo.