Skip to main content
ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #218447
Title: Apo-10’-lycopenoic acid induces Nrf2-mediated expression of phase II antioxidant genes and suppresses H2O2 induced oxidative damage in human bronchial epithelial cells

Author
item LIAN, FUZHI - JM USDA HNRCA @ TUFTS
item Wang, Xiang-Dong

Submitted to: Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2007
Publication Date: 4/5/2008
Citation: Lian, F., Wang, X. 2008. Apo-10’-lycopenoic acid induces Nrf2-mediated expression of phase II antioxidant genes and suppresses H2O2 induced oxidative damage in human bronchial epithelial cells. FASEB Journal. 22:451.7.

Interpretive Summary:

Technical Abstract: Our previous study has demonstrated that apo-10’-lycopenoic acid (ALA), an enzymatic metabolite of lycopene, can suppress lung carcinogenesis in an animal model. However, the potential mechanism(s) underlying this protection is not well defined. It has been suggested that lycopene or its hydrophilic derivatives induce phase II detoxification and antioxidant enzymes by activating the transcription factor Nrf2 (nuclear factor E2-related factor 2). In this study, we investigated whether purified ALA induces Nrf2-mediated expression of phase II antioxidant genes and protects against H2O2-induced oxidative damage. We found that ALA treatment significantly induced the expressions of several phase II enzymes (glutamate-cysteine ligases, heme oxygenase-1, and NAD(P)H : quinone oxidoreductase 1) and resulted in the nuclear accumulation of Nrf2 protein in a time- and dose-dependent manner in BEAS-2B human bronchial epithelial cells. Accordingly, ALA treatment increased total glutathione levels and suppressed endogenous reactive oxygen species generation in BEAs-2B cells. Furthermore, pretreatment of ALA suppressed H2O2-induced oxidative damage in BEA-2B cells as measured by lactate dehydrogenase releasing assay. In conclusion, these data suggest that ALA inhibits lung carcinogenesis by activating Nrf2 mediated antioxidant defense system.