Broccoli could promote lung health, study
The findings, published in the second issue for September of the American Journal of Respiratory and Critical Care Medicine, adds to the list of benefits linked to the antioxidant-rich cruciferous vegetable, which has already been found to be good for the heart, brain and cancer.
The latest study focused on chronic obstructive pulmonary disease (COPD), which is considered to be the fourth leading cause of death in the US, affecting some 16m Americans.
Researchers led by Dr Shyam Biswal found that the severity of COPD in smokers is linked to lower concentrations of NRF2-dependant antioxidants, which are key components of the lung’s defense system against inflammatory injury.
Broccoli has already been found to help prevent the degradation of NRF2, and could form the basis of new research to further examine its link with lung health.
The key to the vegetable’s protective effects is the naturally-occurring sulforaphane.
Sulforaphane was first discovered by scientists at John Hopkins University School of Medicine in 1992, and a raft of scientific studies have indicated SGS (sulforaphane glucosinolate) found in broccoli sprouts to be a long-lasting anti-oxidant and detoxifier, and to contribute to the integrity of cells, promoting the body's immune defense systems for overall health and well being.
Sulforapane has been shown to be able to restore antioxidant gene expression in human epithelial tissue in which DJ-1 has been reduced. DJ-1 is a biochemical regulator that stabilizes NRF2, while KEAP1 – another regulator – inhibits NRF2.
Isothicyanate compounds such as that found in broccoli inhibit KEAP1, and thus prevent it from degrading NRF2, according to Dr Peter Barnes, of the National Heart and Lung Institute in London, who wrote an accompanying editorial.
“While clinical trials to date of antioxidants have been disappointing in improving the clinical course of patients with COPD, this study points to a possibility of benefit from restoring NRF2 levels in damaged lungs by reducing the action of KEAP1, which is an inhibitor of NRF2,” he wrote.
"[I]ncreasing NRF2 may also restore important detoxifying enzymes to counteract other effects of tobacco smoke. This has been achieved in vitro and in vivo by isothiocynate compounds, such as sulforaphane, which occurs naturally in broccoli and [wasabi]."
In the current study, researchers examined tissue samples from the lungs of smokers with and without COPD to determine if there were differences in measured levels of NRF2 expression and the level of KEAP1 and DJ-1.
The lungs of patients with COPD showed markedly decreased levels of NRF2-dependent antioxidants and increased oxidative stress markers, compared to non-COPD lungs.
"NRF2-dependent antioxidants and DJ-1 expression was negatively associated with severity of COPD," wrote Dr Biswal, an associate professor in the Bloomberg School's Department of Environmental Health Sciences and Division of Pulmonary and Critical Care at the Johns Hopkins School of Medicine.
"Therapy directed toward enhancing NRF2-regulated antioxidants may be a novel strategy for attenuating the effects of oxidative stress in the pathogenesis of COPD."
Source:‘Decline in NRF2-regulated Antioxidants in Chronic Obstructive Pulmonary Disease Lungs Due to Loss of Its Positive Regulator, DJ-1’, American Journal of Respiratory and Critical Care Medicine Vol 178. pp. 592-604, (2008)doi: 10.1164/rccm.200803-380OCAuthors: Deepti Malhotra1, Rajesh Thimmulappa1,Ana Navas-Acien1, Andrew Sandford, Mark Elliott, Anju Singh1, Linan Chen, Xiaoxi Zhuang, James Hogg, Peter Pare, Rubin M. Tuder, and Shyam Biswal
