COPD (Chronic Obstructive Pulmonary Disease) is a chronic lung disease closely associated with cigarette smoke (CS). CS induces inflammation which is thought to cause oxidative stress and play a major role in COPD pathogeneses. We lack information on the delivery mechanisms of antioxidants to the lung. Scavenger Receptor B1 (SR-B1) has been shown to play a prominent role in the uptake of vitamin E (tocopherol) via HDL. We hypothesize that SR-B1 plays an important role in regulating the vitamin E delivery status of the lung. Our preliminary results indicate that young animal’s lung has higher SR-B1 levels than older animals and CS exposure lowers these levels of SR-B1 even further with the CS exposed old animal group having the lowest SR-B1. These provocative and novel results led us to hypothesize that CS and its attendant oxidative stress initiate a positive feedback loop consuming vitamin E, decreasing expression of SR-B1 and thereby hampering delivery of vitamin E to the lung. These issues will be addressed in mice studies that will 1) Quantitate SR-B1 and elucidate mechanisms responsible for the changes in lung SR-B1 and specifically in lung type II cells, in response to CS 2) Quantitate SR-B1 and elucidate mechanisms responsible for the changes in lung SR-B1 and specifically in lung type II cells, in response to changes in dietary vitamin E and 3) Quantitate SR-B1 and elucidate mechanisms responsible for the changes in lung SR-B1 and specifically in lung type II cells, upon combined CS exposure and vitamin E supplementation.
Does Second Hand Cigarette Smoke modulate Lung Vitamin E uptake?
VALACCHI, Giuseppe
2008
Abstract
COPD (Chronic Obstructive Pulmonary Disease) is a chronic lung disease closely associated with cigarette smoke (CS). CS induces inflammation which is thought to cause oxidative stress and play a major role in COPD pathogeneses. We lack information on the delivery mechanisms of antioxidants to the lung. Scavenger Receptor B1 (SR-B1) has been shown to play a prominent role in the uptake of vitamin E (tocopherol) via HDL. We hypothesize that SR-B1 plays an important role in regulating the vitamin E delivery status of the lung. Our preliminary results indicate that young animal’s lung has higher SR-B1 levels than older animals and CS exposure lowers these levels of SR-B1 even further with the CS exposed old animal group having the lowest SR-B1. These provocative and novel results led us to hypothesize that CS and its attendant oxidative stress initiate a positive feedback loop consuming vitamin E, decreasing expression of SR-B1 and thereby hampering delivery of vitamin E to the lung. These issues will be addressed in mice studies that will 1) Quantitate SR-B1 and elucidate mechanisms responsible for the changes in lung SR-B1 and specifically in lung type II cells, in response to CS 2) Quantitate SR-B1 and elucidate mechanisms responsible for the changes in lung SR-B1 and specifically in lung type II cells, in response to changes in dietary vitamin E and 3) Quantitate SR-B1 and elucidate mechanisms responsible for the changes in lung SR-B1 and specifically in lung type II cells, upon combined CS exposure and vitamin E supplementation.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
