Radiation damage to the lung: mitigation by angiotensin-converting enzyme (ACE) inhibitors. Respirology 2012 Jan;17(1):66-71
Date
10/26/2011Pubmed ID
22023053Pubmed Central ID
PMC3245332DOI
10.1111/j.1440-1843.2011.02092.xScopus ID
2-s2.0-84255176558 (requires institutional sign-in at Scopus site) 89 CitationsAbstract
Concern regarding accidental overexposure to radiation has been raised after the devastating Tohuku earthquake and tsunami which initiated the Fukushima Daiichi nuclear disaster in Japan in March 2011. Radiation exposure is toxic and can be fatal depending on the dose received. Injury to the lung is often reported as part of multi-organ failure in victims of accidental exposures. Doses of radiation >8 Gray to the chest can induce pneumonitis with right ventricular hypertrophy starting after ∼2 months. Higher doses may be followed by pulmonary fibrosis that presents months to years after exposure. Though the exact mechanisms of radiation lung damage are not known, experimental animal models have been widely used to study this injury. Rodent models for pneumonitis and fibrosis exhibit vascular, parenchymal and pleural injuries to the lung. Inflammation is a part of the injuries suggesting involvement of the immune system. Researchers worldwide have tested a number of interventions to prevent or mitigate radiation lung injury. One of the first and most successful class of mitigators are inhibitors of angiotensin-converting enzyme (ACE), an enzyme that is abundant in the lung. These results offer hope that lung injury from radiation accidents may be mitigated, since the ACE inhibitor captopril was effective when started up to 1 week after irradiation.
Author List
Medhora M, Gao F, Jacobs ER, Moulder JEMESH terms used to index this publication - Major topics in bold
Angiotensin-Converting Enzyme InhibitorsAnimals
Disease Models, Animal
Humans
Inflammation
Lung
Pulmonary Fibrosis
Radiation Dosage
Radiation Injuries, Experimental
Radiation Pneumonitis
