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1 National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, USA
2 Department of Medicine, Duke University, Durham, NC, USA
3 Center for Environmental Medicine and Lung Biology, University of North Carolina, Chapel Hill, NC, USA
4 Department of Cellular and Structural Biology, University of Texas at San Antonio, San Antonio, TX, USA
5 Department of Biochemistry, SUNY at Buffalo, Buffalo, NY, USA
* To whom correspondence should be addressed. E-mail: ghio.andy{at}epa.gov.
Exposure to airborne particulates makes the detoxification of metals a continuous challenge for the lungs. Based on the fate of iron in airway epithelial cells, we postulated that divalent metal transporter 1 (DMT1) participated in detoxification of metal associated with particles. Homozygous Belgrade rats, which are functionally deficient in DMT1, exhibited diminished metal transport from the lower respiratory tract and greater lung injury than control littermates when exposed to oil fly ash. Pre-exposure of normal rats to iron in vivo increased expression of the isoform of DMT1 mRNA that lacked an iron response element (-IRE), accelerated metal transport out of the lung, and decreased injury after particle exposure. In contrast, normal rats pre-exposed to vanadium showed less expression of the -IRE isoform of DMT1, decreased metal transport, and greater pulmonary injury after particle instillation. Respiratory epithelial cells in culture gave similar results. Also, DMT1 mRNA and protein expression for the -IRE isoform increased or decreased in these cells when exposed to iron or vanadium, respectively. These results thus demonstrate for the first time a primary role for DMT1 in lung metal transport and detoxification.
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