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Zinc Ions as Effectors of Environmental Oxidative Lung Injury
Wu, W., P. Bromberg, AND J. Samet. Zinc Ions as Effectors of Environmental Oxidative Lung Injury. Free Radical Biology and Medicine. Elsevier Science Ltd, New York, NY, 65:57-69, (2013).
The non-redox active transition metal Zn is a micronutrient that plays essential roles in protein structure, catalysis and regulation of function. Inhalational exposure to ZnO or Zn salts in occupational and environmental settings leads to adverse health effects, the severity of which appears dependent on the flux of Zn2+ presented to the airway and alveolar cells. The toxicity of exogenous Zn2+ exposure is characterized by cellular responses that include mitochondrial dysfunction, elevated production of reactive oxygen species and loss of signaling quiescence leading to cell death and increased expression of adaptive and inflammatory genes. Central to the molecular effects of Zn2+ is its interactions with cysteinyl thiols, which alters their functionality by modulating their reactivity and participation in redox reactions. Ongoing studies aimed at elucidating the molecular toxicology of Zn2+ in the lung are contributing valuable information about its role in redox biology and cellular homeostasis in normal and pathophysiology.
A review on the molecular toxicology of Zinc inhalation.
Record Details:Record Type: DOCUMENT (JOURNAL/PEER REVIEWED JOURNAL)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LAB
ENVIRONMENTAL PUBLIC HEALTH DIVISION
CLINICAL RESEARCH BRANCH