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ZINC-DEFICIENCY ENHANCES PRO-INFLAMMATORY RESPONSES AFTER OZONE EXPOSURE
Citation:
BRIDGE, K., M. DOYLE, K. SEXTON, H. JEFFERIES, E. HO, M. STYBLO, AND I. JASPERS. ZINC-DEFICIENCY ENHANCES PRO-INFLAMMATORY RESPONSES AFTER OZONE EXPOSURE. Presented at Society of Toxicology (SOT), New Orleans, LA, March 06 - 10, 2005.
Description:
Epidemiological and controlled exposure studies have demonstrated that humans are differentially susceptible to adverse health effects induced by exposure to ozone. Serum analysis of vitamins and trace elements have shown that the elderly (people >65 years) are deficient in several key vitamins and trace elements, including zinc (Zn). While it is well known that the elderly are especially susceptible to adverse health effects induced by exposure to air pollutants, it is not known to what extend their nutritional status could contribute to these effects. The trace element Zn is essential for the function of several key signaling molecules and antioxidant enzymes. Thus, insufficient dietary Zn intake and consequently low intracellular Zn levels could potentially alter the susceptibility to pollutant-induced adverse health effects. We have established an in vitro model of human respiratory epithelial cells (A549 cells) grown under Zn-deficient (Zn-DF) or Zn-adequate (Zn-AD) conditions. Analysis of these cells show that culturing these cells under Zn-DF conditions significantly reduces their intracellular Zn levels and the activity of key Zn-dependent enzymes, such as Cu,Zn-SOD, while the activity Zn-independent antioxidant enzymes, such as catalase and glutathione peroxidase, remain unchanged. Zn-AD and Zn-DF cells grown on Transwell" membranes were exposed to 0.2 ppm ozone for 5 hours and subsequently analyzed for LDH release and the release of pro-inflammatory cytokines, such as IL-8, MCP-1, and IL-6. Ozone exposure caused similar LDH release in both Zn-AD and Zn-DF cells. Interestingly, ozone induced greater release of IL-8, MCP-1, and IL-6 into the apical compartment of Zn-DF cells as compared to Zn-AD cells, while ozone-induced cytokine release into the basolateral compartment was similar in Zn-DF and Zn-AD cells. These data suggest that Zn-DF respiratory epithelial cells are more susceptible to adverse inflammatory effects induced by ozone exposure and that ozone-induced cytokine release is greater towards the apical side than the basolateral side. In addition, these results suggest that the nutritional status of individuals could influence their susceptibility to air pollutant-induced health effec