You are here:
FERRITIN EXPRESSION AFTER IN VITRO EXPOSURES OF HUMAN ALVEOLAR MACROPHAGES TO SILICA IS IRON-DEPENDENT
Citation:
Ghio, A. J., J D. Carter, J M. Samet, J. L. Quay, I. Wortman, J. E. Richards, T. P. Kennedy, AND R. B. Devlin. FERRITIN EXPRESSION AFTER IN VITRO EXPOSURES OF HUMAN ALVEOLAR MACROPHAGES TO SILICA IS IRON-DEPENDENT. AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY 17:533-540, (1997).
Description:
The increased availability of catalytically active iron after silica exposure can present an oxidative injury to a living system. Sequestration of reactive iron would, therefore, confer a protective effect. The intracellular storage of iron by ferritin within macrophages can limit the potential for radical generation and cellular injury resulting from exposure to a metal chelate. We tested the hypothesis that in vitro exposure of human alveolar macrophages to silica increases the expression of ferritin through a posttranscriptional mechanism. Exposure of 1.0 x 10(6) macrophages to 100 microg/ml silica for 4 h increased light-subunit (L)-ferritin protein concentrations in both cell supernatants and lysates. Inclusion of 1.0 mM deferoxamine in the reaction mixtures inhibited increases in ferritin after silica. To test for a posttranscriptional regulation of ferritin protein expression, cells were incubated with acid-washed particles, silica with complexed zinc cation, and silica with complexed iron cation. L-ferritin protein concentrations were increased in both cell supernatants and lysates after 4 h of exposure to silica with complexed iron cation. There were no increases in L-ferritin after incubations with acid-washed particles or silica with complexed zinc cation. There were no significant differences in levels of L-ferritin cDNA between any of the exposures, suggesting a posttranscriptional control of ferritin expression.