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Blood, Vol. 94 No. 7 (October 1), 1999:
pp. 2365-2373
Eosinophil Apoptosis Is Mediated by Stimulators of Cellular Oxidative
Metabolisms and Inhibited by Antioxidants: Involvement of a
Thiol-Sensitive Redox Regulation in Eosinophil Cell Death
Bettina Wedi,
Julia Straede,
Britta Wieland, and
Alexander Kapp
From the Department of Dermatology and Allergology, Hannover Medical
University, Hannover, Germany.
The mechanisms for induction of eosinophil apoptosis remain
uncertain. The role of oxidative stress has not been investigated. The
present study was undertaken to determine the role of reactive oxygen
species (ROS) and selective antioxidants in eosinophil apoptosis.
Eosinophils were cultured with sodium arsenite (SA) known to induce
intracellular oxidative metabolites. There was a significant increase
in the rate of eosinophil apoptosis with low concentrations of
arsenite, whereas high concentrations showed rates of apoptosis similar
to control medium. Investigating the role of intracellular oxidants by
flow cytometry, we found that while inducing apoptosis, SA more than
anti-Fas resulted in a significant dose-dependent production of
intracellular H2O2. In contrast, the
extracellular release of superoxide decreased after stimulation with SA
or anti-Fas as assessed by lucigenin-dependent chemiluminescence. Coincubation experiments demonstrated that arsenite-induced apoptosis can be nearly completely prevented by
selective antioxidants such as glutathione (GSH) and N-acetyl-cysteine (NAC), but not dimethyl sulfoxide (DMSO) or taurine (TAUR). Moreover, GSH and NAC significantly reduced eosinophil apoptosis mediated by a
monoclonal antibody directed to Fas antigen. Next it was shown that GSH
and NAC, but not DMSO or TAUR, were able to significantly delay
spontaneous apoptosis in unstimulated eosinophils. Taken together,
these data point to an important role of oxygen-dependent mechanisms in
the regulation of eosinophil survival and apoptosis. We propose that
eosinophil apoptosis may be related to the ability of the cell to
maintain an appropriate oxidant-antioxidant balance.
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