The aim of the present work was to evaluate whether the treatment of human neutrophils with phenanthrene (PHN) can alter the phagocytic and microbicidal capacity of these cells by causing a disruption in redox balance. Peripheral neutrophils from healthy subjects were treated for up to 24 h with increasing concentrations of phenanthrene. Phagocytic/microbicidal activities, antioxidant enzymes, oxidative lesions (thiobarbituric acid-reactive substances and protein thiol and carbonyl groups) and redox signaling compounds (intracellular Ca(2+), superoxide, hydrogen peroxide and nitric oxide) were monitored on neutrophils exposed to 10 microg PHN ml(-1). Cell viability decreased abruptly at PHN concentrations above 10 microg ml(-1) (LC50 = 20.86 +/- 0.51 microg ml(-1) and p-sigmoidal slope = 19.88 +/- 10.11). Phagocytic and microbicidal capacities were decreased by 60 and 82%, respectively. Substantial increases in total-/Mn-SOD, catalase, glutathione peroxidase and glutathione reductase activities (by 61, 15, 87, 245 and 70%, respectively) matched the oxidative injury obtained in TBARS (2.5-fold higher) and protein thiol (54% lower). Diminished productions of superoxide by 18% and hydrogen peroxide by 29% were observed in association to exacerbated calcium (27%) and nitric oxide (63%) levels. The data indicate that phenanthrene might be associated with substantial reduction in human neutrophil functions due to severe intracellular redox imbalances.
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