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Functional responses of human neutrophils to sodium sulfite (Na2SO3) in vitro

Institut National de la Recherche Scientifique-Santé (INRS-Santé), UniversitéduQuébec, Pointe-Claire, Québec, H9R 1G6 Canada

Martin Pelletier

Institut National de la Recherche Scientifique-Santé (INRS-Santé), UniversitéduQuébec, Pointe-Claire, Québec, H9R 1G6 Canada

Felix O Omara

Institut National de la Recherche Scientifique-Santé (INRS-Santé), UniversitéduQuébec, Pointe-Claire, Québec, H9R 1G6 Canada

Denis Girard

Institut National de la Recherche Scientifique-Santé (INRS-Santé), UniversitéduQuébec, Pointe-Claire, Québec, H9R 1G6 Canada

An influx of neutrophils into the airways is a common feature observed during pulmonary inflammation induced by air pollutants, including sulfur dioxide and sulfates. In the present study focusing on the in vitro interactions of sodium sulfite (Na₂SO₃) with human neutrophils, we confirm results indicating that this sulfite induces superoxide production (O₂ ⁷) by itself. We demonstrated that this response can occur more rapidly than previously reported (within 5 min), and that Na₂SO₃ can act as a priming agent, in a concentration-dependent fashion, to the bacterial tripeptide N-formyl-methionineleucine-phenylalanine (fMLP) by increasing O₂ ⁷ production. In addition, our results show that Na₂SO₃ induces gene expression in human neutrophils in a concentration-dependent manner as assessed by incorporation of 5-[³H] uridine into total RNA. However, it does not induce cell shape changes. We also demonstrated that Na₂SO₃ does not modulate neutrophil apoptosis nor reverse the well-known delaying effect of granulocyte-macrophage colony-stimulating factor (GM-CSF) on apoptosis. We conclude that Na₂SO₃ acts rapidly on neutrophil physiology, within a few minutes with respect to superoxide production, and a few hours (4 h) with respect to gene expression without altering a biological process such as the rate of apoptosis evaluated after a long period of incubation (20 h). We further conclude that Na₂SO₃-induced production of O₂ ⁷ does not drive neutrophils to undergo apoptosis, a mechanism known to occur in other conditions. Therefore, the potential toxicity of Na₂SO₃ during pulmonary inflammation or lung-associated diseases may be related to its ability to induce superoxide production without altering neutrophil apoptosis rate.

Key Words: sodium sulfite • neutrophils • superoxide • gene expression • apoptosis

Human & Experimental Toxicology, Vol. 17, No. 11, 600-605 (1998)
DOI: 10.1177/096032719801701103


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