Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages

Our plain-English summary of Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages, by P. Nyberg (Environmental Research, 1991).

The study

• Author: P. Nyberg
• Journal: Environmental Research
• Published: 1991;55(2):157-64
• Cited by: 10 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Polyvinylpyridine-N-oxide (PVPNO) and carboxymethyl cellulose (CMC) are known to inhibit the cytotoxic effects of quartz particles and chrysotile asbestos fibers, respectively. The effect of PVPNO and CMC on mineral dust-induced production of reactive oxygen species (ROS) by human monocyte-derived macrophages was studied using lucigenin-dependent chemiluminescence. Ten micrograms of PVPNO inhibited the ROS production induced by 100 micrograms of quartz completely, but caused only 25% inhibition of the response to 100 micrograms of chrysotile. Ten micrograms of CMC inhibited the chrysotile-induced ROS production to 70%, but had a weak effect on the responses to quartz. Neither PVPNO nor CMC caused any inhibition of the ROS responses to serum-opsonized zymosan. PVPNO was bound to both quartz and chrysotile, but no binding of CMC to either dust could be detected. Neither PVPNO nor CMC had any superoxide scavenging effect. In conclusion, PVPNO and CMC seem to selectively modify mineral dust surface properties, which are of importance in the induction of ROS production by phagocytes. These observations may be useful in describing the pathogenesis of mineral dust-induced diseases, and may also have therapeutic implications.

In plain English

This laboratory study, from Finland, used human macrophage-like cells grown from the blood of healthy donors. The author tested whether two chemicals, polyvinylpyridine-N-oxide (PVPNO) and carboxymethyl cellulose (CMC), reduced the cells' production of reactive oxygen species (measured as light output) after exposure to 100 micrograms of quartz or of UICC chrysotile A asbestos. Ten micrograms of PVPNO stopped the quartz response completely but cut the chrysotile response by less than 25% at any amount tested. Chrysotile alone caused almost no response. When a polyclonal immunoglobulin (antibody) preparation was added, the response rose markedly, and 10 micrograms of CMC then reduced it by 70%. CMC had only a weak effect on the quartz response. PVPNO had no effect and CMC almost no effect on the response to serum-opsonized zymosan, and neither chemical neutralized superoxide directly. PVPNO attached to both dusts. No CMC attachment was detected, though the author noted the test may not have been sensitive enough. The author concluded that these polymers can selectively block dust-induced oxygen species production, which may have therapeutic implications.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: laboratory (in vitro) experiment on cultured human cells
• Who was studied: Human monocytes from healthy blood donors (number of donors not stated), cultured 3 days into macrophage-like cells; Institute of Occupational Health, Helsinki, Finland; article received January 1991
• Exposure: 100 micrograms of quartz particles or UICC chrysotile A asbestos, with serum-opsonized zymosan for comparison. Responses were modified with PVPNO or CMC (0.01 to 10 micrograms) and with polyclonal immunoglobulin.
• Main results:
  • 10 micrograms of PVPNO completely inhibited the quartz-induced response (representative curves from an experiment repeated 13 times)
  • PVPNO inhibited the chrysotile-induced response by less than 25% at any concentration tested
  • PVPNO had no effect on the response to serum-opsonized zymosan
  • PVPNO added to the cells 1 hour before quartz exposure had no inhibitory effect
  • Chrysotile alone caused almost no response. Adding polyclonal immunoglobulin enhanced it markedly, and 10 micrograms of CMC reduced that response by 70%.
  • CMC had almost no inhibitory effect on the response to zymosan
  • CMC had only a weak inhibitory effect on the quartz-induced response
  • CMC also inhibited the response to chrysotile that had been pre-coated with immunoglobulin
  • PVPNO bound to both quartz and chrysotile; no detectable CMC bound to either dust
  • Neither PVPNO nor CMC had a superoxide-scavenging effect in a cell-free test
• The authors' conclusion: The author concluded that mineral dust-induced reactive oxygen species production by these cells can be selectively blocked by surface-active polymers. The author added that this may help describe disease-relevant dust properties and may have therapeutic implications.
• Limitations the authors state:
  • The CMC binding assay may not have been sensitive enough to detect CMC binding to chrysotile
  • CMC's effect on chrysotile might have worked by blocking immunoglobulin binding to the fibers rather than by interfering with the fiber-cell interaction

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Medical terms in this study, explained in our Lexicon: Reactive Oxygen Species (ROS), Macrophage, Chrysotile, Superoxide.

Related studies

• Increased mineral dust-induced production of reactive oxygen species by blood monocytes from patients with malignant diseases — P.W. Nyberg, S.A. Nordman, et al. (1994)
• Measurement of reactive oxygen metabolites produced by human monocyte-derived macrophages exposed to mineral dusts — P. Nyberg, M. Klockars (1990)
• A synergistic interaction between Bacillus Calmette-Guérin (BCG) and NADPH oxidase stimulants on the production of reactive oxygen metabolites by human mononuclear phagocytes — P.W. Nyberg, S.A. Nordman, et al. (1994)
• Interleukin 1 production and accessory cell function of rat alveolar macrophages exposed to mineral dust particles — Y. Oghiso, Y. Kubota (1987)
• Production of reactive oxygen species by man-made vitreous fibres in human polymorphonuclear leukocytes — M. Ruotsalainen, M.R. Hirvonen, et al. (1999)
• Production of reactive oxygen intermediates by human macrophages exposed to soot particles and asbestos fibers and increase in NF-kappa B p50/p105 mRNA — R. Oettinger, K. Drumm, et al. (1999)

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