Role of free radicals in the toxicity of airborne fine particulate matter

B. Dellinger; W. A. Pryor; R. Cueto; G. L. Squadrito; V. Hegde; W. A. Deutsch

doi:10.1021/tx010050x

Role of free radicals in the toxicity of airborne fine particulate matter

B. Dellinger, W. A. Pryor, R. Cueto, G. L. Squadrito, V. Hegde, W. A. Deutsch

Nutritional Sciences

Research output: Contribution to journal › Article › peer-review

450 Scopus citations

Abstract

Exposure to airborne fine particles (PM_2.5) is implicated in excess of 50 000 yearly deaths in the USA as well as a number of chronic respiratory illnesses. Despite intense interest in the toxicity of PM_2.5, the mechanisms by which it causes illnesses are poorly understood. Since the principal source of airborne fine particles is combustion and combustion sources generate free radicals, we suspected that PM_2.5 may contain radicals. Using electron paramagnetic resonance (EPR), we examined samples of PM_2.5 and found large quantities of radicals with characteristics similar to semiquinone radicals. Semiquinone radicals are known to undergo redox cycling and ultimately produce biologically damaging hydroxyl radicals. Aqueous extracts of PM_2.5 samples induced damage to DNA in human cells and supercoiled phage DNA. PM_2.5-mediated DNA damage was abolished by superoxide dismutase, catalase, and deferoxamine, implicating superoxide radical, hydrogen peroxide, and the hydroxyl radical in the reactions inducing DNA damage.

Original language	English
Pages (from-to)	1371-1377
Number of pages	7
Journal	Chemical Research in Toxicology
Volume	14
Issue number	10
DOIs	https://doi.org/10.1021/tx010050x
State	Published - 2001

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title = "Role of free radicals in the toxicity of airborne fine particulate matter",

abstract = "Exposure to airborne fine particles (PM2.5) is implicated in excess of 50 000 yearly deaths in the USA as well as a number of chronic respiratory illnesses. Despite intense interest in the toxicity of PM2.5, the mechanisms by which it causes illnesses are poorly understood. Since the principal source of airborne fine particles is combustion and combustion sources generate free radicals, we suspected that PM2.5 may contain radicals. Using electron paramagnetic resonance (EPR), we examined samples of PM2.5 and found large quantities of radicals with characteristics similar to semiquinone radicals. Semiquinone radicals are known to undergo redox cycling and ultimately produce biologically damaging hydroxyl radicals. Aqueous extracts of PM2.5 samples induced damage to DNA in human cells and supercoiled phage DNA. PM2.5-mediated DNA damage was abolished by superoxide dismutase, catalase, and deferoxamine, implicating superoxide radical, hydrogen peroxide, and the hydroxyl radical in the reactions inducing DNA damage.",

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AU - Dellinger, B.

AU - Pryor, W. A.

AU - Cueto, R.

AU - Squadrito, G. L.

AU - Hegde, V.

AU - Deutsch, W. A.

PY - 2001

Y1 - 2001

N2 - Exposure to airborne fine particles (PM2.5) is implicated in excess of 50 000 yearly deaths in the USA as well as a number of chronic respiratory illnesses. Despite intense interest in the toxicity of PM2.5, the mechanisms by which it causes illnesses are poorly understood. Since the principal source of airborne fine particles is combustion and combustion sources generate free radicals, we suspected that PM2.5 may contain radicals. Using electron paramagnetic resonance (EPR), we examined samples of PM2.5 and found large quantities of radicals with characteristics similar to semiquinone radicals. Semiquinone radicals are known to undergo redox cycling and ultimately produce biologically damaging hydroxyl radicals. Aqueous extracts of PM2.5 samples induced damage to DNA in human cells and supercoiled phage DNA. PM2.5-mediated DNA damage was abolished by superoxide dismutase, catalase, and deferoxamine, implicating superoxide radical, hydrogen peroxide, and the hydroxyl radical in the reactions inducing DNA damage.

AB - Exposure to airborne fine particles (PM2.5) is implicated in excess of 50 000 yearly deaths in the USA as well as a number of chronic respiratory illnesses. Despite intense interest in the toxicity of PM2.5, the mechanisms by which it causes illnesses are poorly understood. Since the principal source of airborne fine particles is combustion and combustion sources generate free radicals, we suspected that PM2.5 may contain radicals. Using electron paramagnetic resonance (EPR), we examined samples of PM2.5 and found large quantities of radicals with characteristics similar to semiquinone radicals. Semiquinone radicals are known to undergo redox cycling and ultimately produce biologically damaging hydroxyl radicals. Aqueous extracts of PM2.5 samples induced damage to DNA in human cells and supercoiled phage DNA. PM2.5-mediated DNA damage was abolished by superoxide dismutase, catalase, and deferoxamine, implicating superoxide radical, hydrogen peroxide, and the hydroxyl radical in the reactions inducing DNA damage.

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Role of free radicals in the toxicity of airborne fine particulate matter

Abstract

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