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. 1990 Jul;87:337–341. doi: 10.1289/ehp.9087337

Evidence of an oxidative mechanism for the hemolytic activity of silica particles.

B L Razzaboni 1, P Bolsaitis 1
PMCID: PMC1567824  PMID: 2176590

Abstract

The formation of reactive oxygen species resulting from the interaction of silica dust particles with red blood cell membranes was investigated; particularly, the effect of surface hydroxyl (silanol) group concentration on the rate of formation of such reactive oxygen species was investigated. The rate of formation was measured indirectly through the effect of catalase, a hemoprotein peroxidase, on silica-induced hemolysis. It was found that the addition of exogenous catalase to erythrocytes markedly reduces the hemolysis caused by silica particles. Furthermore, the amount of catalase required for deactivation of silica per unit area of particle surface is lower for fumed silica particles and calcined crystalline particles than for uncalcined, crystalline silica, suggesting a correlation between the concentration of OH groups at the silica particle surface and its potential for generation of H2O2. The addition of albumin, a copper chelator, also decreases hemolysis. These results suggest that the hemolysis caused by silica particles is at least partly related to the formation of H2O2 at the particle surface and its subsequent reaction with Cu+ ions. The relationship between the concentration of surface silanol groups on the silica surface and the amount of catalase required to decrease hemolysis may also provide a method for testing potential fibrogenicity of respirable dusts.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Gabor S., Anca Z., Zugravu E. In vitro action of quartz on alveolar macrophage lipid peroxides. Arch Environ Health. 1975 Oct;30(10):499–501. doi: 10.1080/00039896.1975.10666761. [DOI] [PubMed] [Google Scholar]
  2. Gulumian M., van Wyk A. Free radical scavenging properties of polyvinylpyridine N-oxide: a possible mechanism for its action in pneumoconiosis. Med Lav. 1987 Mar-Apr;78(2):124–128. [PubMed] [Google Scholar]
  3. Gutteridge J. M., Wilkins S. Copper salt-dependent hydroxyl radical formation. Damage to proteins acting as antioxidants. Biochim Biophys Acta. 1983 Aug 23;759(1-2):38–41. doi: 10.1016/0304-4165(83)90186-1. [DOI] [PubMed] [Google Scholar]
  4. Halliwell B. Albumin--an important extracellular antioxidant? Biochem Pharmacol. 1988 Feb 15;37(4):569–571. doi: 10.1016/0006-2952(88)90126-8. [DOI] [PubMed] [Google Scholar]
  5. Hodgson E. K., Fridovich I. The interaction of bovine erythrocyte superoxide dismutase with hydrogen peroxide: inactivation of the enzyme. Biochemistry. 1975 Dec 2;14(24):5294–5299. doi: 10.1021/bi00695a010. [DOI] [PubMed] [Google Scholar]
  6. Kappus H. Oxidative stress in chemical toxicity. Arch Toxicol. 1987;60(1-3):144–149. doi: 10.1007/BF00296968. [DOI] [PubMed] [Google Scholar]
  7. Nolan R. P., Langer A. M., Harington J. S., Oster G., Selikoff I. J. Quartz hemolysis as related to its surface functionalities. Environ Res. 1981 Dec;26(2):503–520. doi: 10.1016/0013-9351(81)90226-7. [DOI] [PubMed] [Google Scholar]
  8. Pandurangi R. S., Seehra M. S., Razzaboni B. L., Bolsaitis P. Surface and bulk infrared modes of crystalline and amorphous silica particles: a study of the relation of surface structure to cytotoxicity of respirable silica. Environ Health Perspect. 1990 Jun;86:327–336. doi: 10.1289/ehp.9086327. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Shi X. L., Dalal N. S., Vallyathan V. ESR evidence for the hydroxyl radical formation in aqueous suspension of quartz particles and its possible significance to lipid peroxidation in silicosis. J Toxicol Environ Health. 1988;25(2):237–245. doi: 10.1080/15287398809531205. [DOI] [PubMed] [Google Scholar]
  10. Stansell M. J., Deutsch H. F. Preparation of crystalline erythrocuprein and catalase from human erythrocytes. J Biol Chem. 1965 Nov;240(11):4299–4305. [PubMed] [Google Scholar]
  11. Stöber W., Brieger H. On the theory of silicosis. IV. The topochemical interaction. Arch Environ Health. 1968 May;16(5):706–708. doi: 10.1080/00039896.1968.10665131. [DOI] [PubMed] [Google Scholar]
  12. Vallyathan V., Shi X. L., Dalal N. S., Irr W., Castranova V. Generation of free radicals from freshly fractured silica dust. Potential role in acute silica-induced lung injury. Am Rev Respir Dis. 1988 Nov;138(5):1213–1219. doi: 10.1164/ajrccm/138.5.1213. [DOI] [PubMed] [Google Scholar]
  13. WILLS E. D. THE EFFECT OF INORGANIC IRON ON THE THIOBARBITURIC ACID METHOD FOR THE DETERMINATION OF LIPID PEROXIDES. Biochim Biophys Acta. 1964 Aug 5;84:475–477. doi: 10.1016/0926-6542(64)90016-2. [DOI] [PubMed] [Google Scholar]
  14. Williams R. J. Introduction to silicon chemistry and biochemistry. Ciba Found Symp. 1986;121:24–39. doi: 10.1002/9780470513323.ch3. [DOI] [PubMed] [Google Scholar]

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