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Journal of Cellular and Molecular Medicine logoLink to Journal of Cellular and Molecular Medicine
. 2007 May 1;5(3):285–294. doi: 10.1111/j.1582-4934.2001.tb00162.x

The total peroxyl radical trapping potential in serum ‐ an assay to define the stage of atherosclerosis

L Niculescu 1, Camelia Stancu 1, Anca Sima 1, Daniela Toporan 2, Maya Simionescu 1,
PMCID: PMC6741316  PMID: 12067487

Abstract

Lipid peroxides were identified among the factors that contribute to the atherosclerotic plaque formation in the arterial wall. We hypothesised that a correlation may exist between the content of antioxidant constituents in the serum and the gravity of atherosclerosis. To this purpose, we have determined the serum total peroxyl radical‐ trapping potential (TRAP), which is the combined capacity of all antioxidants to neutralize free radicals in serum and followed its variation in hyperlipemic animals in correlation with the stage of atherosclerosis. In addition, we compared TRAP values in the sera of coronary heart disease (CHD) patients, with or without type II diabetes mellitus. Results showed that after 18 weeks of hyperlipemic diet, the mean TRAP values measured in sera isolated from hyperlipemic hamsters exhibited an about 44% decrease, in good agreement with the increase of serum cholesterol and triglycerides. In the 3 groups of CHD patients, TRAP values decreased with about 10% in sera of stable angina patients, 20% in unstable patients, as compared with normal subjects. The lowest TRAP values were detected in the sera of patients with acute myocardial infarction. The results obtained for different experimental animals and for CHD patients sera indicate that the TRAP method, as adapted in our laboratory, is a reliable and reproducible assay, fit to be used in clinical studies as an ex vivo measurable parameter that correlates with the stage of the atherosclerosis.

Keywords: atherosclerosis, hyperlipemia, oxidative stress, antioxidant potential, hyperlipemic hamster, coronary heart disease, lipid peroxides

References

  • 1. Obrien K.D., Chait A., The biology of artery wall in atherogenesis, Med. Clin. North Am., 78: 41–67, 1994. [DOI] [PubMed] [Google Scholar]
  • 2. Chait A., Progression of atherosclerosis: The cell biology, Eur. Heart J., 8 (Suppl. E): 15–22, 1987. [DOI] [PubMed] [Google Scholar]
  • 3. Tsai E.C., Hirsch I.B., Brunzell J.D., Chait A., Reduced plasma peroxyl radical trapping capacity and increased susceptibility of LDL to oxidation in poorly controlled IDDM, Diabetes, 43: 1010–1014, 1994. [DOI] [PubMed] [Google Scholar]
  • 4. Heller F.R., Descamps O., Hondekjin J‐C., LDL oxidation: therapeutic perspectives, Atherosclerosis, 137 (Suppl), S25–S31, 1998. [DOI] [PubMed] [Google Scholar]
  • 5. Salonen J.T., Nyjssonen K., Tuomainen T.P., Maenpaa P.H., Korpela H., Kaplan G.A., Lynch J., Helmrich S.P., Salonen R., Increased risk of noninsulin dependent diabetes mellitus at low plasma vitamin E concentrations; a four years fellow up study in men, Brit. Med. J., 311: 1124–1127, 1995. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6. Frei B., Molecular and biological mechanisms of antioxidant action, FASEB J., 13(9): 963–964, 1999. [DOI] [PubMed] [Google Scholar]
  • 7. Frei B., Keany J.F., Chen K., Vitamins C and E and LDL oxidation, Vitamins and Hormones, 52: 1–28, 1996. [DOI] [PubMed] [Google Scholar]
  • 8. Pryor W.A., Vitamin E and heart disease: Basic science to clinical intervention trials, Free Radic. Biol. Med., 28(1): 141–164, 2000. [DOI] [PubMed] [Google Scholar]
  • 9. Schwenke D.C., Antioxidants and atherogenesis, J. Nutr. Biochem., 9: 424–445, 1998. [Google Scholar]
  • 10. Fruebis J., Bird D.A., Pattison J., Palinski W., Extent of antioxidant protection of plasma LDL is not a predictor of the antiatherogenic effect of antioxidants, J. Lipid Res., 38: 2455–2464; 1997. [PubMed] [Google Scholar]
  • 11. Valkonen M., Kuusi T., Spectrophotometric assay for total peroxyl radical‐trapping antioxidant potential in human serum, J. Lipid. Res., 28: 823–833, 1997. [PubMed] [Google Scholar]
  • 12. Nistor A., Bulla A., Filip D.A., Radu A., The hyperlipidemic hamster as a model of experimental atherosclerosis, Atherosclerosis, 68: 159–173, 1987. [DOI] [PubMed] [Google Scholar]
  • 13. Sima A., Popov D., Starodub O., Stancu C., Cristea C., Stern D., Simionescu M., Pathobiology of the heart in experimental diabetes: immunolocalization of LDL, IgG and AGE‐proteins in diabetic and/or hyperlipidemic hamster, Lab. Invest., 76: 960–972, 1997. [PubMed] [Google Scholar]
  • 14. Sullivan M.P., Cerda J.J., Robbins F.L., Burgin C.W., Beatty R.J., The gerbil, hamster, and guinea pig as rodent models of hyperlipidemia, Lab. Animal Sci., 43: 575–578, 1993. [PubMed] [Google Scholar]
  • 15. Bishop R.W., Structure of the hamster low density lipoprotein receptor gene, J. Lipid Res., 33: 549–557, 1992. [PubMed] [Google Scholar]
  • 16. Sima A., Stancu C., Constantinescu E., Simionescu M., In vivo uptake and transcytosis of LDL. XIth International Vascular Biology Meeting, Geneve, 5th ‐ 9th september, 2000, J. Submicrosc. Cytol. Pathol., 32: 359, 2000. [Google Scholar]
  • 17. Fogelman A.M., Schechter I., Seager, J. , Hokom, M. , Child J. S., Edwards P.A., Malondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocytemacrophages, Proc. Natl. Acad. Sci. USA, 77: 2214–2218, 1986. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18. Sima A., Bulla A., Simionescu N., Experimental obstructive coronary atherosclerosis in the hyperlipidemic hamster, J. Submicrosc. Cytol. Pathol., 22: 1–16, 1990. [PubMed] [Google Scholar]
  • 19. Filip D., Nistor A., Bulla A., Radu A., Lupu F., Simionescu M., Cellular events in the development of valvular atherosclerotic lesions induced by experimental hypercholesterolemia, Atherosclerosis, 67: 199–214, 1987. [DOI] [PubMed] [Google Scholar]
  • 20. Simionescu N., Vasile E., Lupu F., Popescu G., Simionescu M., Prelesional events in atherogenesis: accumulation of extracellular cholesterol rich liposomes in the arterial intima and cardiac valves of hyperlipidemic rabbits, Am. J. Pathol., 123: 85–101, 1986. [PMC free article] [PubMed] [Google Scholar]
  • 21. Simionescu N., Sima A., Dobrian A., Tirziu D., Simionescu M., Pathobiochemical changes of the arterial wall at the inception of atherosclerosis In: Vollmer/Roessner, (eds.), Current Topics in Pathology, Springer ‐ Verlag, Berlin , 1993, pp. 1–45. [DOI] [PubMed] [Google Scholar]
  • 22. Simionescu N., Endothelial cell dysfunction and injury in experimental hyperlipidemic atherogenesis In: Simionescu N. and Simionescu M., (eds.), Endothelial Cell Dysfunction, Plenum Press, New York , 1992, pp. 321–346. [Google Scholar]
  • 23. Pitman W.A., Osgood D.P., Smith D., Schaefer E.J., Ordovas J.M., The effects of diet and lovastatin on regression of fatty streak lesions and on hepatic and intestinal mRNA levels for the LDL receptor and HMG CoA reductase in F1B hamsters, Atherosclerosis, 138: 43–52, 1998. [DOI] [PubMed] [Google Scholar]
  • 24. Sima A., Hobai I., Stancu C., Cinteza M., Gherasim L., Correlated biochemical modifications of plasma lipoproteins in coronary heart disease: an accelerating pathologic factor, Rom. J. Internal. Med., 34: 55–64, 1996. [PubMed] [Google Scholar]
  • 25. Naito C., Nakamura M., Yamamoto Y., Lipid peroxides as the initiating factor of atheroslerosis, Ann. NY Acad. Sci., 676: 27–45, 1993. [DOI] [PubMed] [Google Scholar]
  • 26. Jain S.K., Palmer M., The effect of oxygen radicals metabolites and vitamin E on glycosylation of proteins, Free Radic. Biol. Med., 22: 593–596; 1997. [DOI] [PubMed] [Google Scholar]

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