Abstract
Paraoxonase (PON1) protects low and high-density lipoproteins (LDL and HDL) against oxidation induced by reactive oxygen species formation facilitated by iron (Fe) and copper (Cu) ions. Plasma PON1, arylesterase, oxidized LDL (Ox-LDL), Cu, Fe, thiobarbituric acid-reactive substances (TBARS), lipid, lipoprotein, and apolipoprotein profile in bronchial asthma were determined and the relations among these parameters in different steps of asthma were interpreted. A total of 58 individuals, 30 asthmatics and 28 controls, were included into the scope of this study. Plasma PON1, arylesterase, and TBARS levels were measured spectrophotometrically. Determination of plasma oxidized LDL, Cu, and Fe levels were performed by enzyme-linked immunosorbent assay, atomic absorption spectrophotometry, and the automated TPTZ method, respectively. Apo-A-1 and Apo-B levels were determined immunoturbidometrically. Plasma total cholesterol, triglyceride, and HDL cholesterol levels were enzymatically determined. Plasma LDL levels were estimated using the Fridewald formula. The average plasma PON1 and arylesterase activities in the group of patients were lower than those of the individuals in the control group, but there was no statistically significant difference found between them (p>0.05). No significant difference was found in plasma Apo-A-1, Apo-B, total cholesterol, triglyceride, HDL, and LDL concentrations between the control and patient groups (p>0.05). Plasma oxidized LDL (p<0.05), Cu (p<0.01), Fe (p<0.01), and TBARS (p<0.001) levels in patients with asthma were found to be significantly higher than for the control group. Increases in Cu, Fe, lipid peroxidation, and oxidized LDL levels supported by relative decreases in PON1 activities observed in asthmatic patients might be introduced as the striking findings as well as the possible potential indicators of this airway disease, the prevalence of which has increased dramatically over recent decades.
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References
S. de Magalhaes Simoes, M. A. dos Santos, M. da Silva Oliveira, E. S. Fontes, and S. Fernezlian, Inflammatory cell mapping of the respiratory tract in fatal asthma, Clin. Exp. Allergy 35, 602–611 (2005).
P. Jeffery, Anti-inflammatory effects of inhaled corticosteroids in chronic obstructive pulmonary disease: similarities and differences to asthma, Expert Opin. Invest. Drugs 14, 619–632 (2005).
C. Maziere, P. Morliere, Z. Massy, et al., Oxidized low-density lipoprotein elicits and intracellular calcium rise an increases the binding activity of the transcription factor NFAT, Free Radical Biol. Med. 38, 472–480 (2005).
H. J. Dhong, H. Y. Kim, and D. Y. Cho, Histopathologic characterstics of chronic sinusitis with bronchial asthma, Acta Otolaryngol. 125, 169–176 (2005).
J. B. Sedgwick, Y. S. Hwang, H. A. Gerbyshak, H. Kita, and W. W. Busse, Oxidized low density lipoprotein activates migration and degranulation of human granulocytes, Am. J. Respir. Cell. Mol. Biol. 29, 702–709 (2003).
G. M. Chisolm and D. Steinberg, The oxidative modification hypothesis of atherogenesis: an overview, Free Radical Biol. Med. 28, 1818–1826 (2000).
F. W. Kemp, J. DeCandia, W. Li, K. Bruening, H. Baker, and D. Rigassio, Relationships between immunity and dietary and serum antioxidants, trace metals, B vitamins, and homocysteine in elderly men and women. Nutr. Res. 22, 45–53 (2002).
M. Navab, J. A. Berliner, G. Subbanagounder, et al., HDL and inflammatory response induced by LDL-derived oxidized phospholipids, Arterioscler. Thromb. Vasc. Biol. 21, 481–488 (2001).
O. Raveh, I. Pinchuk, F. Menahem, and D. Lichtenberg, Kinetic of lipid peroxidation in mixtures of HDL and LDL, mutual effects, Free Radical Biol. Med. 3, 1486–1497 (2001).
M. Aviram, S. Billecke, and R. Sorenson, Paraoxonase active site required for protection against LDL oxidation involves its free sulfhydryl group and is different than that required for its arylesterase/paraoxonase activities: selective action of human paraoxonase alloenzymes Q and R, Arterioscler. Thromb. Vasc. Biol. 18, 1617–1624 (1998).
B. T. Heijmans, R. G. J. Westendorp, A. M. Lagaay, D. L. Knook, C. Kluft, and P. E. Slagboom, Common paraoxonase gene variants, mortality risk and fatal cardiovascular events in elderly subjects, Atherosclerosis 149, 91–97 (2000).
M. Aviram, M. Rosenblat, and C. L. Bisgair, Paraoxonase inhibits high density lipoprotein (HDL) oxidation and preserves its functions: a possible peroxidative role for paraoxonase, J. Clin. Invest. 101, 1581–1590 (1998).
C. Lenfant, Global Strategy for Asthma Management and Prevention, National Institutes of Health, Bethesda, MD (2002).
N. Rifai, P. S. Bachorik, and J. J. Albers, Lipids, lipoproteins, and apolipoproteins, in Tietz Textbook of Clinical Chemistry, 3rd ed., C. A. Burtis and E. R. Ashwood, eds., WB Saunders, Philadelphia, pp. 820–826 (1999).
J. A. Buege and S. D. Aust, Microsomal lipid peroxidation methods, Enzymology 12, 302–310 (1978).
M. Harangi, E. Remenyik, I. Seres, Z. Varga, E. Katona, and G. Paragh, Determination of DNA damage induced by oxidative stress in hyperlipidemic patients, Mutat. Res. 513, 17–25 (2002).
O. Hasselwander, D. A. Savage, D. McMaster, C. M. Loughrey, and P. T. McNamee, Paraoxonase polymorphisms are not associated iwth cardiovascular risk in renal transplant recipients, Kidney Int. 56, 289–298 (1999).
N. W. Alcock, Copper, in Methods in Clinical Chemistry, A. J. Pasce and L. A. Kaplan, eds., Mosby, St Louis, MO, pp. 527–538 (1987).
Shimadzu Corp., Atomic Absorption Spectrophotometry Cookbook, Shimadzu Corp., Kyoto, Sect. 1–4, p. 10 (1998).
D. B. Milne, Trace elements, in Tietz Textbook of Clinical Chemistry, 3rd ed., C. A. Burtis and E. R. Ashwood, eds., WB Saunders, Philadelphia, pp. 1029–1055 (1999).
M. Paoli-de Valeri, Y. Zerpa-de Miliani, E. G. Valeri-Davila, and G. Bellabarba, Adrenal function and lipid metabolism in asthmatic children treated with budesonide, Salud Public. Mex. 41, 119–123 (1999).
E. Turley, A. McKeown, M. P. Bonham, etal., Copper supplementation in humans does not affect the susceptibility of low density lipoprotein to in vitro induced oxidation (Foodcue Project), Free Radical Biol. Med. 29, 1129–1134 (2000).
J. Gallego-Nicasio, G. Lopez-Rodriquez, R. Martinez, M. J. Tarancon, M. V. Fraile, and P. Carmona, Structural changes of low density lipoproteins with Cu2+ and glucose induced oxidation, Biopolymers 72, 514–520 (2003).
X. Cheng, Y. Cui, Y. Chen, and X. Zhang, Effects of alpha-tocopherol and beta-carotene on the oxidized low density lipoprotein induced by Cu2+, Wei Sheng Yan Jiu 29, 229–231 (2000).
E. Sarandöl, Ö. Şafak, M. Dirican, and G. Uncu, Oxidizability of apolipoprotein B-containing lipoproteins and serum paraoxonase/arylesterase activities in preeclampsia, Clin. Biochem. 37, 990–996 (2004).
M. Aviram, M. Rosenblat, B. Scott, et al., Human serum paraoxonase (PON 1) is inactivated by oxidized low density lipoprotein and preserved by antioxidants, Free Radical Biol. Med. 26, 892–904 (1999).
A. Ayub, M. I. Mackness, S. Arrol, B. Mackness, J. Patel, and P. N. Durrington, Serum paraoxonase after myocardial infarction, Arterioscler. Thromb. Vasc. Biol. 19, 330–335 (1999).
D. B. Rousselot, P. Therond, J. L. Beaudux, J. Peynet, A. Legrand, and J. Delattre, High density lipoprotein (HDL) and the oxidative hypothesis of atherosclerosis, Clin. Chem. Lab. Med. 37, 939–948 (1999).
P. M. Laplaud, T. Dantoine, and M. J. Chapman, Paraoxonase as a risk marker for cardiovascular disease: facts and hypotheses, Clin. Chem. Lab. Med. 36, 431–444 (1998).
M. I. Mackness, S. Arool, and P. N. Durrington, Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein, FEBS 286, 152–154 (1991).
M. I. Mackness, S. Arrol, C. Abbott, and P. N. Durrington. Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase, Atherosclerosis 104, 129–135 (1993).
M. I. Mackness, D. Harty, D. Bhartnagar, et al., Serum paraoxonase activity in familial hypercholesterolaemia and insulin-dependent diabetes mellitus, Atherosclerosis 86, 193–199 (1999).
D. Steinberg, Low density lipoprotein oxidation and its pathobiological significance, J. Biol. Chem. 272, 20,963–20,966 (1997).
G. Gornicka, J. Beltowski, G. Wojcicka, and A. Jamroz, Serum paraoxonase activity, total antioxidant potential and lipid peroxidation products in children with bronchial asthma exacerbation, Wiad. Lek. 55, 257–263 (2002).
B. Mackness, R. Hunt, P. N. Durrington, and M. I. Mackness, Increased immunolocalization of paraoxonase, clusterin, and apolipoprotein A-1 in the human artery wall with the progression of atherosclerosis, Arterioscler. Thromb. Vasc. Biol. 17, 1233–1238 (1997).
S. Wiersbitzky, E. H. Ballke, R. Burghart, et al., Long-term study of various immunologic functions in children with chronic nonspecific lung disease, Z. Erk. Atmungsorg. 164, 241–253 (1985).
F. Mateos, J. H. Brock, and J. L. Perez-Arellano, Iron metabolism in the lower respiratory tract, Thorax 53, 594–600 (1998).
H. Vural, K. Uzun, E. Uz, A. Kocyigit, A. Cigli, and O. Akyol, Concentrations of copper, zinc and various elements in serum of patients with bronchial asthma. J. Trace Elements Med. Biol. 14, 88–91 (2000).
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Ekmekci, O.B., Donma, O., Ekmekci, H. et al. Plasma paroaoxonase activities, lipoprotein oxidation, and trace element interaction in asthmatic patients. Biol Trace Elem Res 111, 41–52 (2006). https://doi.org/10.1385/BTER:111:1:41
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DOI: https://doi.org/10.1385/BTER:111:1:41