Araştırma Makalesi
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Investigation of dysfunctional HDL using myeloperoxidase / paraoxonase ratio in lymphoma

Yıl 2019, Cilt: 16 Sayı: 2, 358 - 364, 29.08.2019
https://doi.org/10.35440/hutfd.579011

Öz

Background: The aim of this
study is to investigate the myeloperoxidase/paraoxonase ratio which indicates
dysfunction of high-density lipoprotein in various types of lymphoma
characterized by abnormal lipid metabolism, oxidative stress, and inflammation.

Methods: Thirty lymphoma
patients and 30 healthy subjects were enrolled in this study. Serum
myeloperoxidase, paraoxonase, arylesterase, lipid hydroperoxide and routine
biochemistry tests levels were measured on an automated analyzer. The diagnosis
of lymphoma patients was made according to the histological examination of the
biopsy material.

Results: Compared with
healthy control group; the albumin, arylesterase, high-density lipoprotein,
thiol, and Hemoglobin levels were significantly lower while myeloperoxidase /
paraoxonase, myeloperoxidase/arylesterase, and lipid hydroperoxide levels were
significantly higher, in patients with lymphoma. Also, lipid hydroperoxide
level was significantly correlated with myeloperoxidase / paraoxonase and
myeloperoxidase / arylesterase (r= 0.330, p=0.046; r=
0.588, p< 0.001, respectively).







Conclusions: We think that
dysfunctional high-density lipoprotein is an important factor in the
inflammatory process, atherosclerosis, oxidative stress, and impaired lipid
metabolism that can be observed in patients with lymphoma. We believe that in
the future the myeloperoxidase/paraoxonase ratio can be used as a treatment
criterion to prevent diseases that cause dysfunctional high-density
lipoprotein.

Kaynakça

  • 1. Ansell, S.M. Hodgkin lymphoma: diagnosis and treatment. in Mayo Clinic Proceedings. 2015. Elsevier.
  • 2. Ansell, S.M. Non-Hodgkin lymphoma: diagnosis and treatment. in Mayo Clinic Proceedings. 2015. Elsevier.
  • 3. Imbesi, S., C. Musolino, A. Allegra, A. Saija, F. Morabito, G. Calapai, et al., Oxidative stress in oncohematologic diseases: an update. Expert review of hematology, 2013. 6(3): p. 317-325.
  • 4. Memişoğulları, R., Paraoksonaz ve kanser. Konuralp Tıp Dergisi, 2010. 2010(2): p. 22-26.
  • 5. Morabito, F., M. Cristani, A. Saija, C. Stelitano, V. Callea, A. Tomaino, et al., Lipid peroxidation and protein oxidation in patients affected by Hodgkin's lymphoma. Mediators of inflammation, 2004. 13(5-6): p. 381-383.
  • 6. Lim, U., T. Gayles, H.A. Katki, R. Stolzenberg-Solomon, S.J. Weinstein, P. Pietinen, et al., Serum high-density lipoprotein cholesterol and risk of non-hodgkin lymphoma. Cancer Research, 2007. 67(11): p. 5569-5574.
  • 7. Yang, S., M.G. Damiano, H. Zhang, S. Tripathy, A.J. Luthi, J.S. Rink, et al., Biomimetic, synthetic HDL nanostructures for lymphoma. Proceedings of the National Academy of Sciences, 2013. 110(7): p. 2511-2516.
  • 8. Rho, Y.H., C.P. Chung, A. Oeser, J.F. Solus, T. Gebretsadik, A. Shintani, et al., Interaction between oxidative stress and high‐density lipoprotein cholesterol is associated with severity of coronary artery calcification in rheumatoid arthritis. Arthritis care & research, 2010. 62(10): p. 1473-1480.
  • 9. Ferretti, G., T. Bacchetti, A. Nègre-Salvayre, R. Salvayre, N. Dousset, and G. Curatola, Structural modifications of HDL and functional consequences. Atherosclerosis, 2006. 184(1): p. 1-7.
  • 10. McMahon, K.M., L. Foit, N.L. Angeloni, F.J. Giles, L.I. Gordon, and C.S. Thaxton, Synthetic high-density lipoprotein-like nanoparticles as cancer therapy, in Nanotechnology-Based Precision Tools for the Detection and Treatment of Cancer. 2015, Springer. p. 129-150.
  • 11. Deakin, S.P. and R.W. James, Genetic and environmental factors modulating serum concentrations and activities of the antioxidant enzyme paraoxonase-1. Clinical Science, 2004. 107(5): p. 435-447.
  • 12. Kulka, M., A review of paraoxonase 1 properties and diagnostic applications. Polish journal of veterinary sciences, 2016. 19(1): p. 225-232.
  • 13. Mackness, M.I., S. Arrol, and P.N. Durrington, Paraoxonase prevents accumulation of lipoperoxides in low‐density lipoprotein. FEBS letters, 1991. 286(1-2): p. 152-154.
  • 14. Kurban, S. and I. Mehmetoglu, Effects of acetylsalicylic acid on serum paraoxonase activity, Ox-LDL, coenzyme Q10 and other oxidative stress markers in healthy volunteers. Clinical biochemistry, 2010. 43(3): p. 287-290.
  • 15. Mackness, B., M.I. Mackness, S. Arrol, W. Turkie, and P.N. Durrington, Effect of the molecular polymorphisms of human paraoxonase (PON1) on the rate of hydrolysis of paraoxon. British journal of pharmacology, 1997. 122(2): p. 265-268.
  • 16. Humbert, R., D.A. Adler, C.M. Disteche, C. Hassett, C.J. Omiecinski, and C.E. Furlong, The molecular basis of the human serum paraoxonase activity polymorphism. Nature genetics, 1993. 3(1): p. 73.
  • 17. Cao, H., A. Girard-Globa, F. Berthezene, and P. Moulin, Paraoxonase protection of LDL against peroxidation is independent of its esterase activity towards paraoxon and is unaffected by the Q R genetic polymorphism. Journal of lipid research, 1999. 40(1): p. 133-139.
  • 18. Kontush, A. and M.J. Chapman, Antiatherogenic small, dense HDL guardian angel of the arterial wall? Nature Reviews Cardiology, 2006. 3(3): p. 144.
  • 19. Razavi, A.E., G. Basati, J. Varshosaz, and S. Abdi, Association between HDL particles size and myeloperoxidase/paraoxonase-1 (MPO/PON1) ratio in patients with acute coronary syndrome. Acta Medica Iranica, 2013. 51(6): p. 365-371.
  • 20. Haraguchi, Y., R. Toh, M. Hasokawa, H. Nakajima, T. Honjo, K. Otsui, et al., Serum myeloperoxidase/paraoxonase 1 ratio as potential indicator of dysfunctional high-density lipoprotein and risk stratification in coronary artery disease. Atherosclerosis, 2014. 234(2): p. 288-294.
  • 21. Bradley, P.P., D.A. Priebat, R.D. Christensen, and G. Rothstein, Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. Journal of Investigative Dermatology, 1982. 78(3): p. 206-209.
  • 22. Eckerson, H.W., C.M. Wyte, and B. La Du, The human serum paraoxonase/arylesterase polymorphism. American journal of human genetics, 1983. 35(6): p. 1126.
  • 23. Haagen, L. and A. Brock, A new automated method for phenotyping arylesterase (EC 3.1. 1.2) based upon inhibition of enzymatic hydrolysis of 4-nitrophenyl acetate by phenyl acetate. Clinical Chemistry and Laboratory Medicine, 1992. 30(7): p. 391-396.
  • 24. Arab, K. and J.-P. Steghens, Plasma lipid hydroperoxides measurement by an automated xylenol orange method. Analytical biochemistry, 2004. 325(1): p. 158-163.
  • 25. Ellman, G. and H. Lysko, A precise method for the determination of whole blood and plasma sulfhydryl groups. Analytical biochemistry, 1979. 93: p. 98-102.
  • 26. Huang, Y., Z. Wu, M. Riwanto, S. Gao, B.S. Levison, X. Gu, et al., Myeloperoxidase, paraoxonase-1, and HDL form a functional ternary complex. The Journal of clinical investigation, 2013. 123(9): p. 3815-3828.
  • 27. Carbone, A., C. Tripodo, C. Carlo-Stella, A. Santoro, and A. Gloghini, The role of inflammation in lymphoma, in Inflammation and Cancer. 2014, Springer. p. 315-333.28. Navab, M., S.Y. Hama, G. Anantharamaiah, K. Hassan, G.P. Hough, A.D. Watson, et al., Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. Journal of lipid research, 2000. 41(9): p. 1495-1508.
  • 29. Perségol, L., M. Foissac, L. Lagrost, A. Athias, P. Gambert, B. Vergès, et al., HDL particles from type 1 diabetic patients are unable to reverse the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation. Diabetologia, 2007. 50(11): p. 2384-2387.
  • 30. Riwanto, M., L. Rohrer, B. Roschitzki, C. Besler, P. Mocharla, M. Mueller, et al., Altered activation of endothelial anti-and pro-apoptotic pathways by high-density lipoprotein from patients with coronary artery disease: role of HDL-proteome remodeling. Circulation, 2013: p. CIRCULATIONAHA. 112.108753.
  • 31. Kontush, A. and M.J. Chapman, Antiatherogenic function of HDL particle subpopulations: focus on antioxidative activities. Current opinion in lipidology, 2010. 21(4): p. 312-318.
  • 32. Hansel, B., P. Giral, E. Nobecourt, S. Chantepie, E. Bruckert, M.J. Chapman, et al., Metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity. The Journal of Clinical Endocrinology & Metabolism, 2004. 89(10): p. 4963-4971.
  • 33. Banka, C., T. Yuan, M. De Beer, M. Kindy, L. Curtiss, and F. De Beer, Serum amyloid A (SAA): influence on HDL-mediated cellular cholesterol efflux. Journal of lipid research, 1995. 36(5): p. 1058-1065.
  • 34. Cavallero, E., F. Brites, B. Delfly, N. Nicolaı̈ew, C. Decossin, C. De Geitere, et al., Abnormal reverse cholesterol transport in controlled type II diabetic patients: studies on fasting and postprandial LpA-I particles. Arteriosclerosis, thrombosis, and vascular biology, 1995. 15(12): p. 2130-2135.
  • 35. Rosenson, R.S., H.B. Brewer Jr, B.J. Ansell, P. Barter, M.J. Chapman, J.W. Heinecke, et al., Dysfunctional HDL and atherosclerotic cardiovascular disease. Nature reviews cardiology, 2016. 13(1): p. 48.
  • 36. Huang, J., H. Lee, A.M. Zivkovic, J.T. Smilowitz, N. Rivera, J.B. German, et al., Glycomic analysis of high density lipoprotein shows a highly sialylated particle. Journal of proteome research, 2014. 13(2): p. 681-691.
  • 37. Nicholls, S.J. and S.L. Hazen, Myeloperoxidase, modified lipoproteins, and atherogenesis. Journal of lipid research, 2009. 50(Supplement): p. S346-S351.
  • 38. Aviram, M. and J. Vaya, Paraoxonase 1 activities, regulation, and interactions with atherosclerotic lesion. Current opinion in lipidology, 2013. 24(4): p. 339-344.
  • 39. Shao, B. and J.W. Heinecke, HDL, lipid peroxidation, and atherosclerosis. Journal of lipid research, 2009. 50(4): p. 599-601.
  • 40. Smith, J.D., Dysfunctional HDL as a diagnostic and therapeutic target. Arteriosclerosis, thrombosis, and vascular biology, 2010. 30(2): p. 151-155.
  • 41. Cervellati, C., A. Trentini, A. Romani, T. Bellini, C. Bosi, B. Ortolani, et al., Serum paraoxonase and arylesterase activities of paraoxonase 1 (PON 1), mild cognitive impairment, and 2 year conversion to dementia: A pilot study. Journal of neurochemistry, 2015. 135(2): p. 395-401.

Lenfomada miyeloperoksidaz/paraoksonaz oranı kullanılarak disfonksiyonel HDL’nin araştırılması

Yıl 2019, Cilt: 16 Sayı: 2, 358 - 364, 29.08.2019
https://doi.org/10.35440/hutfd.579011

Öz

Amaç: Bu çalışmanın amacı, anormal lipid metabolizması, oksidatif stres ve
inflamasyon ile karakterize çeşitli lenfoma tiplerinde disfonksiyonel HDL'yi
gösteren miyeloperoksidaz / paraoksonaz oranını araştırmaktır.

Materyal ve Metot: Çalışmaya 30 lenfoma hastası ve 30 sağlıklı birey alındı. Otomatik
analizörde serum myeloperoksidaz, paraoksonaz, arilesteraz, lipid hidroperoksit
parametrelerinin ve rutin biyokimya testlerinin düzeyleri ölçüldü. Lenfoma
hastalarının tanısı biyopsi materyalinin histolojik incelemesine göre konuldu.

Bulgular: Sağlıklı kontrol grubu ile karşılaştırıldığında; albumin, arilesteraz,
HDL, tiyol ve Hemoglobin seviyeleri anlamlı derecede düşükken, myeloperoksidaz
/ paraoksonaz oranı, myeloperoksidaz / arilesteraz oranı ve lipid hidroperoksit
seviyeleri, lenfomalı hastalarda anlamlı olarak daha yüksekti. Ayrıca lipid
hidroperoksit düzeyi, miyeloperoksidaz / paraoksonaz oranı ve miyeloperoksidaz
/ paraoksonaz oranı ile anlamlı şekilde ilişkiliydi
(sırasıyla r= 0.330, p=0.046; r=
0.588, p< 0.001)







Sonuç: Biz disfonksiyonel HDL'nin, lenfoma hastalarında gözlenen inflamatuar
süreç, ateroskleroz, oksidatif stres ve bozulmuş lipid metabolizmasında önemli
bir faktör olduğunu düşünüyoruz. Gelecekte myeloperoxidase / paraoxonase
oranının, disfonksiyonel HDL'ye sebep olan hastalıkları önlemek için bir tedavi
kriteri olarak kullanılabileceğine inanıyoruz.

Kaynakça

  • 1. Ansell, S.M. Hodgkin lymphoma: diagnosis and treatment. in Mayo Clinic Proceedings. 2015. Elsevier.
  • 2. Ansell, S.M. Non-Hodgkin lymphoma: diagnosis and treatment. in Mayo Clinic Proceedings. 2015. Elsevier.
  • 3. Imbesi, S., C. Musolino, A. Allegra, A. Saija, F. Morabito, G. Calapai, et al., Oxidative stress in oncohematologic diseases: an update. Expert review of hematology, 2013. 6(3): p. 317-325.
  • 4. Memişoğulları, R., Paraoksonaz ve kanser. Konuralp Tıp Dergisi, 2010. 2010(2): p. 22-26.
  • 5. Morabito, F., M. Cristani, A. Saija, C. Stelitano, V. Callea, A. Tomaino, et al., Lipid peroxidation and protein oxidation in patients affected by Hodgkin's lymphoma. Mediators of inflammation, 2004. 13(5-6): p. 381-383.
  • 6. Lim, U., T. Gayles, H.A. Katki, R. Stolzenberg-Solomon, S.J. Weinstein, P. Pietinen, et al., Serum high-density lipoprotein cholesterol and risk of non-hodgkin lymphoma. Cancer Research, 2007. 67(11): p. 5569-5574.
  • 7. Yang, S., M.G. Damiano, H. Zhang, S. Tripathy, A.J. Luthi, J.S. Rink, et al., Biomimetic, synthetic HDL nanostructures for lymphoma. Proceedings of the National Academy of Sciences, 2013. 110(7): p. 2511-2516.
  • 8. Rho, Y.H., C.P. Chung, A. Oeser, J.F. Solus, T. Gebretsadik, A. Shintani, et al., Interaction between oxidative stress and high‐density lipoprotein cholesterol is associated with severity of coronary artery calcification in rheumatoid arthritis. Arthritis care & research, 2010. 62(10): p. 1473-1480.
  • 9. Ferretti, G., T. Bacchetti, A. Nègre-Salvayre, R. Salvayre, N. Dousset, and G. Curatola, Structural modifications of HDL and functional consequences. Atherosclerosis, 2006. 184(1): p. 1-7.
  • 10. McMahon, K.M., L. Foit, N.L. Angeloni, F.J. Giles, L.I. Gordon, and C.S. Thaxton, Synthetic high-density lipoprotein-like nanoparticles as cancer therapy, in Nanotechnology-Based Precision Tools for the Detection and Treatment of Cancer. 2015, Springer. p. 129-150.
  • 11. Deakin, S.P. and R.W. James, Genetic and environmental factors modulating serum concentrations and activities of the antioxidant enzyme paraoxonase-1. Clinical Science, 2004. 107(5): p. 435-447.
  • 12. Kulka, M., A review of paraoxonase 1 properties and diagnostic applications. Polish journal of veterinary sciences, 2016. 19(1): p. 225-232.
  • 13. Mackness, M.I., S. Arrol, and P.N. Durrington, Paraoxonase prevents accumulation of lipoperoxides in low‐density lipoprotein. FEBS letters, 1991. 286(1-2): p. 152-154.
  • 14. Kurban, S. and I. Mehmetoglu, Effects of acetylsalicylic acid on serum paraoxonase activity, Ox-LDL, coenzyme Q10 and other oxidative stress markers in healthy volunteers. Clinical biochemistry, 2010. 43(3): p. 287-290.
  • 15. Mackness, B., M.I. Mackness, S. Arrol, W. Turkie, and P.N. Durrington, Effect of the molecular polymorphisms of human paraoxonase (PON1) on the rate of hydrolysis of paraoxon. British journal of pharmacology, 1997. 122(2): p. 265-268.
  • 16. Humbert, R., D.A. Adler, C.M. Disteche, C. Hassett, C.J. Omiecinski, and C.E. Furlong, The molecular basis of the human serum paraoxonase activity polymorphism. Nature genetics, 1993. 3(1): p. 73.
  • 17. Cao, H., A. Girard-Globa, F. Berthezene, and P. Moulin, Paraoxonase protection of LDL against peroxidation is independent of its esterase activity towards paraoxon and is unaffected by the Q R genetic polymorphism. Journal of lipid research, 1999. 40(1): p. 133-139.
  • 18. Kontush, A. and M.J. Chapman, Antiatherogenic small, dense HDL guardian angel of the arterial wall? Nature Reviews Cardiology, 2006. 3(3): p. 144.
  • 19. Razavi, A.E., G. Basati, J. Varshosaz, and S. Abdi, Association between HDL particles size and myeloperoxidase/paraoxonase-1 (MPO/PON1) ratio in patients with acute coronary syndrome. Acta Medica Iranica, 2013. 51(6): p. 365-371.
  • 20. Haraguchi, Y., R. Toh, M. Hasokawa, H. Nakajima, T. Honjo, K. Otsui, et al., Serum myeloperoxidase/paraoxonase 1 ratio as potential indicator of dysfunctional high-density lipoprotein and risk stratification in coronary artery disease. Atherosclerosis, 2014. 234(2): p. 288-294.
  • 21. Bradley, P.P., D.A. Priebat, R.D. Christensen, and G. Rothstein, Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. Journal of Investigative Dermatology, 1982. 78(3): p. 206-209.
  • 22. Eckerson, H.W., C.M. Wyte, and B. La Du, The human serum paraoxonase/arylesterase polymorphism. American journal of human genetics, 1983. 35(6): p. 1126.
  • 23. Haagen, L. and A. Brock, A new automated method for phenotyping arylesterase (EC 3.1. 1.2) based upon inhibition of enzymatic hydrolysis of 4-nitrophenyl acetate by phenyl acetate. Clinical Chemistry and Laboratory Medicine, 1992. 30(7): p. 391-396.
  • 24. Arab, K. and J.-P. Steghens, Plasma lipid hydroperoxides measurement by an automated xylenol orange method. Analytical biochemistry, 2004. 325(1): p. 158-163.
  • 25. Ellman, G. and H. Lysko, A precise method for the determination of whole blood and plasma sulfhydryl groups. Analytical biochemistry, 1979. 93: p. 98-102.
  • 26. Huang, Y., Z. Wu, M. Riwanto, S. Gao, B.S. Levison, X. Gu, et al., Myeloperoxidase, paraoxonase-1, and HDL form a functional ternary complex. The Journal of clinical investigation, 2013. 123(9): p. 3815-3828.
  • 27. Carbone, A., C. Tripodo, C. Carlo-Stella, A. Santoro, and A. Gloghini, The role of inflammation in lymphoma, in Inflammation and Cancer. 2014, Springer. p. 315-333.28. Navab, M., S.Y. Hama, G. Anantharamaiah, K. Hassan, G.P. Hough, A.D. Watson, et al., Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. Journal of lipid research, 2000. 41(9): p. 1495-1508.
  • 29. Perségol, L., M. Foissac, L. Lagrost, A. Athias, P. Gambert, B. Vergès, et al., HDL particles from type 1 diabetic patients are unable to reverse the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation. Diabetologia, 2007. 50(11): p. 2384-2387.
  • 30. Riwanto, M., L. Rohrer, B. Roschitzki, C. Besler, P. Mocharla, M. Mueller, et al., Altered activation of endothelial anti-and pro-apoptotic pathways by high-density lipoprotein from patients with coronary artery disease: role of HDL-proteome remodeling. Circulation, 2013: p. CIRCULATIONAHA. 112.108753.
  • 31. Kontush, A. and M.J. Chapman, Antiatherogenic function of HDL particle subpopulations: focus on antioxidative activities. Current opinion in lipidology, 2010. 21(4): p. 312-318.
  • 32. Hansel, B., P. Giral, E. Nobecourt, S. Chantepie, E. Bruckert, M.J. Chapman, et al., Metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity. The Journal of Clinical Endocrinology & Metabolism, 2004. 89(10): p. 4963-4971.
  • 33. Banka, C., T. Yuan, M. De Beer, M. Kindy, L. Curtiss, and F. De Beer, Serum amyloid A (SAA): influence on HDL-mediated cellular cholesterol efflux. Journal of lipid research, 1995. 36(5): p. 1058-1065.
  • 34. Cavallero, E., F. Brites, B. Delfly, N. Nicolaı̈ew, C. Decossin, C. De Geitere, et al., Abnormal reverse cholesterol transport in controlled type II diabetic patients: studies on fasting and postprandial LpA-I particles. Arteriosclerosis, thrombosis, and vascular biology, 1995. 15(12): p. 2130-2135.
  • 35. Rosenson, R.S., H.B. Brewer Jr, B.J. Ansell, P. Barter, M.J. Chapman, J.W. Heinecke, et al., Dysfunctional HDL and atherosclerotic cardiovascular disease. Nature reviews cardiology, 2016. 13(1): p. 48.
  • 36. Huang, J., H. Lee, A.M. Zivkovic, J.T. Smilowitz, N. Rivera, J.B. German, et al., Glycomic analysis of high density lipoprotein shows a highly sialylated particle. Journal of proteome research, 2014. 13(2): p. 681-691.
  • 37. Nicholls, S.J. and S.L. Hazen, Myeloperoxidase, modified lipoproteins, and atherogenesis. Journal of lipid research, 2009. 50(Supplement): p. S346-S351.
  • 38. Aviram, M. and J. Vaya, Paraoxonase 1 activities, regulation, and interactions with atherosclerotic lesion. Current opinion in lipidology, 2013. 24(4): p. 339-344.
  • 39. Shao, B. and J.W. Heinecke, HDL, lipid peroxidation, and atherosclerosis. Journal of lipid research, 2009. 50(4): p. 599-601.
  • 40. Smith, J.D., Dysfunctional HDL as a diagnostic and therapeutic target. Arteriosclerosis, thrombosis, and vascular biology, 2010. 30(2): p. 151-155.
  • 41. Cervellati, C., A. Trentini, A. Romani, T. Bellini, C. Bosi, B. Ortolani, et al., Serum paraoxonase and arylesterase activities of paraoxonase 1 (PON 1), mild cognitive impairment, and 2 year conversion to dementia: A pilot study. Journal of neurochemistry, 2015. 135(2): p. 395-401.
Toplam 40 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Klinik Tıp Bilimleri
Bölüm Araştırma Makalesi
Yazarlar

Salim Neşelioğlu 0000-0002-0974-5717

Gültekin Pekcan Bu kişi benim 0000-0003-3245-4667

Gamze Gök 0000-0002-2804-5548

Emine Feyza Yurt Bu kişi benim 0000-0001-5686-7576

Özcan Erel 0000-0002-2996-3236

Yayımlanma Tarihi 29 Ağustos 2019
Gönderilme Tarihi 19 Haziran 2019
Kabul Tarihi 7 Ağustos 2019
Yayımlandığı Sayı Yıl 2019 Cilt: 16 Sayı: 2

Kaynak Göster

Vancouver Neşelioğlu S, Pekcan G, Gök G, Yurt EF, Erel Ö. Investigation of dysfunctional HDL using myeloperoxidase / paraoxonase ratio in lymphoma. Harran Üniversitesi Tıp Fakültesi Dergisi. 2019;16(2):358-64.

Harran Üniversitesi Tıp Fakültesi Dergisi  / Journal of Harran University Medical Faculty