BibTex RIS Cite

Deformability of Erythrocytes and Oxidative Damage in Alzheimer Disease

Year 2012, Volume: 37 Issue: 2, 65 - 75, 01.06.2012

Abstract

Purpose: A lowered cerebral perfusion as a consequence of hemodynamic microcirculatory insufficiency is one of the factors underlying in Alzheimer's disease, which is a neurodegenerative disorder leading to progressive cognitive impairment. Erythrocyte deformability is one of the major factors affecting the microcirculatory hemodynamics which is closely related to the oxidative damage. The aim of this study is to investigate the relationship between the erythrocyte deformability, nitric oxide levels and oxidative stress in Alzheimer's disease. Methods: The blood samples of 30 elderly people in three groups consisting of healthy control and different severities of the disease (low and severe) were used. Then the erythrocytes were isolated and the deformability of erythrocytes was determined by Rheodyne SSD evaluating the elongation indexes of the erythrocytes under different shear stress. The catalase, glutathione peroxidase and plasma nitric oxide levels were measured spectrophotometric ally. Results: The plasma nitric oxide levels, catalase activities were found significantly higher and glutathione peroxidase activity was significantly lower in severe Alzheimer's disease patients compared to the control group. However, the deformability of erythrocytes was not significantly affected from these alterations. Conclusion: the oxidant-antioxidant status is dramatically changed in Alzheimer's disease patients with the severity of the disease and similar alterations were seen in the nitric oxide levels without any significant change in erythrocyte deformability.

References

  • King ME, Kan HM, Baas PW, Erisir A, Glabe CG, Bloom GS. Tau-dependent microtubule disassembly initiated by prefibrillar beta-amyloid. J Cell Biol. 2006; 175:541-6.
  • Mesulam MM. Neuroplasticity failure in Alzheimer's disease: bridging the gap between plaques and tangles. Neuron. 1999; 24:521-529.
  • Bozner P, Grishko V, LeDoux SP, Wilson GL, Chyan YC, Pappolla MA. J. The amyloid beta protein induces oxidative damage of mitochondrial DNA. Neuropathol. Exp Neurol. 1997; 56:1356–1362.
  • Glenner GG, Wong CW. Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun. 1984; 120:885–90.
  • Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci U SA. 1985; 82:4245–49.
  • Murray IV, Liu L, Komatsu H, Uryu K, Xiao G, Lawson JA, Axelsen PH. Membrane mediated amyloidogenesis and the promotion of oxidative lipid damage by amyloid beta proteins. J Biol Chem. 2007; 282:9335-45.
  • Loh KP, Huang SH, De Silva R, Tan BK, Zhu YZ. Oxidative stress: apoptosis in neuronal injury. Curr Alzheimer Res. 2006; 3:327-37.
  • Miranda S, Opaza C, Larrondo LF, Munoz FJ, Ruiz F, Leighton F, Inestrosa NC. The role of oxidative stress in the toxicity induced by amyloid b-peptide in Alzheimer's disease. Prog Neurobiol. 2000; 62:633- 48. 9. Onyango IG, Khan SM. Oxidative stress, mitochondrial dysfunction, and stress signaling in Alzheimer's disease. Curr Alzheimer Res. 2006; 3:339-49.
  • Pappolla MA, Chyan YJ, Poeggeler B, Frangione B, Wilson G, Ghiso J, Reiter RJ. An assessment of the antioxidant and the antiamyloidogenic properties of melatonin: implications for alzheimer's disease. J Neural Transm. 2000; 107:203-231.
  • Kawamoto EM, Munhoz CM, Glezer I, Bahai VS, Caramelli P, Nitrini R, et al. Oxidative state in platelets and erythrocytes in aging and Alzheimer’s disease. Neurobiology of Aging. 2005; 26:857–864.
  • Smith MA, Hirai K, Hsiao K, Pappolla MA, Harris PLR, Siedlak SL, et al. Amyloid-beta deposition in Alzheimer transgenic mice is associated with oxidative stress. J Neurochem. 1998; 70:2212–15.
  • Bourdel-Marchasson I, Delmas-Beauvieux MC, Peuchant E, Richard-Harston S, Decamps A, Reignier B, et al. Antioxidant defences and oxidative stress markers in erythrocytes and plasma from normally nourished elderly Alzheimer patients. Age Ageing. 2001; 30:235-41.
  • Bourdel-Marchasson I, Joseph PA, Dehail P, Biran M, Faux P, Rainfray M, et al. Functional and metabolic early changes in calf muscle occurring during nutritional repletion in malnourished elderly patients. Am J Clin Nutr. 2001; 73(4):832-8.
  • Repetto MG, Reides CG, Evelson P, Kohan S, de Lustig ES, Llesuy SF. Peripheral markers of oxidative stress in probable Alzheimer patients. European J Clin Invest. 1999; 29:643–49.
  • Rinaldi P, Polidori MC, Metastasio A, Mariani E, Mattioli P, Cherubini A, et al. Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer’s disease. Neurobiology of Aging. 2003; 24: 915–19.
  • Tarkowski E, Ringqvist A, Blennow K, Wallin A, Wennmalm A. Intrathecal release of nitric oxid in Alzheimer’s disease and vascular dementia. Dement Geriatr Cogn Disord. 2000; 11:322–26.
  • Puzzo D, Palmeri A, Arancio O. Involvement of the nitric oxide pathway in synaptic dysfunction following amyloid elevation in Alzheimer's disease. Rev Neurosci. 2006; 17:497-523.
  • Benz D, Cadet P, Mantione K, Zhu W, Stefano G. Tonal nitric oxide and health – a free radical and a scavenger of free radicals. Med Sci Monit. 2002; 8:RA1–RA4.
  • Maiese K, Chong ZZ. Insights into oxidative stress and potential novel therapeutic targets for Alzheimer disease. Restor Neurol Neurosci. 2004; 22:87–104.
  • de la Torre JC, Stefano GB. Evidence that Alzheimer’s disease is a microvascular disorder: The role of constitutive nitric oxide. Brain Res Rev. 2000; 34:119–36.
  • Pak T, Cadet P, Mantione KJ, Stefano GB. Morphine via nitric oxide modulates b-amyloid metabolism: a novel protective mechanism for Alzheimer’s disease. Med Sci Monit. 2005;11:BR357-366.
  • Yerer MB, Aydoğan S. The in vivo antioxidant effectiveness of -tocopherol in oxidative stress induced by sodiumnitro prusside in rat red blood cells. Clinical Hemorheol. Microcirc. 2004; 30: 323- 29.
  • Yerer M B., Aydogan S, The importance of circadian rhythm alterations in erythrocyte deformability, Clinical Hemorheol Microcirc. 2006; 35:143-7.
  • Folstein MF, Folstein SE and McHugh PR. Mini- Mental State – A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189–198
  • Beers RF, Sizer IW. A spectrophotometric method for measuring the breakdown of hydrogen peroxide by catalase. J Biol Chem. 1952; 95:133-140. 27. Fairbanks VF, Klee GG. Measurement of hemoglobin concentration in whole blood. In:Tietz(ed) Textbook of Clinical Chemistry. Philadelphia: WB Saunders Company. 1986: 1532-34.
  • Flohe L, Gunzler WA. Assays for glutathione peroxidase. Methods Enzymol. 1984; 105:114-121.
  • Arto K, Sandra T. The calcium dependent nitric oxide production of human vascular endothelial cell in preeclampsia. Am 174:1056-60.
  • Rondanelli M, Melzi d’Eril GV, Anesi A, Ferrari M Altered oxidative stress in healthy old subjects. Aging. 1997; 9:221-3.
  • Calabrese V, Sultana R, Scapagnini G, Guagliano E, Sapienza M, et al. Nitrosative stress, cellular stress response, and thiol homeostasis in patients with Alzheimer's disease. Antioxid Redox Signal. 2006; 8:1975-86.
  • Harris DE. Regulation of antioxidant enzymes. FASEB J. 1992; 6:1675–83.
  • Folin M, Baiguera S, Gallucci M, Conconi MT, Liddo R, Zanardo A, Parnigotto PP. A cross-sectional study of homocysteine-, NO-levels, and CT-findings in Alzheimer dementia, vascular dementia and controls. Biogerontology. 2005; 6:255–60.
  • Dawson VL, Dawson TM. neurodegeneration. Prog Brain Res. 1998; 118: 215– 29. Nitric oxide in deformability. Am J Physiol Heart Circ Physiol. 2003; 284:H1577-84.

Alzheimer Hastalığında Eritrosit Deformabilitesi ve Oksidatif Hasar

Year 2012, Volume: 37 Issue: 2, 65 - 75, 01.06.2012

Abstract

Amaç: Progresif kognitif bozukluğa yol açan bir nörodejeneratif hastalık olan Alzheimer hastalığı’nın altında yatan faktörlerden biri hemodinamik mikro dolaşım yetmezliğe bağlı gelişen azalmış serebral perfüzyondur. Oksidatif hasarla yakından bağlantılı olan eritrosit deformabilitesi, mikro dolaşım hemodinamiğini etkileyen başlıca faktörlerden biridir. Bu çalışmanın amacı Alzheimer hastalığı’nda eritrosit deformabilitesi, nitrik oksit seviyesi ve oksidatif stres arasındaki bağlantıyı araştırmaktır. Yöntem: Sağlıklı kontrol grubu ve farklı şiddette hastalığı (hafif, ağır) olan gruplar şeklinde üç grup yaşlı kişinin kan örnekleri kullanıldı. Sonrasında eritrositler izole edildi ve eritrosit deformabilitesi, Rheodyne SSD ile farklı shear streste eritrosit uzama indeksleri çalışılarak belirlendi. Katalaz, glutathion peroksidaz ve plazma nitrik oksit seviyeleri spektrofotometrik olarak belirlendi. Bulgular: Kontrol grubu ile karşılaştırıldığında şiddetli Alzheimer hastalığı olan hastalarda plazma nitrik oksit ve katalaz aktivitelerinin önemli derecede yüksek ve glutathion peroksidaz aktivitesinin ise önemli oranda düşük olduğu bulundu. Bununla birlikte eritrosit deformabilitesinin bu değişikliklerden önemli şekilde etkilenmediği gözlendi. Sonuç: Alzheimer hastalığı’nda hastalığın şiddetlenmesi ile oksidan-antioksidan durumu dramatik olarak değişmekte ve benzer değişimler önemli oranda eritrosit deformabilitesi eşlik etmeden nitrik oksit seviyelerinde de görülmektedir.

References

  • King ME, Kan HM, Baas PW, Erisir A, Glabe CG, Bloom GS. Tau-dependent microtubule disassembly initiated by prefibrillar beta-amyloid. J Cell Biol. 2006; 175:541-6.
  • Mesulam MM. Neuroplasticity failure in Alzheimer's disease: bridging the gap between plaques and tangles. Neuron. 1999; 24:521-529.
  • Bozner P, Grishko V, LeDoux SP, Wilson GL, Chyan YC, Pappolla MA. J. The amyloid beta protein induces oxidative damage of mitochondrial DNA. Neuropathol. Exp Neurol. 1997; 56:1356–1362.
  • Glenner GG, Wong CW. Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein. Biochem Biophys Res Commun. 1984; 120:885–90.
  • Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci U SA. 1985; 82:4245–49.
  • Murray IV, Liu L, Komatsu H, Uryu K, Xiao G, Lawson JA, Axelsen PH. Membrane mediated amyloidogenesis and the promotion of oxidative lipid damage by amyloid beta proteins. J Biol Chem. 2007; 282:9335-45.
  • Loh KP, Huang SH, De Silva R, Tan BK, Zhu YZ. Oxidative stress: apoptosis in neuronal injury. Curr Alzheimer Res. 2006; 3:327-37.
  • Miranda S, Opaza C, Larrondo LF, Munoz FJ, Ruiz F, Leighton F, Inestrosa NC. The role of oxidative stress in the toxicity induced by amyloid b-peptide in Alzheimer's disease. Prog Neurobiol. 2000; 62:633- 48. 9. Onyango IG, Khan SM. Oxidative stress, mitochondrial dysfunction, and stress signaling in Alzheimer's disease. Curr Alzheimer Res. 2006; 3:339-49.
  • Pappolla MA, Chyan YJ, Poeggeler B, Frangione B, Wilson G, Ghiso J, Reiter RJ. An assessment of the antioxidant and the antiamyloidogenic properties of melatonin: implications for alzheimer's disease. J Neural Transm. 2000; 107:203-231.
  • Kawamoto EM, Munhoz CM, Glezer I, Bahai VS, Caramelli P, Nitrini R, et al. Oxidative state in platelets and erythrocytes in aging and Alzheimer’s disease. Neurobiology of Aging. 2005; 26:857–864.
  • Smith MA, Hirai K, Hsiao K, Pappolla MA, Harris PLR, Siedlak SL, et al. Amyloid-beta deposition in Alzheimer transgenic mice is associated with oxidative stress. J Neurochem. 1998; 70:2212–15.
  • Bourdel-Marchasson I, Delmas-Beauvieux MC, Peuchant E, Richard-Harston S, Decamps A, Reignier B, et al. Antioxidant defences and oxidative stress markers in erythrocytes and plasma from normally nourished elderly Alzheimer patients. Age Ageing. 2001; 30:235-41.
  • Bourdel-Marchasson I, Joseph PA, Dehail P, Biran M, Faux P, Rainfray M, et al. Functional and metabolic early changes in calf muscle occurring during nutritional repletion in malnourished elderly patients. Am J Clin Nutr. 2001; 73(4):832-8.
  • Repetto MG, Reides CG, Evelson P, Kohan S, de Lustig ES, Llesuy SF. Peripheral markers of oxidative stress in probable Alzheimer patients. European J Clin Invest. 1999; 29:643–49.
  • Rinaldi P, Polidori MC, Metastasio A, Mariani E, Mattioli P, Cherubini A, et al. Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer’s disease. Neurobiology of Aging. 2003; 24: 915–19.
  • Tarkowski E, Ringqvist A, Blennow K, Wallin A, Wennmalm A. Intrathecal release of nitric oxid in Alzheimer’s disease and vascular dementia. Dement Geriatr Cogn Disord. 2000; 11:322–26.
  • Puzzo D, Palmeri A, Arancio O. Involvement of the nitric oxide pathway in synaptic dysfunction following amyloid elevation in Alzheimer's disease. Rev Neurosci. 2006; 17:497-523.
  • Benz D, Cadet P, Mantione K, Zhu W, Stefano G. Tonal nitric oxide and health – a free radical and a scavenger of free radicals. Med Sci Monit. 2002; 8:RA1–RA4.
  • Maiese K, Chong ZZ. Insights into oxidative stress and potential novel therapeutic targets for Alzheimer disease. Restor Neurol Neurosci. 2004; 22:87–104.
  • de la Torre JC, Stefano GB. Evidence that Alzheimer’s disease is a microvascular disorder: The role of constitutive nitric oxide. Brain Res Rev. 2000; 34:119–36.
  • Pak T, Cadet P, Mantione KJ, Stefano GB. Morphine via nitric oxide modulates b-amyloid metabolism: a novel protective mechanism for Alzheimer’s disease. Med Sci Monit. 2005;11:BR357-366.
  • Yerer MB, Aydoğan S. The in vivo antioxidant effectiveness of -tocopherol in oxidative stress induced by sodiumnitro prusside in rat red blood cells. Clinical Hemorheol. Microcirc. 2004; 30: 323- 29.
  • Yerer M B., Aydogan S, The importance of circadian rhythm alterations in erythrocyte deformability, Clinical Hemorheol Microcirc. 2006; 35:143-7.
  • Folstein MF, Folstein SE and McHugh PR. Mini- Mental State – A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189–198
  • Beers RF, Sizer IW. A spectrophotometric method for measuring the breakdown of hydrogen peroxide by catalase. J Biol Chem. 1952; 95:133-140. 27. Fairbanks VF, Klee GG. Measurement of hemoglobin concentration in whole blood. In:Tietz(ed) Textbook of Clinical Chemistry. Philadelphia: WB Saunders Company. 1986: 1532-34.
  • Flohe L, Gunzler WA. Assays for glutathione peroxidase. Methods Enzymol. 1984; 105:114-121.
  • Arto K, Sandra T. The calcium dependent nitric oxide production of human vascular endothelial cell in preeclampsia. Am 174:1056-60.
  • Rondanelli M, Melzi d’Eril GV, Anesi A, Ferrari M Altered oxidative stress in healthy old subjects. Aging. 1997; 9:221-3.
  • Calabrese V, Sultana R, Scapagnini G, Guagliano E, Sapienza M, et al. Nitrosative stress, cellular stress response, and thiol homeostasis in patients with Alzheimer's disease. Antioxid Redox Signal. 2006; 8:1975-86.
  • Harris DE. Regulation of antioxidant enzymes. FASEB J. 1992; 6:1675–83.
  • Folin M, Baiguera S, Gallucci M, Conconi MT, Liddo R, Zanardo A, Parnigotto PP. A cross-sectional study of homocysteine-, NO-levels, and CT-findings in Alzheimer dementia, vascular dementia and controls. Biogerontology. 2005; 6:255–60.
  • Dawson VL, Dawson TM. neurodegeneration. Prog Brain Res. 1998; 118: 215– 29. Nitric oxide in deformability. Am J Physiol Heart Circ Physiol. 2003; 284:H1577-84.
There are 32 citations in total.

Details

Primary Language Turkish
Journal Section Research
Authors

Mükerrem Betül Yerer This is me

Sami Aydogan This is me

Emel Köseoğlu This is me

Recep Baştuğ This is me

Publication Date June 1, 2012
Published in Issue Year 2012 Volume: 37 Issue: 2

Cite

MLA Yerer, Mükerrem Betül et al. “Alzheimer Hastalığında Eritrosit Deformabilitesi Ve Oksidatif Hasar”. Cukurova Medical Journal, vol. 37, no. 2, 2012, pp. 65-75.