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PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY

Yıl 2014, Cilt: 19 Sayı: 4, 169 - 174, 23.03.2015

Öz

Objectives: Paraoxonase-1 (PON-1) has been thought to be an antioxidant enzyme that hydrolyzes lipid peroxides. Experimental and epidemiologic numerous studies have  shown that oxygen-free-radicals are elevated in uncontrolled DM. The present study was undertaken to make comparison of the activity of serum PON1, Malondialdehyde (MDA) and Glutathione Reductase (GR) in type 2 diabetic (T2DM) patients with nephropathy (DN).

Methods: 70 subjects were included in the study: 30 as control, 20 with T2DM with nephropathy, 20 T2DM without nephropathy. All studied groups are subjected to the following laboratory investigations after their consents: fasting and postprandial blood sugars, HbA1c, blood urea, serum creatinine and microalbumin in urine, serum PON-1 activity level, serum MDA, and serum GR activity.

Results: serum PON-1 activity and GR levels showed significant decrease in both T2DM patients with and without nephropathy compared to the control group with significant decrease in its activity in DN group while there was clearly a rise in amount of MDA in diabetic groups than control with significant rise in DN, fasting blood glucose levels, post prandial and HbA1c was significantly higher in DN group than diabetic group or control (p= 0.0001) for all. Serum creatinine show significant rise in DN group than diabetic or control group (p=0.0001). Microalbuminuria show significant rise in DN group than control or diabetic group as well as in diabetic group than control group (p= 0.0001 for all.

Conclusions: The decreased antioxidant enzyme activities in DN subjects suggesting that antioxidant may give rise to the occurrence of DN along with other microvascular complications. So, measurement of PNO1, MDA level and supplementing the antioxidants could manage the seriousness of DN.

Recommendations: Further researches is strongly recommended to examine genetic polymorphism distribution in large population to accomplish a concise overview which could explain variability in PON1  and its particular relationship with all the additional factors that associate the condition and its particular complications.

Kaynakça

  • Tandogan B, Ulusu NN. Kinetic mechanism and molecular properties of glutathione reductase. FABAD J pharm sci 2006; 31: 230-237
  • Kamerbeek N, Zwieten R, de Boer M, et al. Molecular basis of glutathione reductase deficiency in human blood cells. Blood 2007; 109: 3560-3566.
  • Gross JL, de Azevedo MJ, Silveiro SP, et al. Diabetic nephropathy: diagnosis, prevention, and treatment. Diabetes Care 2005; 28: 164-176.
  • Ferré N, Camps J, Prats E, et al. Serum paraoxonase activity: a new additional test for the improved evaluation of chronic liver damage. Clin Chem 2002; 48: 261-268.
  • Kalghatgi S, Spina CS, Costello JC, et al. Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells. Sci Transl Med 2013; 5: 192ra85.
  • Krishan P, Chakkarwar VA. Diabetic nephropathy: Aggressive involvement of oxidative stress. J Pharm Educ Res June 2011; Vol. 2, Issue No. 1.
  • Rosario RF, Prabhakar S. Lipids and diabetic nephropathy. Curr Diab Rep 2006; 6: 455-462.
  • Chen HC, Guh JY, Chang JM, et al. Role of lipid control in diabetic nephropathy. Kidney Int Suppl 2005; 60-62.
  • Ruan XZ, Varghese Z, Moorhead JF. Inflammation modifies lipid-mediated renal injury. Nephrol Dial Transplant 2003; 18: 27-32.
  • Raimundo M, Lopes JA. Metabolic syndrome, chronic kidney disease and cardiovascular disease: a dynamic and life-threatening triad. Cardiol Res Pract 2011; 747-861.
  • Jyoti D, Purnima D. Oxidative with homocysteine, lipoprotein (A) and lipid profile in diabetic nephropathy. IJABPT 2010; 840-846.
  • Maha EW, Gamila SM, Safinaz E, et al. Oxidative DNA damage in patients with type 2 diabetes mellitus. Diabetologia Croatica 2012; 41-44.
  • Davi G, Falco A, Patrono C. Lipid peroxidation in diabetes mellitus. Antioxid Redox Signal 2005; 256- 268.
  • Nowak M, Wielkoszyński T, Marek B, et al. Antioxidant potential, Paraoxonase 1, ceruloplasmin activity and C‑ reactive protein concentration in diabetic retinopathy. Clin Exp MED 2010; 10: 185- 192.
  • Rosenblat M, Sapir O, Aviram M. The paraoxonases: their role in disease development and xenobiotic metabolism. In Glucose inactivates Paraoxonase 1 (PON1) and displaces it from high density lipoprotein (HDL) to a free PON1 form. Edited by Mackness B, Mackness M, Aviram M, Paragh G. New York: Springer 2008; 35-51.
  • Rozenberg O, Rosenblat M, Coleman R, Shih DM, Aviram M. Paraoxonase (PON1) deficiency is associated with increased macrophage oxidative stress: studies in PON1-knockout mice. Free Radic Biol Med 2003; 34: 774-784.
  • Mastorikou M, Mackness B, Liu Y, Mackness M. Glycation of paraoxonase 1 inhibit its activity and impair the ability of high‑ density lipoprotein to metabolize membrane lipid hydroperoxides. Diabetes MED 2008; 25: 1049-1055.
  • Shao B, Heineke JW. HDL, lipid peroxidation, and atherosclerosis. J Lipid Res 2009; 50: 716-722.
  • Aksoy H, Aksoy AN, Ozkan A, Polat H. Serum lipid profile, oxidative status, and paraoxonase 1 activity in hyperemesis gravidarum. J Clin Lab Anal 2009; 23:105-109.
  • Younis NN, Soran H, Charlton-Menys V, et al. High- density lipoprotein impedes glycation of low-density lipoprotein. Diab Vasc Dis Res 2013; 10: 152-160.
  • Al-Shamma Z and Yassin H. Glutathion, Glutathion Reductase and Gama-glutamyl Transferase Biomarkers for type 2 diabetes Mellitus and Coronary Heart Disease. IRAQI J MED SCI 2011; 9: 218-226.
  • Sailaja Y, Baskar R, Saralakumari D. The antioxidant status during maturation of reticulocytes to erythrocytes in type 2 diabetics. Free Radic Biol MED 2003; 35: 133-139.
Yıl 2014, Cilt: 19 Sayı: 4, 169 - 174, 23.03.2015

Öz

Kaynakça

  • Tandogan B, Ulusu NN. Kinetic mechanism and molecular properties of glutathione reductase. FABAD J pharm sci 2006; 31: 230-237
  • Kamerbeek N, Zwieten R, de Boer M, et al. Molecular basis of glutathione reductase deficiency in human blood cells. Blood 2007; 109: 3560-3566.
  • Gross JL, de Azevedo MJ, Silveiro SP, et al. Diabetic nephropathy: diagnosis, prevention, and treatment. Diabetes Care 2005; 28: 164-176.
  • Ferré N, Camps J, Prats E, et al. Serum paraoxonase activity: a new additional test for the improved evaluation of chronic liver damage. Clin Chem 2002; 48: 261-268.
  • Kalghatgi S, Spina CS, Costello JC, et al. Bactericidal antibiotics induce mitochondrial dysfunction and oxidative damage in Mammalian cells. Sci Transl Med 2013; 5: 192ra85.
  • Krishan P, Chakkarwar VA. Diabetic nephropathy: Aggressive involvement of oxidative stress. J Pharm Educ Res June 2011; Vol. 2, Issue No. 1.
  • Rosario RF, Prabhakar S. Lipids and diabetic nephropathy. Curr Diab Rep 2006; 6: 455-462.
  • Chen HC, Guh JY, Chang JM, et al. Role of lipid control in diabetic nephropathy. Kidney Int Suppl 2005; 60-62.
  • Ruan XZ, Varghese Z, Moorhead JF. Inflammation modifies lipid-mediated renal injury. Nephrol Dial Transplant 2003; 18: 27-32.
  • Raimundo M, Lopes JA. Metabolic syndrome, chronic kidney disease and cardiovascular disease: a dynamic and life-threatening triad. Cardiol Res Pract 2011; 747-861.
  • Jyoti D, Purnima D. Oxidative with homocysteine, lipoprotein (A) and lipid profile in diabetic nephropathy. IJABPT 2010; 840-846.
  • Maha EW, Gamila SM, Safinaz E, et al. Oxidative DNA damage in patients with type 2 diabetes mellitus. Diabetologia Croatica 2012; 41-44.
  • Davi G, Falco A, Patrono C. Lipid peroxidation in diabetes mellitus. Antioxid Redox Signal 2005; 256- 268.
  • Nowak M, Wielkoszyński T, Marek B, et al. Antioxidant potential, Paraoxonase 1, ceruloplasmin activity and C‑ reactive protein concentration in diabetic retinopathy. Clin Exp MED 2010; 10: 185- 192.
  • Rosenblat M, Sapir O, Aviram M. The paraoxonases: their role in disease development and xenobiotic metabolism. In Glucose inactivates Paraoxonase 1 (PON1) and displaces it from high density lipoprotein (HDL) to a free PON1 form. Edited by Mackness B, Mackness M, Aviram M, Paragh G. New York: Springer 2008; 35-51.
  • Rozenberg O, Rosenblat M, Coleman R, Shih DM, Aviram M. Paraoxonase (PON1) deficiency is associated with increased macrophage oxidative stress: studies in PON1-knockout mice. Free Radic Biol Med 2003; 34: 774-784.
  • Mastorikou M, Mackness B, Liu Y, Mackness M. Glycation of paraoxonase 1 inhibit its activity and impair the ability of high‑ density lipoprotein to metabolize membrane lipid hydroperoxides. Diabetes MED 2008; 25: 1049-1055.
  • Shao B, Heineke JW. HDL, lipid peroxidation, and atherosclerosis. J Lipid Res 2009; 50: 716-722.
  • Aksoy H, Aksoy AN, Ozkan A, Polat H. Serum lipid profile, oxidative status, and paraoxonase 1 activity in hyperemesis gravidarum. J Clin Lab Anal 2009; 23:105-109.
  • Younis NN, Soran H, Charlton-Menys V, et al. High- density lipoprotein impedes glycation of low-density lipoprotein. Diab Vasc Dis Res 2013; 10: 152-160.
  • Al-Shamma Z and Yassin H. Glutathion, Glutathion Reductase and Gama-glutamyl Transferase Biomarkers for type 2 diabetes Mellitus and Coronary Heart Disease. IRAQI J MED SCI 2011; 9: 218-226.
  • Sailaja Y, Baskar R, Saralakumari D. The antioxidant status during maturation of reticulocytes to erythrocytes in type 2 diabetics. Free Radic Biol MED 2003; 35: 133-139.
Toplam 22 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Bölüm Articles
Yazarlar

Waleed Mohamed

Mohammed Hassanien Bu kişi benim

Khalid Abokhosheim

Yayımlanma Tarihi 23 Mart 2015
Yayımlandığı Sayı Yıl 2014 Cilt: 19 Sayı: 4

Kaynak Göster

APA Mohamed, W., Hassanien, M., & Abokhosheim, K. (2015). PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY. EASTERN JOURNAL OF MEDICINE, 19(4), 169-174.
AMA Mohamed W, Hassanien M, Abokhosheim K. PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY. EASTERN JOURNAL OF MEDICINE. Mart 2015;19(4):169-174.
Chicago Mohamed, Waleed, Mohammed Hassanien, ve Khalid Abokhosheim. “PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY”. EASTERN JOURNAL OF MEDICINE 19, sy. 4 (Mart 2015): 169-74.
EndNote Mohamed W, Hassanien M, Abokhosheim K (01 Mart 2015) PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY. EASTERN JOURNAL OF MEDICINE 19 4 169–174.
IEEE W. Mohamed, M. Hassanien, ve K. Abokhosheim, “PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY”, EASTERN JOURNAL OF MEDICINE, c. 19, sy. 4, ss. 169–174, 2015.
ISNAD Mohamed, Waleed vd. “PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY”. EASTERN JOURNAL OF MEDICINE 19/4 (Mart 2015), 169-174.
JAMA Mohamed W, Hassanien M, Abokhosheim K. PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY. EASTERN JOURNAL OF MEDICINE. 2015;19:169–174.
MLA Mohamed, Waleed vd. “PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY”. EASTERN JOURNAL OF MEDICINE, c. 19, sy. 4, 2015, ss. 169-74.
Vancouver Mohamed W, Hassanien M, Abokhosheim K. PARAOXONASE-1, MALONDIALDEHYDE, AND GLUTATHIONE REDUCTASE IN TYPE 2 DIABETIC PATIENTS WITH NEPHROPATHY. EASTERN JOURNAL OF MEDICINE. 2015;19(4):169-74.