Role of paraoxonase 1 activity and PON1 gene polymorphisms in sickle cell disease

[1]  P. Jagodziński,et al.  Paraoxonase 1 concerning dyslipidaemia, cardiovascular diseases, and mortality in haemodialysis patients , 2021, Scientific Reports.

[2]  S. C. M. A. Yahouédéhou,et al.  Investigation of Lipid Profile and Clinical Manifestations in SCA Children , 2020, Disease markers.

[3]  Y. Oztas,et al.  Altered HDL particle in sickle cell disease: decreased cholesterol content is associated with hemolysis, whereas decreased Apolipoprotein A1 is linked to inflammation , 2019, Lipids in Health and Disease.

[4]  V. Pinto,et al.  Sickle cell disease: a review for the internist , 2019, Internal and Emergency Medicine.

[5]  M. Gidlund,et al.  Paraoxonases (PON) 1, 2, and 3 Polymorphisms and PON-1 Activities in Patients with Sickle Cell Disease , 2019, Antioxidants.

[6]  A. Valladares-Salgado,et al.  Genotypes of Common Polymorphisms in the PON1 Gene Associated with Paraoxonase Activity as Cardiovascular Risk Factor. , 2018, Archives of medical research.

[7]  Mou-Ze Liu,et al.  Association of PON2 Gene Polymorphisms (Ser311Cys and Ala148Gly) With the Risk of Developing Type 2 Diabetes Mellitus in the Chinese Population , 2018, Front. Endocrinol..

[8]  P. Wilgenbus,et al.  Paraoxonase-2 regulates coagulation activation through endothelial tissue factor. , 2018, Blood.

[9]  D. Weatherall,et al.  Sickle cell disease , 2018, Nature Reviews Disease Primers.

[10]  A. Alayash.  Oxidative pathways in the sickle cell and beyond. , 2017, Blood cells, molecules & diseases.

[11]  Rayra P Santiago,et al.  Association of classical markers and establishment of the dyslipidemic sub-phenotype of sickle cell anemia , 2017, Lipids in Health and Disease.

[12]  Lingshu Wang,et al.  The Mechanism of Proinflammatory HDL Generation in Sickle Cell Disease Is Linked to Cell-Free Hemoglobin via Haptoglobin , 2016, PloS one.

[13]  M. Mackness,et al.  Human paraoxonase-1 (PON1): Gene structure and expression, promiscuous activities and multiple physiological roles. , 2015, Gene.

[14]  J. G. Mohanty,et al.  The pathophysiology of extracellular hemoglobin associated with enhanced oxidative reactions , 2015, Front. Physiol..

[15]  K. Akinlade,et al.  Defective lipid metabolism in sickle cell anaemia subjects in vaso-occlusive crisis , 2014, Nigerian medical journal : journal of the Nigeria Medical Association.

[16]  E. Youness,et al.  Oxidant-antioxidant status in Egyptian children with sickle cell anemia: a single center based study. , 2014, Jornal de pediatria.

[17]  M. Phillips.  New insights into the determination of HDL structure by apolipoproteins1 , 2013, Journal of Lipid Research.

[18]  R. Couto,et al.  Levels of high-density lipoprotein cholesterol (HDL-C) among children with steady-state sickle cell disease , 2010, Lipids in Health and Disease.

[19]  G. Vercellotti,et al.  Heme degradation and vascular injury. , 2010, Antioxidants & redox signaling.

[20]  Michele Ana Flores Chaves,et al.  Oxidative process in erythrocytes of individuals with hemoglobin S , 2008, Hematology.

[21]  J. Freedman.  Oxidative stress and platelets. , 2008, Arteriosclerosis, thrombosis, and vascular biology.

[22]  R. D. Couto,et al.  Estrutura, metabolismo e funes fisiolgicas da lipoprotena de alta densidade , 2006 .

[23]  N. Santos,et al.  Frequency of the Q192R and L55M polymorphisms of the human serum paraoxonase gene (PON1) in ten Amazonian Amerindian tribes , 2005 .

[24]  M. Phillips,et al.  High density lipoprotein structure. , 2003, Frontiers in bioscience : a journal and virtual library.

[25]  M. Aviram,et al.  Oxidative stress increases the expression of the CD36 scavenger receptor and the cellular uptake of oxidized low-density lipoprotein in macrophages from atherosclerotic mice: protective role of antioxidants and of paraoxonase. , 2002, Atherosclerosis.

[26]  A. von Eckardstein,et al.  HDL and arteriosclerosis: beyond reverse cholesterol transport. , 2002, Atherosclerosis.

[27]  D. Steinberg,et al.  The oxidative modification hypothesis of atherogenesis: an overview. , 2000, Free radical biology & medicine.

[28]  M. Aviram,et al.  Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions: PON1 esterase and peroxidase-like activities. , 2000, Circulation.

[29]  D. Weatherall,et al.  Red cells I: inherited anaemias , 2000, The Lancet.

[30]  S. Scherer,et al.  Human PON2 gene at 7q21.3: cloning, multiple mRNA forms, and missense polymorphisms in the coding sequence. , 1998, Gene.

[31]  P. Durrington,et al.  Effect of the human serum paraoxonase 55 and 192 genetic polymorphisms on the protection by high density lipoprotein against low density lipoprotein oxidative modification , 1998, FEBS letters.

[32]  P. Lane.  Sickle cell disease. , 1996, Pediatric clinics of North America.

[33]  R. Hegele,et al.  Paraoxonase: biochemistry, genetics and relationship to plasma lipoproteins , 1996, Current opinion in lipidology.

[34]  A. Boulton,et al.  Serum paraoxonase activity, concentration, and phenotype distribution in diabetes mellitus and its relationship to serum lipids and lipoproteins. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[35]  C. Abbott,et al.  Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. , 1993, Atherosclerosis.

[36]  A. Czinner,et al.  Human paraoxonase polymorphism: Hungarian population studies in children and adults. , 1991, International journal of clinical pharmacology, therapy and toxicology.

[37]  P. Mahadevan,et al.  An overview , 2007, Journal of Biosciences.

[38]  L. Iuliano.  The oxidant stress hypothesis of atherogenesis , 2001, Lipids.

[39]  A. Lusis,et al.  Paraoxonase-gene polymorphisms associated with coronary heart disease: support for the oxidative damage hypothesis? , 1998, American journal of human genetics.

[40]  D. Adler,et al.  The molecular basis of the human serum paraoxonase activity polymorphism , 1993, Nature Genetics.