Protective effects of high-density lipoprotein against oxidative stress are impaired in haemodialysis patients
Introduction. Cardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major cardiovascular risk factor, implicated in atherosclerotic plaque formation. It has been suggested that high-density lipoprotein (HD) has t...
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Published in | Nephrology, dialysis, transplantation Vol. 15; no. 3; pp. 389 - 395 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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Oxford University Press
01.03.2000
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Abstract | Introduction. Cardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major cardiovascular risk factor, implicated in atherosclerotic plaque formation. It has been suggested that high-density lipoprotein (HD) has the capacity to reduce the oxidative modifications of LDL. The aim of this study is to analyse the protective effects of HDL in HD patients. Methods.In vitro copper-induced LDL oxidation was evaluated in 12 patients with chronic renal failure (mean age 61.0±12.8 years) and compared to 25 healthy subjects (mean age 57.3±19.2 years). LDL were incubated in oxygen-saturated PBS, LDL oxidation was initiated by Cu (II) in the presence and absence of HDL and assessed by measuring the absorbance (abs) increase at 234 nm due to conjugated diene formation. Duration of lag time, maximum velocity (Vmax.) of lipid peroxidation, oxidation slope and half-time of maximum diene formation (T ½) were obtained by kinetic modelling analysis. Results. HDL (1.06±0.31 vs 1.23±0.39 mmol/l) and Apo AI (1.17±0.39 vs 1.49±0.20 g/l) levels were decreased in HD patients. In the absence of HDL, LDL obtained from HD patients showed an enhanced susceptibility to oxidation in vitro as demonstrated by the significant decrease in lag time (54.5±22.2 vs 79.4±37.8 min) and a significant increase in Vmax. (0.026±0.006 vs 0.017±0.005 abs/min). In all cases, HDL (from 0.1 to 2 μM) prevented LDL oxidation in vitro; however, this effect was significantly reduced in HD patients: increase in lag time 54.2% vs 150.4% in HD vs controls; increase in T ½ 52.2% vs 124.6% in HD vs controls; decrease in Vmax. 13.5% vs 38.5% in HD vs controls. Conclusions. These results suggest that qualitative abnormalities such as an impairment of HDL-associated enzymes are associated with a decrease of HDL levels during HD. Hence, in addition to the known impairment of reverse cholesterol transport, the reduction of HDL protective capacity against oxidative stress could be involved in the development of HD-induced atherosclerosis. |
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AbstractList | INTRODUCTIONCardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major cardiovascular risk factor, implicated in atherosclerotic plaque formation. It has been suggested that high-density lipoprotein (HD) has the capacity to reduce the oxidative modifications of LDL. The aim of this study is to analyse the protective effects of HDL in HD patients.METHODSIn vitro copper-induced LDL oxidation was evaluated in 12 patients with chronic renal failure (mean age 61.0+/-12.8 years) and compared to 25 healthy subjects (mean age 57.3+/-19.2 years). LDL were incubated in oxygen-saturated PBS, LDL oxidation was initiated by Cu (II) in the presence and absence of HDL and assessed by measuring the absorbance (abs) increase at 234 nm due to conjugated diene formation. Duration of lag time, maximum velocity (V(max.)) of lipid peroxidation, oxidation slope and half-time of maximum diene formation (T (1/2)) were obtained by kinetic modelling analysis.RESULTSHDL (1.06+/-0.31 vs 1.23+/-0.39 mmol/l) and Apo AI (1. 17+/-0.39 vs 1.49+/-0.20 g/l) levels were decreased in HD patients. In the absence of HDL, LDL obtained from HD patients showed an enhanced susceptibility to oxidation in vitro as demonstrated by the significant decrease in lag time (54.5+/-22.2 vs 79.4+/-37.8 min) and a significant increase in V(max.) (0.026+/-0.006 vs 0.017+/-0. 005 abs/min). In all cases, HDL (from 0.1 to 2 microM) prevented LDL oxidation in vitro; however, this effect was significantly reduced in HD patients: increase in lag time 54.2% vs 150.4% in HD vs controls; increase in T (1/2) 52.2% vs 124.6% in HD vs controls; decrease in V(max). 13.5% vs 38.5% in HD vs controls.CONCLUSIONSThese results suggest that qualitative abnormalities such as an impairment of HDL-associated enzymes are associated with a decrease of HDL levels during HD. Hence, in addition to the known impairment of reverse cholesterol transport, the reduction of HDL protective capacity against oxidative stress could be involved in the development of HD-induced atherosclerosis. Cardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major cardiovascular risk factor, implicated in atherosclerotic plaque formation. It has been suggested that high-density lipoprotein (HD) has the capacity to reduce the oxidative modifications of LDL. The aim of this study is to analyse the protective effects of HDL in HD patients. In vitro copper-induced LDL oxidation was evaluated in 12 patients with chronic renal failure (mean age 61.0+/-12.8 years) and compared to 25 healthy subjects (mean age 57.3+/-19.2 years). LDL were incubated in oxygen-saturated PBS, LDL oxidation was initiated by Cu (II) in the presence and absence of HDL and assessed by measuring the absorbance (abs) increase at 234 nm due to conjugated diene formation. Duration of lag time, maximum velocity (V(max.)) of lipid peroxidation, oxidation slope and half-time of maximum diene formation (T (1/2)) were obtained by kinetic modelling analysis. HDL (1.06+/-0.31 vs 1.23+/-0.39 mmol/l) and Apo AI (1. 17+/-0.39 vs 1.49+/-0.20 g/l) levels were decreased in HD patients. In the absence of HDL, LDL obtained from HD patients showed an enhanced susceptibility to oxidation in vitro as demonstrated by the significant decrease in lag time (54.5+/-22.2 vs 79.4+/-37.8 min) and a significant increase in V(max.) (0.026+/-0.006 vs 0.017+/-0. 005 abs/min). In all cases, HDL (from 0.1 to 2 microM) prevented LDL oxidation in vitro; however, this effect was significantly reduced in HD patients: increase in lag time 54.2% vs 150.4% in HD vs controls; increase in T (1/2) 52.2% vs 124.6% in HD vs controls; decrease in V(max). 13.5% vs 38.5% in HD vs controls. These results suggest that qualitative abnormalities such as an impairment of HDL-associated enzymes are associated with a decrease of HDL levels during HD. Hence, in addition to the known impairment of reverse cholesterol transport, the reduction of HDL protective capacity against oxidative stress could be involved in the development of HD-induced atherosclerosis. Introduction. Cardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major cardiovascular risk factor, implicated in atherosclerotic plaque formation. It has been suggested that high-density lipoprotein (HD) has the capacity to reduce the oxidative modifications of LDL. The aim of this study is to analyse the protective effects of HDL in HD patients. Methods.In vitro copper-induced LDL oxidation was evaluated in 12 patients with chronic renal failure (mean age 61.0±12.8 years) and compared to 25 healthy subjects (mean age 57.3±19.2 years). LDL were incubated in oxygen-saturated PBS, LDL oxidation was initiated by Cu (II) in the presence and absence of HDL and assessed by measuring the absorbance (abs) increase at 234 nm due to conjugated diene formation. Duration of lag time, maximum velocity (Vmax.) of lipid peroxidation, oxidation slope and half-time of maximum diene formation (T ½) were obtained by kinetic modelling analysis. Results. HDL (1.06±0.31 vs 1.23±0.39 mmol/l) and Apo AI (1.17±0.39 vs 1.49±0.20 g/l) levels were decreased in HD patients. In the absence of HDL, LDL obtained from HD patients showed an enhanced susceptibility to oxidation in vitro as demonstrated by the significant decrease in lag time (54.5±22.2 vs 79.4±37.8 min) and a significant increase in Vmax. (0.026±0.006 vs 0.017±0.005 abs/min). In all cases, HDL (from 0.1 to 2 μM) prevented LDL oxidation in vitro; however, this effect was significantly reduced in HD patients: increase in lag time 54.2% vs 150.4% in HD vs controls; increase in T ½ 52.2% vs 124.6% in HD vs controls; decrease in Vmax. 13.5% vs 38.5% in HD vs controls. Conclusions. These results suggest that qualitative abnormalities such as an impairment of HDL-associated enzymes are associated with a decrease of HDL levels during HD. Hence, in addition to the known impairment of reverse cholesterol transport, the reduction of HDL protective capacity against oxidative stress could be involved in the development of HD-induced atherosclerosis. |
Author | Dantoine, Thierry Descomps, Bernard Morena, Marion Cristol, Jean-Paul Carbonneau, Marie-Annette Canaud, Bernard |
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Cites_doi | 10.1016/0014-5793(94)80553-9 10.1016/S0272-6386(12)80473-2 10.1051/jbio/1999193020211 10.1093/clinchem/44.1.179 10.1093/ndt/13.9.2281 10.1056/NEJM198904063201407 10.1016/S0022-2275(20)40756-4 10.1681/ASN.V9112082 10.1038/ki.1994.115 10.1016/0021-9150(96)05853-4 10.1007/BF00841817 10.1016/0021-9150(94)05524-M 10.1159/000186303 10.1038/ki.1995.288 10.1056/NEJM197403282901301 10.1016/0891-5849(96)00233-X 10.1016/S0021-9150(96)06040-6 10.1038/ki.1996.186 10.1042/bj3240001 10.1016/0014-5793(91)80962-3 10.1016/0076-6879(86)28066-0 10.1093/oxfordjournals.qjmed.a068888 10.1038/ki.1981.62 10.1161/01.ATV.16.6.784 10.1159/000187287 10.7326/0003-4819-85-1-29 10.3109/10715768909073429 10.1056/NEJM199901143400207 10.1038/ki.1997.233 10.1016/0009-8981(95)06221-1 10.1016/0021-9150(91)90215-O 10.1016/0021-9150(93)90063-Z 10.4049/jimmunol.161.5.2524 10.1016/0021-9150(93)90183-U 10.1016/0891-5849(92)90181-F 10.1038/ki.1992.204 10.1016/0021-9150(94)90203-8 10.1093/ndt/12.11.2312 10.1038/ki.1990.123 10.1093/ndt/14.suppl_1.76 |
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Keywords | Human Kidney disease Oxidative stress Urinary system disease Hemodialysis Male Antioxidant Extrarenal dialysis Chronic Treatment Renal failure Adult Female Lipoprotein HDL Protection |
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Snippet | Introduction. Cardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a... Cardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major... INTRODUCTIONCardiovascular diseases represent the major cause of mortality in haemodialysis (HD) patients. Oxidized low-density lipoprotein (Ox-LDL) is a major... |
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SubjectTerms | Adult Aged Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Copper - pharmacology Emergency and intensive care: renal failure. Dialysis management Female high-density lipoprotein Humans Intensive care medicine Kidney Failure, Chronic - blood lipid peroxidation Lipids - blood Lipoproteins - blood Lipoproteins, HDL - physiology Lipoproteins, LDL - metabolism low-density lipoprotein Male Medical sciences Middle Aged Oxidation-Reduction - drug effects Oxidative Stress - physiology Renal Dialysis - adverse effects |
Title | Protective effects of high-density lipoprotein against oxidative stress are impaired in haemodialysis patients |
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