Reduced Atherosclerotic Burden in Subjects With Genetically Determined Low Oxidative Stress
OBJECTIVE—NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role in human atherosclerosis is still unclear. We hypothesized that a reduced activity of NADPH oxidase might be linked to a reduced at...
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| Published in | Arteriosclerosis, thrombosis, and vascular biology Vol. 33; no. 2; pp. 406 - 412 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Heart Association, Inc
01.02.2013
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| Online Access | Get full text |
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| Abstract | OBJECTIVE—NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role in human atherosclerosis is still unclear. We hypothesized that a reduced activity of NADPH oxidase might be linked to a reduced atherosclerotic burden.
METHODS AND RESULTS—Thirty-one women carriers of hereditary deficiency of NOX2, the catalytic subunit of NADPH oxidase, were matched for sex and age with 31 controls and 31 obese women. Flow-mediated dilation and intima-media thickness, 2 surrogate markers of atherosclerosis, serum activity of NOX2, urinary isoprostanes, serum levels of nitrite/nitrate, and platelet production of isoprostanes and nitrite/nitrate were determined. Compared with controls (5.7±3.0% and 0.60±0.11 mm), carriers of NOX2 deficiency had higher flow-mediated dilation (9.2±5.0%; P<0.001) and lower intima-media thickness (0.50±0.11 mm; P=0.002), whereas obese women had lower flow-mediated dilation (3.2±2.1%; P=0.007) and higher intima-media thickness (0.71±0.15 mm; P<0.001). Compared with controls, carriers of NOX2 deficiency had lower urinary isoprostanes (132.6±87.3 versus 82.3±46.0 pg/mg creatinine; P=0.007) and serum NOX2 activity (24.9±19.3 versus 12.8±11.9 pg/mL; P=0.004) and higher serum nitrite/nitrate (23.8±7.6 versus 30.5±6.3 µmol/L; P<0.001), whereas obese women had higher urinary isoprostanes (132.6±87.3 versus 182.2±84.6 pg/mg creatinine; P=0.008) and serum NOX2 activity (24.9±19.3 versus 36.1±18.6 pg/mL; P=0.008) and lower serum nitrite/nitrate (23.8±7.6 versus 12.6±4.2 µmol/L; P<0.001). Flow-mediated dilation correlated with intima-media thickness (r=–0.433; P<0.001), serum NOX2 activity (r=–325; P<0.001), and urinary isoprostanes (r=–0.314; P=0.002). Ex vivo study showed that, compared with controls, platelets from carriers of NOX2 deficiency had lower isoprostanes (P<0.001) and higher nitrite/nitrate (P<0.001), whereas platelets from obese women had higher isoprostanes (P<0.001) and lower nitrite/nitrate (P=0.013).
CONCLUSION—The study shows reduced atherosclerotic burden in carriers of NOX2 deficiency, suggesting that oxidative stress generated by this enzymatic pathway is implicated in human atherosclerosis. |
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| AbstractList | OBJECTIVE—NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role in human atherosclerosis is still unclear. We hypothesized that a reduced activity of NADPH oxidase might be linked to a reduced atherosclerotic burden.
METHODS AND RESULTS—Thirty-one women carriers of hereditary deficiency of NOX2, the catalytic subunit of NADPH oxidase, were matched for sex and age with 31 controls and 31 obese women. Flow-mediated dilation and intima-media thickness, 2 surrogate markers of atherosclerosis, serum activity of NOX2, urinary isoprostanes, serum levels of nitrite/nitrate, and platelet production of isoprostanes and nitrite/nitrate were determined. Compared with controls (5.7±3.0% and 0.60±0.11 mm), carriers of NOX2 deficiency had higher flow-mediated dilation (9.2±5.0%; P<0.001) and lower intima-media thickness (0.50±0.11 mm; P=0.002), whereas obese women had lower flow-mediated dilation (3.2±2.1%; P=0.007) and higher intima-media thickness (0.71±0.15 mm; P<0.001). Compared with controls, carriers of NOX2 deficiency had lower urinary isoprostanes (132.6±87.3 versus 82.3±46.0 pg/mg creatinine; P=0.007) and serum NOX2 activity (24.9±19.3 versus 12.8±11.9 pg/mL; P=0.004) and higher serum nitrite/nitrate (23.8±7.6 versus 30.5±6.3 µmol/L; P<0.001), whereas obese women had higher urinary isoprostanes (132.6±87.3 versus 182.2±84.6 pg/mg creatinine; P=0.008) and serum NOX2 activity (24.9±19.3 versus 36.1±18.6 pg/mL; P=0.008) and lower serum nitrite/nitrate (23.8±7.6 versus 12.6±4.2 µmol/L; P<0.001). Flow-mediated dilation correlated with intima-media thickness (r=–0.433; P<0.001), serum NOX2 activity (r=–325; P<0.001), and urinary isoprostanes (r=–0.314; P=0.002). Ex vivo study showed that, compared with controls, platelets from carriers of NOX2 deficiency had lower isoprostanes (P<0.001) and higher nitrite/nitrate (P<0.001), whereas platelets from obese women had higher isoprostanes (P<0.001) and lower nitrite/nitrate (P=0.013).
CONCLUSION—The study shows reduced atherosclerotic burden in carriers of NOX2 deficiency, suggesting that oxidative stress generated by this enzymatic pathway is implicated in human atherosclerosis. NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role in human atherosclerosis is still unclear. We hypothesized that a reduced activity of NADPH oxidase might be linked to a reduced atherosclerotic burden.OBJECTIVENADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role in human atherosclerosis is still unclear. We hypothesized that a reduced activity of NADPH oxidase might be linked to a reduced atherosclerotic burden.Thirty-one women carriers of hereditary deficiency of NOX2, the catalytic subunit of NADPH oxidase, were matched for sex and age with 31 controls and 31 obese women. Flow-mediated dilation and intima-media thickness, 2 surrogate markers of atherosclerosis, serum activity of NOX2, urinary isoprostanes, serum levels of nitrite/nitrate, and platelet production of isoprostanes and nitrite/nitrate were determined. Compared with controls (5.7±3.0% and 0.60±0.11 mm), carriers of NOX2 deficiency had higher flow-mediated dilation (9.2±5.0%; P<0.001) and lower intima-media thickness (0.50±0.11 mm; P=0.002), whereas obese women had lower flow-mediated dilation (3.2±2.1%; P=0.007) and higher intima-media thickness (0.71±0.15 mm; P<0.001). Compared with controls, carriers of NOX2 deficiency had lower urinary isoprostanes (132.6±87.3 versus 82.3±46.0 pg/mg creatinine; P=0.007) and serum NOX2 activity (24.9±19.3 versus 12.8±11.9 pg/mL; P=0.004) and higher serum nitrite/nitrate (23.8±7.6 versus 30.5±6.3 µmol/L; P<0.001), whereas obese women had higher urinary isoprostanes (132.6±87.3 versus 182.2±84.6 pg/mg creatinine; P=0.008) and serum NOX2 activity (24.9±19.3 versus 36.1±18.6 pg/mL; P=0.008) and lower serum nitrite/nitrate (23.8±7.6 versus 12.6±4.2 µmol/L; P<0.001). Flow-mediated dilation correlated with intima-media thickness (r=-0.433; P<0.001), serum NOX2 activity (r=-325; P<0.001), and urinary isoprostanes (r=-0.314; P=0.002). Ex vivo study showed that, compared with controls, platelets from carriers of NOX2 deficiency had lower isoprostanes (P<0.001) and higher nitrite/nitrate (P<0.001), whereas platelets from obese women had higher isoprostanes (P<0.001) and lower nitrite/nitrate (P=0.013).METHODS AND RESULTSThirty-one women carriers of hereditary deficiency of NOX2, the catalytic subunit of NADPH oxidase, were matched for sex and age with 31 controls and 31 obese women. Flow-mediated dilation and intima-media thickness, 2 surrogate markers of atherosclerosis, serum activity of NOX2, urinary isoprostanes, serum levels of nitrite/nitrate, and platelet production of isoprostanes and nitrite/nitrate were determined. Compared with controls (5.7±3.0% and 0.60±0.11 mm), carriers of NOX2 deficiency had higher flow-mediated dilation (9.2±5.0%; P<0.001) and lower intima-media thickness (0.50±0.11 mm; P=0.002), whereas obese women had lower flow-mediated dilation (3.2±2.1%; P=0.007) and higher intima-media thickness (0.71±0.15 mm; P<0.001). Compared with controls, carriers of NOX2 deficiency had lower urinary isoprostanes (132.6±87.3 versus 82.3±46.0 pg/mg creatinine; P=0.007) and serum NOX2 activity (24.9±19.3 versus 12.8±11.9 pg/mL; P=0.004) and higher serum nitrite/nitrate (23.8±7.6 versus 30.5±6.3 µmol/L; P<0.001), whereas obese women had higher urinary isoprostanes (132.6±87.3 versus 182.2±84.6 pg/mg creatinine; P=0.008) and serum NOX2 activity (24.9±19.3 versus 36.1±18.6 pg/mL; P=0.008) and lower serum nitrite/nitrate (23.8±7.6 versus 12.6±4.2 µmol/L; P<0.001). Flow-mediated dilation correlated with intima-media thickness (r=-0.433; P<0.001), serum NOX2 activity (r=-325; P<0.001), and urinary isoprostanes (r=-0.314; P=0.002). Ex vivo study showed that, compared with controls, platelets from carriers of NOX2 deficiency had lower isoprostanes (P<0.001) and higher nitrite/nitrate (P<0.001), whereas platelets from obese women had higher isoprostanes (P<0.001) and lower nitrite/nitrate (P=0.013).The study shows reduced atherosclerotic burden in carriers of NOX2 deficiency, suggesting that oxidative stress generated by this enzymatic pathway is implicated in human atherosclerosis.CONCLUSIONSThe study shows reduced atherosclerotic burden in carriers of NOX2 deficiency, suggesting that oxidative stress generated by this enzymatic pathway is implicated in human atherosclerosis. NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role in human atherosclerosis is still unclear. We hypothesized that a reduced activity of NADPH oxidase might be linked to a reduced atherosclerotic burden. Thirty-one women carriers of hereditary deficiency of NOX2, the catalytic subunit of NADPH oxidase, were matched for sex and age with 31 controls and 31 obese women. Flow-mediated dilation and intima-media thickness, 2 surrogate markers of atherosclerosis, serum activity of NOX2, urinary isoprostanes, serum levels of nitrite/nitrate, and platelet production of isoprostanes and nitrite/nitrate were determined. Compared with controls (5.7±3.0% and 0.60±0.11 mm), carriers of NOX2 deficiency had higher flow-mediated dilation (9.2±5.0%; P<0.001) and lower intima-media thickness (0.50±0.11 mm; P=0.002), whereas obese women had lower flow-mediated dilation (3.2±2.1%; P=0.007) and higher intima-media thickness (0.71±0.15 mm; P<0.001). Compared with controls, carriers of NOX2 deficiency had lower urinary isoprostanes (132.6±87.3 versus 82.3±46.0 pg/mg creatinine; P=0.007) and serum NOX2 activity (24.9±19.3 versus 12.8±11.9 pg/mL; P=0.004) and higher serum nitrite/nitrate (23.8±7.6 versus 30.5±6.3 µmol/L; P<0.001), whereas obese women had higher urinary isoprostanes (132.6±87.3 versus 182.2±84.6 pg/mg creatinine; P=0.008) and serum NOX2 activity (24.9±19.3 versus 36.1±18.6 pg/mL; P=0.008) and lower serum nitrite/nitrate (23.8±7.6 versus 12.6±4.2 µmol/L; P<0.001). Flow-mediated dilation correlated with intima-media thickness (r=-0.433; P<0.001), serum NOX2 activity (r=-325; P<0.001), and urinary isoprostanes (r=-0.314; P=0.002). Ex vivo study showed that, compared with controls, platelets from carriers of NOX2 deficiency had lower isoprostanes (P<0.001) and higher nitrite/nitrate (P<0.001), whereas platelets from obese women had higher isoprostanes (P<0.001) and lower nitrite/nitrate (P=0.013). The study shows reduced atherosclerotic burden in carriers of NOX2 deficiency, suggesting that oxidative stress generated by this enzymatic pathway is implicated in human atherosclerosis. |
| Author | Cirillo, Emilia Angelico, Francesco Sanguigni, Valerio Rossi, Paolo Soresina, Annarosa Violi, Francesco Pignatelli, Pasquale Pignata, Claudio Loffredo, Lorenzo Plebani, Alessandro Carnevale, Roberto Finocchi, Andrea Catasca, Elisa |
| AuthorAffiliation | From the Clinica Medica I, Sapienza University of Rome, Rome, Italy (F.V., P.P., R.C., E.C., F.A., L.L.); Department of Pediatrics, University of Naples, Naples, Italy (C.P., E.C.); Department of Pediatrics and Institute of Molecular Medicine “A. Nocivelli”, University of Brescia, Brescia, Italy (A.P., A.S.); University-Hospital Pediatric Department, Bambino Gesù Children Hospital- University of Rome Tor Vergata, Rome, Italy (P.R., A.F.); and Department of Internal Medicine, University of Rome “Tor Vergata”, Rome, Italy (V.S.) |
| AuthorAffiliation_xml | – name: From the Clinica Medica I, Sapienza University of Rome, Rome, Italy (F.V., P.P., R.C., E.C., F.A., L.L.); Department of Pediatrics, University of Naples, Naples, Italy (C.P., E.C.); Department of Pediatrics and Institute of Molecular Medicine “A. Nocivelli”, University of Brescia, Brescia, Italy (A.P., A.S.); University-Hospital Pediatric Department, Bambino Gesù Children Hospital- University of Rome Tor Vergata, Rome, Italy (P.R., A.F.); and Department of Internal Medicine, University of Rome “Tor Vergata”, Rome, Italy (V.S.) |
| Author_xml | – sequence: 1 givenname: Francesco surname: Violi fullname: Violi, Francesco organization: From the Clinica Medica I, Sapienza University of Rome, Rome, Italy (F.V., P.P., R.C., E.C., F.A., L.L.); Department of Pediatrics, University of Naples, Naples, Italy (C.P., E.C.); Department of Pediatrics and Institute of Molecular Medicine “A. Nocivelli”, University of Brescia, Brescia, Italy (A.P., A.S.); University-Hospital Pediatric Department, Bambino Gesù Children Hospital- University of Rome Tor Vergata, Rome, Italy (P.R., A.F.); and Department of Internal Medicine, University of Rome “Tor Vergata”, Rome, Italy (V.S.) – sequence: 2 givenname: Pasquale surname: Pignatelli fullname: Pignatelli, Pasquale – sequence: 3 givenname: Claudio surname: Pignata fullname: Pignata, Claudio – sequence: 4 givenname: Alessandro surname: Plebani fullname: Plebani, Alessandro – sequence: 5 givenname: Paolo surname: Rossi fullname: Rossi, Paolo – sequence: 6 givenname: Valerio surname: Sanguigni fullname: Sanguigni, Valerio – sequence: 7 givenname: Roberto surname: Carnevale fullname: Carnevale, Roberto – sequence: 8 givenname: Annarosa surname: Soresina fullname: Soresina, Annarosa – sequence: 9 givenname: Andrea surname: Finocchi fullname: Finocchi, Andrea – sequence: 10 givenname: Emilia surname: Cirillo fullname: Cirillo, Emilia – sequence: 11 givenname: Elisa surname: Catasca fullname: Catasca, Elisa – sequence: 12 givenname: Francesco surname: Angelico fullname: Angelico, Francesco – sequence: 13 givenname: Lorenzo surname: Loffredo fullname: Loffredo, Lorenzo |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23288160$$D View this record in MEDLINE/PubMed |
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| Snippet | OBJECTIVE—NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but... NADPH oxidase, one of the most important enzymes producing reactive oxidant species, is suggested to play a role in experimental atherosclerosis, but its role... |
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| SubjectTerms | Adult Atherosclerosis - enzymology Atherosclerosis - genetics Atherosclerosis - pathology Atherosclerosis - physiopathology Atherosclerosis - prevention & control Biomarkers - blood Biomarkers - urine Brachial Artery - physiopathology Carotid Intima-Media Thickness Case-Control Studies Chi-Square Distribution Female Genetic Predisposition to Disease Humans Isoprostanes - blood Isoprostanes - urine Italy Linear Models Membrane Glycoproteins - blood Membrane Glycoproteins - genetics Middle Aged NADPH Oxidase 2 NADPH Oxidases - blood NADPH Oxidases - genetics Nitrates - blood Nitrites - blood Obesity - enzymology Obesity - pathology Obesity - physiopathology Oxidative Stress - genetics Phenotype Predictive Value of Tests Vasodilation |
| Title | Reduced Atherosclerotic Burden in Subjects With Genetically Determined Low Oxidative Stress |
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