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The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation
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Zeitschriftentitel: | British Journal of Clinical Pharmacology |
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Personen und Körperschaften: | , , |
In: | British Journal of Clinical Pharmacology, 44, 1997, 1, S. 94-97 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Wiley
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Schlagwörter: |
author_facet |
Wen, Y. Cooke, T. Feely, J. Wen, Y. Cooke, T. Feely, J. |
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author |
Wen, Y. Cooke, T. Feely, J. |
spellingShingle |
Wen, Y. Cooke, T. Feely, J. British Journal of Clinical Pharmacology The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation Pharmacology (medical) Pharmacology |
author_sort |
wen, y. |
spelling |
Wen, Y. Cooke, T. Feely, J. 0306-5251 1365-2125 Wiley Pharmacology (medical) Pharmacology http://dx.doi.org/10.1046/j.1365-2125.1997.00623.x <jats:p> <jats:italic>Aims Vitamin C (ascorbic acid) is a powerful antioxidant but there is limited information on its ability to prevent LDL oxidation and its interaction with other natural antioxidants in vivo. We assessed the effect of 4 weeks pharmacological supplementation with vitamin C 1 g day<jats:sup>−1</jats:sup></jats:italic> on copper induced LDL oxidation and lipid peroxidation.</jats:p><jats:p> <jats:italic>Methods</jats:italic> Blood samples were obtained at baseline and at the end of 4 weeks supplementation from 11 healthy non‐smokers and also from nine control subjects. Plasma lipid peroxides were measured as malondialdehyde (MDA) by h.p.l.c. The relationship between vitamin C and two other important antioxidants, vitamin E and glutathione, was also studied.</jats:p><jats:p> <jats:italic>Results There was no difference in baseline values between the two groups and the oxidizability of LDL, assessed as the lag phase of conjugated dienes production and the formation of thiobarbituric acid reactive substances (TBARS), remained unchanged after 4 weeks. In the vitamin C supplemented group only, there was a 2.2‐fold increase in plasma ascorbic acid level and a 28% increase in red cell reduced glutathione (GSH) (P<0.001). Vitamin E, measured as α‐tocopherol, in red cells increased significantly (P<0.02) and plasma MDA was reduced (P</jats:italic><0.01).</jats:p><jats:p> <jats:italic>Conclusions</jats:italic> Vitamin C did not alter LDL oxidation but it may have a protective role against lipid peroxidation as shown by decreased plasma MDA levels and enhanced vitamin E and GSH status.</jats:p> The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation British Journal of Clinical Pharmacology |
doi_str_mv |
10.1046/j.1365-2125.1997.00623.x |
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Chemie und Pharmazie |
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Wiley, 1997 |
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1997 |
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Wiley |
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British Journal of Clinical Pharmacology |
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title |
The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_unstemmed |
The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_full |
The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_fullStr |
The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_full_unstemmed |
The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_short |
The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_sort |
the effect of pharmacological supplementation with vitamin c on low‐density lipoprotein oxidation |
topic |
Pharmacology (medical) Pharmacology |
url |
http://dx.doi.org/10.1046/j.1365-2125.1997.00623.x |
publishDate |
1997 |
physical |
94-97 |
description |
<jats:p> <jats:italic>Aims Vitamin C (ascorbic acid) is a powerful antioxidant but there is limited information on its ability to prevent LDL oxidation and its interaction with other natural antioxidants in vivo. We assessed the effect of 4 weeks pharmacological supplementation with vitamin C 1 g day<jats:sup>−1</jats:sup></jats:italic> on copper induced LDL oxidation and lipid peroxidation.</jats:p><jats:p> <jats:italic>Methods</jats:italic> Blood samples were obtained at baseline and at the end of 4 weeks supplementation from 11 healthy non‐smokers and also from nine control subjects. Plasma lipid peroxides were measured as malondialdehyde (MDA) by h.p.l.c. The relationship between vitamin C and two other important antioxidants, vitamin E and glutathione, was also studied.</jats:p><jats:p> <jats:italic>Results There was no difference in baseline values between the two groups and the oxidizability of LDL, assessed as the lag phase of conjugated dienes production and the formation of thiobarbituric acid reactive substances (TBARS), remained unchanged after 4 weeks. In the vitamin C supplemented group only, there was a 2.2‐fold increase in plasma ascorbic acid level and a 28% increase in red cell reduced glutathione (GSH) (P<0.001). Vitamin E, measured as α‐tocopherol, in red cells increased significantly (P<0.02) and plasma MDA was reduced (P</jats:italic><0.01).</jats:p><jats:p> <jats:italic>Conclusions</jats:italic> Vitamin C did not alter LDL oxidation but it may have a protective role against lipid peroxidation as shown by decreased plasma MDA levels and enhanced vitamin E and GSH status.</jats:p> |
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author | Wen, Y., Cooke, T., Feely, J. |
author_facet | Wen, Y., Cooke, T., Feely, J., Wen, Y., Cooke, T., Feely, J. |
author_sort | wen, y. |
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container_start_page | 94 |
container_title | British Journal of Clinical Pharmacology |
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description | <jats:p> <jats:italic>Aims Vitamin C (ascorbic acid) is a powerful antioxidant but there is limited information on its ability to prevent LDL oxidation and its interaction with other natural antioxidants in vivo. We assessed the effect of 4 weeks pharmacological supplementation with vitamin C 1 g day<jats:sup>−1</jats:sup></jats:italic> on copper induced LDL oxidation and lipid peroxidation.</jats:p><jats:p> <jats:italic>Methods</jats:italic> Blood samples were obtained at baseline and at the end of 4 weeks supplementation from 11 healthy non‐smokers and also from nine control subjects. Plasma lipid peroxides were measured as malondialdehyde (MDA) by h.p.l.c. The relationship between vitamin C and two other important antioxidants, vitamin E and glutathione, was also studied.</jats:p><jats:p> <jats:italic>Results There was no difference in baseline values between the two groups and the oxidizability of LDL, assessed as the lag phase of conjugated dienes production and the formation of thiobarbituric acid reactive substances (TBARS), remained unchanged after 4 weeks. In the vitamin C supplemented group only, there was a 2.2‐fold increase in plasma ascorbic acid level and a 28% increase in red cell reduced glutathione (GSH) (P<0.001). Vitamin E, measured as α‐tocopherol, in red cells increased significantly (P<0.02) and plasma MDA was reduced (P</jats:italic><0.01).</jats:p><jats:p> <jats:italic>Conclusions</jats:italic> Vitamin C did not alter LDL oxidation but it may have a protective role against lipid peroxidation as shown by decreased plasma MDA levels and enhanced vitamin E and GSH status.</jats:p> |
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spelling | Wen, Y. Cooke, T. Feely, J. 0306-5251 1365-2125 Wiley Pharmacology (medical) Pharmacology http://dx.doi.org/10.1046/j.1365-2125.1997.00623.x <jats:p> <jats:italic>Aims Vitamin C (ascorbic acid) is a powerful antioxidant but there is limited information on its ability to prevent LDL oxidation and its interaction with other natural antioxidants in vivo. We assessed the effect of 4 weeks pharmacological supplementation with vitamin C 1 g day<jats:sup>−1</jats:sup></jats:italic> on copper induced LDL oxidation and lipid peroxidation.</jats:p><jats:p> <jats:italic>Methods</jats:italic> Blood samples were obtained at baseline and at the end of 4 weeks supplementation from 11 healthy non‐smokers and also from nine control subjects. Plasma lipid peroxides were measured as malondialdehyde (MDA) by h.p.l.c. The relationship between vitamin C and two other important antioxidants, vitamin E and glutathione, was also studied.</jats:p><jats:p> <jats:italic>Results There was no difference in baseline values between the two groups and the oxidizability of LDL, assessed as the lag phase of conjugated dienes production and the formation of thiobarbituric acid reactive substances (TBARS), remained unchanged after 4 weeks. In the vitamin C supplemented group only, there was a 2.2‐fold increase in plasma ascorbic acid level and a 28% increase in red cell reduced glutathione (GSH) (P<0.001). Vitamin E, measured as α‐tocopherol, in red cells increased significantly (P<0.02) and plasma MDA was reduced (P</jats:italic><0.01).</jats:p><jats:p> <jats:italic>Conclusions</jats:italic> Vitamin C did not alter LDL oxidation but it may have a protective role against lipid peroxidation as shown by decreased plasma MDA levels and enhanced vitamin E and GSH status.</jats:p> The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation British Journal of Clinical Pharmacology |
spellingShingle | Wen, Y., Cooke, T., Feely, J., British Journal of Clinical Pharmacology, The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation, Pharmacology (medical), Pharmacology |
title | The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_full | The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_fullStr | The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_full_unstemmed | The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_short | The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
title_sort | the effect of pharmacological supplementation with vitamin c on low‐density lipoprotein oxidation |
title_unstemmed | The effect of pharmacological supplementation with vitamin C on low‐density lipoprotein oxidation |
topic | Pharmacology (medical), Pharmacology |
url | http://dx.doi.org/10.1046/j.1365-2125.1997.00623.x |