Abstract
Because much data have accrued to support the concept that oxidatively modified LDL (Ox-LDL) can promote atherogenesis, the role of antioxidants in decreasing LDL oxidation has assumed great importance. High-dose α-tocopherol supplementation in humans decreases the susceptibility of LDL to oxidation. Hence, the aim of the present study was to ascertain the minimum dose of α-tocopherol that would decrease the susceptibility of LDL to oxidation. The effect of α-tocopherol in doses of 60, 200, 400, 800, and 1200 IU/d on copper-catalyzed LDL oxidation was tested in a randomized placebo-controlled study over 8 weeks. There were eight subjects in each group. Oxidation of LDL was monitored by measuring the formation of conjugated dienes and lipid peroxides by the thiobarbituric acid-reacting substances (TBARS) assay over an 8-hour time course at baseline and after 8 weeks of supplementation. Neither placebo nor any of the doses of α-tocopherol resulted in any side effects or exerted an adverse effect on the plasma lipoprotein profile. However, there was a dose-dependent increase in plasma and lipid-standardized α-tocopherol levels with increasing doses of α-tocopherol supplementation. LDL α-tocopherol appeared to follow a similar trend. When the time-course curves of LDL oxidation and the kinetics of LDL oxidation were examined, there was no significant effect at 8 weeks compared with baseline in the groups that received placebo or α-tocopherol 60 or 200 IU/d. However, in the groups that received at least 400 IU/d α-tocopherol, there was a decreased susceptibility of LDL to oxidation, as shown by the mean levels in the time-course curves, prolongation in the lag phase, and a decrease in the oxidation rate. Furthermore, both plasma and LDL α-tocopherol correlated significantly with the lag phase of oxidation and inversely with the oxidation rate. The results of the present study show that the minimum dose of α-tocopherol needed to significantly decrease the susceptibility of LDL to oxidation is 400 IU/d.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 190-198 |
| Number of pages | 9 |
| Journal | Arteriosclerosis, Thrombosis, and Vascular Biology |
| Volume | 15 |
| Issue number | 2 |
| State | Published - Feb 1995 |
| Externally published | Yes |
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Keywords
- α-tocopherol
- Antioxidants
- Atherosclerosis
- LDL oxidation
- Lipid peroxidation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
The effect of α-tocopherol supplementation on LDL oxidation : A dose-response study. / Jialal, Ishwarlal; Fuller, Cindy J.; Huet, Beverley A.
In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 15, No. 2, 02.1995, p. 190-198.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The effect of α-tocopherol supplementation on LDL oxidation
T2 - A dose-response study
AU - Jialal, Ishwarlal
AU - Fuller, Cindy J.
AU - Huet, Beverley A.
PY - 1995/2
Y1 - 1995/2
N2 - Because much data have accrued to support the concept that oxidatively modified LDL (Ox-LDL) can promote atherogenesis, the role of antioxidants in decreasing LDL oxidation has assumed great importance. High-dose α-tocopherol supplementation in humans decreases the susceptibility of LDL to oxidation. Hence, the aim of the present study was to ascertain the minimum dose of α-tocopherol that would decrease the susceptibility of LDL to oxidation. The effect of α-tocopherol in doses of 60, 200, 400, 800, and 1200 IU/d on copper-catalyzed LDL oxidation was tested in a randomized placebo-controlled study over 8 weeks. There were eight subjects in each group. Oxidation of LDL was monitored by measuring the formation of conjugated dienes and lipid peroxides by the thiobarbituric acid-reacting substances (TBARS) assay over an 8-hour time course at baseline and after 8 weeks of supplementation. Neither placebo nor any of the doses of α-tocopherol resulted in any side effects or exerted an adverse effect on the plasma lipoprotein profile. However, there was a dose-dependent increase in plasma and lipid-standardized α-tocopherol levels with increasing doses of α-tocopherol supplementation. LDL α-tocopherol appeared to follow a similar trend. When the time-course curves of LDL oxidation and the kinetics of LDL oxidation were examined, there was no significant effect at 8 weeks compared with baseline in the groups that received placebo or α-tocopherol 60 or 200 IU/d. However, in the groups that received at least 400 IU/d α-tocopherol, there was a decreased susceptibility of LDL to oxidation, as shown by the mean levels in the time-course curves, prolongation in the lag phase, and a decrease in the oxidation rate. Furthermore, both plasma and LDL α-tocopherol correlated significantly with the lag phase of oxidation and inversely with the oxidation rate. The results of the present study show that the minimum dose of α-tocopherol needed to significantly decrease the susceptibility of LDL to oxidation is 400 IU/d.
AB - Because much data have accrued to support the concept that oxidatively modified LDL (Ox-LDL) can promote atherogenesis, the role of antioxidants in decreasing LDL oxidation has assumed great importance. High-dose α-tocopherol supplementation in humans decreases the susceptibility of LDL to oxidation. Hence, the aim of the present study was to ascertain the minimum dose of α-tocopherol that would decrease the susceptibility of LDL to oxidation. The effect of α-tocopherol in doses of 60, 200, 400, 800, and 1200 IU/d on copper-catalyzed LDL oxidation was tested in a randomized placebo-controlled study over 8 weeks. There were eight subjects in each group. Oxidation of LDL was monitored by measuring the formation of conjugated dienes and lipid peroxides by the thiobarbituric acid-reacting substances (TBARS) assay over an 8-hour time course at baseline and after 8 weeks of supplementation. Neither placebo nor any of the doses of α-tocopherol resulted in any side effects or exerted an adverse effect on the plasma lipoprotein profile. However, there was a dose-dependent increase in plasma and lipid-standardized α-tocopherol levels with increasing doses of α-tocopherol supplementation. LDL α-tocopherol appeared to follow a similar trend. When the time-course curves of LDL oxidation and the kinetics of LDL oxidation were examined, there was no significant effect at 8 weeks compared with baseline in the groups that received placebo or α-tocopherol 60 or 200 IU/d. However, in the groups that received at least 400 IU/d α-tocopherol, there was a decreased susceptibility of LDL to oxidation, as shown by the mean levels in the time-course curves, prolongation in the lag phase, and a decrease in the oxidation rate. Furthermore, both plasma and LDL α-tocopherol correlated significantly with the lag phase of oxidation and inversely with the oxidation rate. The results of the present study show that the minimum dose of α-tocopherol needed to significantly decrease the susceptibility of LDL to oxidation is 400 IU/d.
KW - α-tocopherol
KW - Antioxidants
KW - Atherosclerosis
KW - LDL oxidation
KW - Lipid peroxidation
UR - http://www.scopus.com/inward/record.url?scp=0028986372&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028986372&partnerID=8YFLogxK
M3 - Article
C2 - 7749825
AN - SCOPUS:0028986372
VL - 15
SP - 190
EP - 198
JO - Arteriosclerosis, Thrombosis, and Vascular Biology
JF - Arteriosclerosis, Thrombosis, and Vascular Biology
SN - 1079-5642
IS - 2
ER -