Thromb Haemost 1985; 54(02): 425-430
DOI: 10.1055/s-0038-1657865
Original Article
Schattauer GmbH Stuttgart

Dietary Supplementation with Vitamin E in Hyperlipoproteinemias: Effects on Plasma Lipid Peroxides, Antioxidant Activity, Prostacyclin Generation and Platelet Aggregability

A Szczeklik
The Departments of Internal Medicine and Pharmacology, Copernicus Academy of Medicine, Cracow, Poland
,
R J Gryglewski
The Departments of Internal Medicine and Pharmacology, Copernicus Academy of Medicine, Cracow, Poland
,
B Domagala
The Departments of Internal Medicine and Pharmacology, Copernicus Academy of Medicine, Cracow, Poland
,
R Dworski
The Departments of Internal Medicine and Pharmacology, Copernicus Academy of Medicine, Cracow, Poland
,
M Basista
The Departments of Internal Medicine and Pharmacology, Copernicus Academy of Medicine, Cracow, Poland
› Author Affiliations
Further Information

Publication History

Received 20 November 1984

Accepted 06 May 1985

Publication Date:
18 July 2018 (online)

Preview

Summary

In a placebo-controlled trial healthy volunteers and patients with hyperlipoproteinemias types II and IV received orally vitamin E at doses of 300 mg and 600 mg daily for 2 weeks. Serum tocopherol levels increased two-fold, but serum concentrations of total lipids, cholesterol, triglycerides, ceruloplasmin and transferrin remained unchanged. Dietary supplementation with vitamin E suppressed elevated concentrations of plasma lipid peroxides and this effect was correlated with an increase in serum antioxidant activity. In patients a mild platelet suppressant effect of vitamin E (600 mg daily) was observed.

Feeding an atherogenic diet to rabbits for a week resulted in elevation of plasma lipid peroxides and a 90% decrease in arterial generation of prostacyclin. Enrichment of the atherogenic diet with 100 mg vitamin E daily prevented the increase in plasma lipid peroxides and protected the prostacyclin generating system in arteries. Thus, in hyperlipoproteinemias vitamin E corrects certain abnormalities of lipid metabolism which might predispose to atherosclerosis.