Do iron and vitamin C co-supplementation influence platelet function or LDL oxidizability in healthy volunteers?

Objective: To examine the effect of co-supplementation with iron and vitami n C on antioxidant status, platelet function and low density lipoprotein ox idation in normal healthy volunteers. Design: The study was carried out with two groups of 20 subjects each actin g as their own control, comparing presupplemention with postsupplemention. One group was supplemented with iron and the RDA level of vitamin C and the second group with iron and 260 mg/d vitamin C. Setting: The International Antioxidant Research Centre, The Guy's, King's C ollege and St Thomas's School of Biomedical Science, Guy's Campus, London. Subjects: Forty normal healthy volunteers, recruited from the staff of the Medical School and Hospital in which two volunteers withdrew during the stu dy. Interventions: Subjects in both studies were randomly assigned to one of tw o groups (5 males and 5 females group) and received supplements containing iron (14 mg/d) and either 60 mg/d (Group A) or 260 mg/d (Group B) vitamin C for 12 wk. Blood samples were taken at 6 wk and 12 wk, and prior to supple mentation and analysed for iron and antioxidant status (transferrin bound i ron, vitamin C and E, and beta-carotene levels) in both studies. Samples fr om the first study were analysed for the susceptibility of LDL isolated fro m plasma to Cu2+-induced oxidation and samples from the second for platelet function. Results: Transferrin-bound iron was significantly increased (P < 0.05) at 1 2 wk, in Group A subjects (from 14.9 +/- 5.3 mu mol/l to 19.5 +/- 2.3 mu mo l/l; mean +/- s.d.; n = 19), whereas those in Group B showed a significant increase (P < 0.05) after 6 wk (from 15.8 +/- 4.5 mu mol/l to 20.4 +/- 6.6 mu mol/l; n = 19) which decreased at 12 wk (16.3 +/- 5.0 mu mol/l). Plasma total ascorbate significantly increased from an initial level of 59.3 +/- 2 1.3 mu mol/l to 87.6 +/- 29.0 mu mol/l after 6 wk and 81.7 +/- 11.4 mu mol/ l after 12 wk following the Group B supplementation, but only after 12 wk i n Group A (from 64.0 +/- 24.8 mu mol/l to 77.2 +/- 13.2 mu mol/l). Plasma a lpha-tocopherol concentrations were significantly increased after 6 wk and 12 wk with both levels of supplementation (from 24.2 +/- 5.7 mu mol/l Group A and 23.4 +/- 5.3 mu mol/l Group B to 26.3 +/- 5.5 mu mol/l and 25.7 +/- 4.7 mu mol/l respectively at 12 wk). The mean lag phase to oxidation of low density lipoprotein (LDL) was significantly increased in subjects in Group B after 12 wk ingestion of iron and 260 mg vitamin C (from 80.0 +/- 14.8 m in to 97.2 +/- 16.9 min; n = 9). Platelet sensitivity to ADP-induced aggreg ation was significantly decreased (P < 0.05) by 12 wk in Group A (from EC50 2.3 +/- 1.3 mu M to 3.7 +/- 2.2 mu M; n = 10), whereas those receiving hig her vitamin C showed a significant decrease (P<0.05; from EC50 1.9 +/- 0.6 mu M to 3.1 +/- 1.8 mu M) after 6 wk which subsequently increased towards p resupplemental levels (2.6 +/- 1.6 mu M). Platelets from the latter subject s showed a significant reduction in ADP-induced ATP secretion at both 6 wk and 12 wk. Conclusion: The results show modest beneficial effects on LDL oxidation and platelet function following supplementation with iron and vitamin C. No ev idence for pro-oxidant effects was observed.