A single high dose of ascorbic acid and iron is not correlated with oxidative stress in healthy volunteers.
Fe (II) is a potential prooxidant in vivo and can induce cellular oxidative stress. Ascorbic acid (AA) is a powerful physiological antioxidant and, in the presence of free Fe (II), can exhibit prooxidant effects in vitro. However, in vivo prooxidant effects of Fe (II) and AA have not yet been indisputably demonstrated. Here we evaluate the potential toxic effect of supplementation of Fe (II) associated with AA. Nine healthy, nonsmoking male volunteers (20-31 years old) participated in the crossover study design. The volunteers were supplemented with either a dose of 2 g of AA, 150 mg of iron carbonyl or 2 g of AA plus 150 mg of iron carbonyl with a washout period of 15 days between each treatment. AA, iron, ferritin, thiobarbituric acid-reactive substances, catalase, delta-aminolevulinic dehydratase and SH thiol groups were measured in the blood of the volunteers. Plasma AA levels were increased at 2, 5 and 24 h after AA or AA plus iron ingestion. Plasma Fe levels were increased at 2 and 5 h in the AA plus iron group. Erythrocyte malondialdehyde levels decreased at 5 and 24 h after AA and 5 h after AA plus iron ingestion. Catalase activity from erythrocytes was increased 5 h after supplementation with AA plus iron. There was no significant difference between groups in the other biochemical parameters evaluated. Thus, the present study does not support the hypothesis that the combination of high plasma concentrations of AA and iron, or iron alone, could cause in vivo oxidative damage after a single supplementation dose.
Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, Brazil.
Elisângela
E
Colpo
Andreza Fabro
AF
de Bem
Simone
S
Pieniz
Sally Danuta
SD
Schettert
Rosane Maria Souza
RM
dos Santos
Iria Luiza Gomes
IL
Farias
Iara
I
Bertoncello
Cleci Menezes
CM
Moreira
Nilda Vargas
NV
Barbosa
Maria Beatriz
MB
Moretto
João Batista Teixeira
JB
Rocha
D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D001205:Ascorbic Acid / Q000009:adverse effects / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D002374:Catalase / Q000097:blood; D018592:Cross-Over Studies; D004347:Drug Interactions; D005293:Ferritins / Q000097:blood; D006801:Humans; D007501:Iron / Q000097:blood; D019266:Iron, Dietary / Q000009:adverse effects / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology*; D008297:Male; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D000623:Porphobilinogen Synthase / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D055815:Young Adult
D000975:Antioxidants; D019266:Iron, Dietary; D017392:Thiobarbituric Acid Reactive Substances; D005293:Ferritins; D007501:Iron; D002374:Catalase; D000623:Porphobilinogen Synthase; D001205:Ascorbic Acid