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Is sulfite an antiatherogenic compound in wine?

To the Editor:

High intake of fats is strongly correlated with high mortality from coronary heart disease. The lack of this correlation not seen in certain regions of France has been attributed to wine consumption (1). Red wine contains phenolic substances. The antioxidant properties of these compounds may delay the onset of atherogenesis by reducing peroxidative reactions. Sodium sulfite is used as a preservative in foods and as an antioxidant in alcoholic beverages. Sulfite is present in finished wines in concentrations up to ~6 mmol/L. We measured the concentration of plasma sulfite in four healthy volunteers (males; age range, 28-37 years) before and after they drank a glass of wine (200 mL of a 1997 Bordeaux red wine containing ~320 mg/L sodium sulfite). Each volunteer fasted for 12 h before the study. Plasma sulfite was determined by a sensitive HPLC method described by Ji et al. (2). Basal concentrations of sulfite were 0.43-1.20 [micro]mol/L (mean [+ or -] SD, 0.72 [+ or -] 0.05 [micro]mol/L). There was a sharp increase in plasma sulfite that reached maximum concentrations (5.8-9.2 [micro]mol/L) in each individual at 0.5-1.0 h after the consumption of wine (Fig. 1). Thereafter, sulfite concentrations gradually decreased, but were higher at 4 h than basal values (paired t-test, P <0.01).

We examined the in vitro capacity of sulfite to prevent plasma lipid peroxidation. Human plasma was oxidized by incubation with 50 mmol/L 2,2'-azobis-(2-aminopropane) hydrochloride (AAPH) at 37[degrees]C for 6 h with continuous shaking under air. This procedure generates alkyl peroxyl radicals at a constant rate (3). We then evaluated the formation of lipid peroxides as N-methyl-2-phenylindole-reactive substance, using the Bioxytech [R] LPO-586 method (OXIS International) and expressed as malondialdehyde equivalents. Sodium sulfite was added at concentrations of 10 and 100 [micro]mol/L to the samples before incubation with AAPH. Sulfite suppressed the formation of lipid peroxides in a dose-dependent manner (lipid peroxide concentrations: control, 3.78 [+ or -] 1.09 /.mol/L; 10 [micro]mol/L sodium sulfite, 2.51 [+ or -] 0.85 [micro]mol/L; 100 [micro]mol/L sodium sulfite, 2.01 [+ or -] 0.62 [micro]mol/L; ANOVA, P <0.01). In parallel, we examined the antioxidant activity of 100 /.mol/L quercetin (lipid peroxide concentration, 2.11 [+ or -] 0.40 [micro]mol/L; P <0.01), a phenolic compound in red wine that may account for the "French paradox" and thus is the subject of great research interest (4). Sulfite is as strong as quercetin in preventing plasma lipid peroxidation.


Finally we examined the antioxidant activity of orally administered sulfite. Three healthy volunteers drank 80 mg of sodium sulfite in water. Plasma samples from the volunteers were assessed for lipid peroxidation by exposure to 50 mmol/L AAPH. Formation of malondialdehyde was significantly lower in the plasma obtained after sulfite loading in each individual (before loading, 4.4 [+ or -] 0.61 [micro]mol/L; after loading, 3.76 [+ or -] 0.62 [micro]mol/L; paired t-test, P <0.01). Plasma sulfite concentrations were 6.4-10.2 [micro]mol/L at this time point, which were similar to those seen in the volunteers who consumed a glass of wine. Thus, orally administered sulfite is capable of suppressing oxidative stress in plasma.

Several antioxidants have been shown to prevent the progression of atherosclerosis. Red wine contains higher amounts of phenolics than white wine, which may partly explain the French paradox. However, there is little information regarding the absorption of orally administered phenolics; this is partly a result of the lack of reliable assay systems for these compounds in the plasma.

We showed here an increase in plasma sulfite, after the consumption of a glass of wine, to a concentration that may account for increased plasma antioxidant activity. We believe that these data justify further study of the role of sulfite as an antioxidant and antiatherogenic agent. Several important questions should be addressed, including whether there is any correlation between plasma sulfite concentrations and wine consumption or development of cardiovascular events in a large cohort.


(1.) Criqui MH, Ringel BL. Does diet or alcohol explain the French paradox? Lancet 1994;344: 1719-23.

(2.) Ji JA, Savon SR, Jacobsen DW. Determination of total serum sulfite by HPLC with fluorescence detection. Clin Chem 1995;41:897-903.

(3.) Lotito SB, Fraga CG. Catechins delay lipid peroxidation and [alpha]-tocopherol and [beta]-carotene depletion following ascorbate depletion in human plasma. Proc Soc Exp Biol Med 2000;224: 32-8.

(4.) Yamamoto N, Moon JH, Tsushida T, Nagao A, Terao J. Inhibitory effect of quercetin metabolites and their related derivatives on copper ion-induced lipid peroxidation in human low-density lipoprotein. Arch Biochem Biophys 1999; 372:347-54.

Hideki Mitsuhashi


Yoshihisa Nojima *

Third Department of Internal Medicine

Gunma University

School of Medicine


Gunma, 371-8511 Japan

* Author for correspondence. E-mail
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Title Annotation:Letters
Author:Mitsuhashi, Hideki; Ikeuchi, Hidekazu; Nojima, Yoshihisa
Publication:Clinical Chemistry
Article Type:Letter to the editor
Date:Oct 1, 2001
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