Considerable evidence exists that smoking significantly lowers the concentration of plasma antioxidants. While for most antioxidants this effect appears to result mainly from altered dietary habits, ascorbic acid has recently been shown to be depleted by smoking per se. However, the direct cause of ascorbate depletion remains unclear. Erythorbic acid is a stereoisomer of ascorbic acid commonly used as antioxidant in foodstuffs and has the same redox properties as ascorbic acid. We therefore investigated if erythorbic acid could be used as a non-isotopic marker of smoking-induced oxidative stress. In a sample of smokers (n 10) and non-smokers (n 10), the pharmacokinetics of erythorbic acid were followed after a single oral dose (1 g) and subsequently, the effect of a 2-week ascorbic acid supplementation (0·5 g/d) on erythorbic acid kinetics was studied in a double-blind, placebo-controlled fashion. There were no significant effects of smoking or supplementation on relative bioavailability (difference in area under curve, AUC0-∞) of erythorbic acid (smokers 357 (SD 119), non-smokers 414 (SD 142) μmol·h/l; P=0·34). Time to reach maximum plasma concentration (Tmax) was significantly less in smokers (P=0·03). If the relative pharmacokinetics of erythorbic acid between smokers and non-smokers compares with those of AA, our present results do not suggest that altered pharmacokinetics is likely to play a major role in the ascorbic acid depletion consistently observed in smokers.