TY - JOUR
T1 - Ascorbic acid recycling in human erythrocytes is induced by smoking in vivo
AU - Lykkesfeldt, Jens
AU - Viscovich, Michael
AU - Poulsen, Henrik E
PY - 2003/12/1
Y1 - 2003/12/1
N2 - Tobacco smoke contains large numbers of radicals that burden the antioxidant defense and, thus, lower plasma antioxidants, in particular vitamin C or ascorbic acid, is commonly observed among smokers. Ascorbic acid recycling describes the process in which ascorbic acid is oxidized to dehydroascorbic acid by various pathways and subsequently reduced back to ascorbic acid intracellularly, e.g., in erythrocytes, thereby preserving the ascorbic acid pool. In humans who are unable to synthesize ascorbic acid, and in smokers in particular, who are prone to oxidation, this process must be very efficient and of great importance. It has previously been reported that isolated erythrocytes subjected to tobacco smoke in vitro had significantly lower ascorbic acid recycling as compared to controls. In contrast to these findings, we now report that freshly isolated erythrocytes from long-term smokers (n = 39) display a significantly increased rate of ascorbic acid recycling in vivo as compared to those isolated from nonsmokers (n = 31; p <.0001). Preliminary data suggests that the increase results from induction of dehydroascorbic acid reductase activity rather than from differences in energy status, glutathione content, or altered transport capacity. The induction of ascorbic acid recycling as a potential adaptation mechanism of the antioxidant defense to oxidative insults is discussed.
AB - Tobacco smoke contains large numbers of radicals that burden the antioxidant defense and, thus, lower plasma antioxidants, in particular vitamin C or ascorbic acid, is commonly observed among smokers. Ascorbic acid recycling describes the process in which ascorbic acid is oxidized to dehydroascorbic acid by various pathways and subsequently reduced back to ascorbic acid intracellularly, e.g., in erythrocytes, thereby preserving the ascorbic acid pool. In humans who are unable to synthesize ascorbic acid, and in smokers in particular, who are prone to oxidation, this process must be very efficient and of great importance. It has previously been reported that isolated erythrocytes subjected to tobacco smoke in vitro had significantly lower ascorbic acid recycling as compared to controls. In contrast to these findings, we now report that freshly isolated erythrocytes from long-term smokers (n = 39) display a significantly increased rate of ascorbic acid recycling in vivo as compared to those isolated from nonsmokers (n = 31; p <.0001). Preliminary data suggests that the increase results from induction of dehydroascorbic acid reductase activity rather than from differences in energy status, glutathione content, or altered transport capacity. The induction of ascorbic acid recycling as a potential adaptation mechanism of the antioxidant defense to oxidative insults is discussed.
KW - Antioxidants/pharmacology
KW - Ascorbic Acid/blood
KW - Cells, Cultured
KW - Dehydroascorbic Acid/metabolism
KW - Dose-Response Relationship, Drug
KW - Erythrocytes/metabolism
KW - Free Radicals
KW - Glutathione/metabolism
KW - Glutathione Reductase/metabolism
KW - Humans
KW - Malondialdehyde/blood
KW - Oxidative Stress
KW - Oxygen/metabolism
KW - Smoking
KW - Vitamins/metabolism
U2 - 10.1016/j.freeradbiomed.2003.08.006
DO - 10.1016/j.freeradbiomed.2003.08.006
M3 - Journal article
C2 - 14642391
SN - 0891-5849
VL - 35
SP - 1439
EP - 1447
JO - Free Radical Biology & Medicine
JF - Free Radical Biology & Medicine
IS - 11
ER -