In vitro immune response of human peripheral blood cells to vitamins C and E.
Since oxygen free radicals exert a noxious effect on cell functions, the purpose of the study was to examine the influence of the antioxidant vitamins C and E on the phagocytic capacity, apoptotic death, production of TNFalpha and IL-10 by human peripheral blood cells. In addition, an attempt to find a correlation between the effect of these vitamins on apoptosis and DNA synthesis was carried out. Peripheral white blood cells obtained from 27 healthy volunteers were incubated for 24 hr without and with vitamins C and E at doses extrapolated from clinical practice. Incubation of cells with vit. C caused a significant increase in the number of latex particles internalized by each individual polymorphonuclear cell, but not by monocytes. Both vitamins did not change the number of cells capable for phagocytosis. By the method of propidium iodide staining for detection of apoptosis, incubation of the cells with 0.2 mg/mL vit. C for 24 hrs caused a 39% increase in the percentage of apoptotic cells, as compared to those kept at the same incubation conditions without vitamin. 0.125 mg/mL of vit. E did not affect the percentage of apoptotic cells. On the other hand, applying the caspase-3 method for apoptosis detection, vitamins C and E did not affect the caspase-3 activity. Both vitamins caused an inhibition of 3H-TdR incorporation, which was dose-dependent for vit. C. Concentrations of the vitamins lower than those mentioned above did not alter DNA synthesis. While TNFalpha production was not affected by both vitamins, the spontaneous secretion of IL-10 was dose-dependently reduced by vit. C but remained unaltered following incubation with vit. E. The results, although observed in vitro, might be of importance when those vitamins are administered to healthy subjects.
Bergman
Michael
M
Department of Medicine C, Rabin Medical Center, Golda Campus, Petah Tiqva, Israel.
Salman
Hertzel
H
Djaldetti
Meir
M
Fish
Lev
L
Punsky
Igor
I
Bessler
Hanna
H
D000975:Antioxidants; D017209:Apoptosis / Q000187:drug effects*; D001205:Ascorbic Acid / Q000494:pharmacology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D016753:Interleukin-10 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000166:cytology / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D009000:Monocytes / Q000166:cytology / Q000187:drug effects / Q000276:immunology / Q000502:physiology; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects / Q000276:immunology / Q000502:physiology*; D010587:Phagocytosis / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology*
D000975:Antioxidants; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D014810:Vitamin E; D001205:Ascorbic Acid