Dietary supplementation with antioxidants improves functions and decreases oxidative stress of leukocytes from prematurely aging mice.
OBJECTIVE
Aging is accompanied by chronic inflammation and oxidative stress, which lead to a marked impairment of immune function and therefore increased mortality. This study assessed the effect of dietary supplementation, for 15 wk, with 5% and 20% (w/w) of biscuits enriched with nutritional doses of vitamins C and E, zinc, selenium, and beta-carotenes on function and oxidative stress parameters of peritoneal leukocytes from middle-aged, prematurely aging mice (PAM) and non-prematurely aging mice (NPAM).


METHODS
After supplementation we measured leukocyte functions (adherence, chemotaxis, phagocytosis, intracellular reactive oxygen species levels, lymphoproliferation, natural killer activity, and interleukin-2 release), antioxidant defenses (superoxide dismutase, glutathione peroxidase, and reduced glutathione), oxidant compounds (extracellular O(2)(-), glutathione disulfide, glutathione disulfide/reduced glutathione ratio, tumor necrosis factor-alpha, nitric oxide, and prostaglandin E(2)), and lipid and DNA oxidative damage, measured by malondialdehyde and 8-oxo,7,8-dihydro-2'-deoxyguanosine levels, respectively.


RESULTS
In general, leukocyte functions were improved and redox homeostasis was restored after intake of antioxidants. In consequence, malondialdehyde and 8-oxo,7,8-dihydro-2'-deoxyguanosine in PAM and NPAM were strikingly decreased after 5% and 20% supplementation (malondialdehyde, P < 0.001 in PAM; P < 0.01 in NPAM after both treatments; 8-oxo,7,8-dihydro-2'-deoxyguanosine, P < 0.01 after 5% supplementation and P < 0.001 after 20% supplementation in PAM and NPAM). Moreover, the effect of the antioxidants was stronger in PAM than in NPAM, and 20% supplementation was more effective than 5%.


CONCLUSIONS
Our data suggest that improvement of leukocyte function and restoration of redox balance after consumption of adequate levels of antioxidants from adulthood may be useful to attain healthy aging, especially in animals with premature aging.
Alvarado
Carmen
C
Department of Physiology (Animal Physiology II), Faculty of Biological Sciences, Complutense University, Madrid, Spain.
Alvarez
Pedro
P
Puerto
Marta
M
Gausserès
Nicolas
N
Jiménez
Liliana
L
De la Fuente
Mónica
M
D000375:Aging / Q000276:immunology*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D001202:Ascitic Fluid / Q000166:cytology; D001205:Ascorbic Acid / Q000008:administration & dosage; D002448:Cell Adhesion; D002455:Cell Division; D002634:Chemotaxis, Leukocyte; D003602:Cytotoxicity, Immunologic; D004249:DNA Damage; D004032:Diet; D019587:Dietary Supplements; D005260:Female; D005978:Glutathione / Q000032:analysis; D005979:Glutathione Peroxidase / Q000378:metabolism; D007962:Leukocytes / Q000187:drug effects* / Q000502:physiology*; D008214:Lymphocytes / Q000187:drug effects / Q000502:physiology; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008813:Mice, Inbred ICR; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010587:Phagocytosis; D012643:Selenium / Q000008:administration & dosage; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage; D015032:Zinc / Q000008:administration & dosage; D019207:beta Carotene / Q000008:administration & dosage
D000975:Antioxidants; D019207:beta Carotene; D014810:Vitamin E; D009569:Nitric Oxide; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D012643:Selenium; D015032:Zinc; D001205:Ascorbic Acid