Increased oxidative damage in vitamin C deficiency is accompanied by induction of ascorbic acid recycling capacity in young but not mature guinea pigs.
Ascorbic acid (AA) recycling, i.e. the intracellular regeneration of AA from its oxidized forms semidehydroascorbyl radical and dehydroascorbic acid (DHA), presumably has a key function in maintaining redox homeostasis. Like humans, guinea pigs cannot synthesize AA. In the present paper, the effects of severe AA deficiency on the AA recycling capacity in erythrocytes (RBCs) and liver homogenates were studied in young and mature guinea pigs. Twelve animals of each age category were divided into weight-matched groups of six animals and fed either an AA deficient or sufficient diet. After 5 weeks, they were sacrificed and RBC and liver ascorbate recycling was estimated along with glutathione, tocopherols, AA, SOD, and malondialdehyde (MDA). For young animals, AA recycling capacity was significantly increased in RBCs from the deficient group as compared to the controls (p < 0.001). RBC MDA was not increased by incubation with t-butylhydroperoxide (TBH) while the initial MDA level was significantly elevated (p < 0.001). In mature animals, neither RBC recycling nor MDA levels depended on AA status. Liver recycling capacity was not affected by age or diet, while liver MDA was significantly higher in young but not in mature deficient animals compared to respective controls (p < 0.01). In young animals, incubation with TBH resulted in significant MDA formation in the deficient compared to sufficient animals in both liver and RBCs (p < 0.05). RBC glutathione was not significantly changed by age or diet indicating that the observed changes in recycling capacity are enzyme dependent. The results suggest that young guinea pigs may have a more adaptable antioxidant defense system compared to mature animals while also being more susceptible to oxidative stress.
Lykkesfeldt
Jens
J
Department of Pharmacology and Pathobiology, Royal Veterinary and Agricultural University, Frederiksberg, Copenhagen, Denmark. jopl@kvl.dk
D000375:Aging / Q000502:physiology*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism*; D001206:Ascorbic Acid Deficiency / Q000378:metabolism*; D001835:Body Weight; D002374:Catalase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004912:Erythrocytes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006168:Guinea Pigs; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000378:metabolism
D000975:Antioxidants; D014810:Vitamin E; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione; D001205:Ascorbic Acid