title: Fructo-oligosaccharide systemically diminished D-galactose-induced oxidative molecule damages in BALB/cJ mice.
abstract: Subcutaneous (s.c.) D-galactose (DG) treatment has been shown to facilitate the development of biomarkers for Alzheimer's disease in C57BL/6J mice. The aim of the present study was to determine whether this treatment in young BALB/cJ mice, another mouse strain, enhanced oxidative stress to similar extents shown in older mice, and to further determine the effects of fructo-oligosaccharide (FO), a prebiotic fibre and vitamin E (antioxidant control) on the DG-induced oxidative damage of lipids, proteins and mitochondrial DNA, and erythrocyte antioxidant enzyme activities. Mice (12 weeks of age, n 40) were divided into four groups: vehicle (s.c. saline)+control (modified rodent chow); DG (s.c. 1·2 g/kg body weight)+control; DG+FO (5 %, w/w); DG+vitamin E (α-tocopherol, 0·2 %). Then, the animals were killed after 52 d of treatment. Another natural ageing (NA) group without any injection was killed at 47 weeks of age, which served as an aged control. The results indicated that the DG treatment enhanced malonaldehyde dimethyl acetal (MDA) levels in the plasma, liver and cerebral cortex, and protein carbonyl levels in the liver and hippocampus to similar levels shown in the NA group. FO, similar to α-tocopherol, systemically normalised DG-induced elevations in the levels of MDA in the plasma, liver and cerebral cortex, protein carbonyls in the liver and hippocampus, hepatic mitochondrial 8-oxo-deoxyguanosine and erythrocyte superoxide dismutase activity. In conclusion, the s.c. DG treatment in younger BALB/cJ mice resembled the oxidative status in older mice. FO supplementation systemically prevented DG-induced oxidative stress, probably through its fermentation products and prebiotic effect.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Changhua Christian Hospital, Changhua, Taiwan, ROC.
authors.forename: Chien-Hsun
authors.initials: CH
authors.lastname: Hsia
authors.forename: Cheng-Hsin
authors.initials: CH
authors.lastname: Wang
authors.forename: Yi-Wen
authors.initials: YW
authors.lastname: Kuo
authors.forename: Ying-Jui
authors.initials: YJ
authors.lastname: Ho
authors.forename: Hsiao-Ling
authors.initials: HL
authors.lastname: Chen
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000367:Age Factors; D000375:Aging / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D004043:Dietary Fiber / Q000494:pharmacology; D019587:Dietary Supplements; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D005690:Galactose / Q000008:administration & dosage / Q000009:adverse effects*; D007279:Injections, Subcutaneous; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009844:Oligosaccharides / Q000494:pharmacology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D056692:Prebiotics; D050050:Protein Carbonylation / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D000975:Antioxidants; D004043:Dietary Fiber; D009844:Oligosaccharides; D056692:Prebiotics; D014810:Vitamin E; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D013482:Superoxide Dismutase; D003849:Deoxyguanosine; D005690:Galactose