Fructo-oligosaccharide systemically diminished D-galactose-induced oxidative molecule damages in BALB/cJ mice

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.