Decline in glutathione peroxidase activity is a reason for brain senescence: consumption of green tea catechin prevents the decline in its activity and protein oxidative damage in ageing mouse brain.

The accumulation of oxidative damage is believed to contribute to senescence. We have previously found that the consumption of green tea catechins (GT-catechin), which are potent antioxidants, decreases oxidative damage to DNA and improves brain function in aged mice with accelerated senescence (SAMP10 mice). To investigate the mechanisms underlying the beneficial effects of GT-catechin, we measured the activities of antioxidative enzymes in the brains of aged SAMP10 mice. The activity of glutathione peroxidase (GPx), an essential enzyme for reduction of hydrogen and lipid peroxides, was significantly lower in aged mice than in younger ones. However, the decline in activity was prevented in aged mice that had consumed GT-catechin. The increased level of carbonyl proteins, a marker of oxidative damage in proteins, was also significantly reduced in aged mice that had consumed GT-catechin. The activities of superoxide dismutase and catalase were not decreased in aged mice. These results suggest that decreased activity of GPx importantly contributes to brain dysfunction in ageing SAMP10 mice. Furthermore, the intake of GT-catechin protected the decline in GPx activity and age-related oxidative damage in the brain.

Daily consumption of green tea catechin delays memory regression in aged mice.

Almost all elderly people show brain atrophy and cognitive dysfunction, even if they are saved from illness, such as cardiac disease, malignancy and diabetes. Prevention or delay of brain senescence would therefore enhance the quality of life for older persons. Because oxidative stress has been implicated in brain senescence, we investigated the effects of green tea catechin (GT-catechin), a potential antioxidant, in senescence-accelerated (SAMP10) mice. The mouse is a model of brain senescence with short life span, cerebral atrophy and cognitive dysfunction. Mice were fed water containing 0.02% GT-catechin from 1- to 15-month-old. The mean dose was about 35 mg/kg/day. We found that daily consumption of GT-catechin prevented memory regression and DNA oxidative damage in these mice. GT-catechin did not prolong the lifetime of SAMP10 mice, but it did delay brain senescence. These findings suggest that continued intake of GT-catechin might promote healthy ageing of the brain in older persons.