Although the study cannot be directly compared with effects in humans, it appears to counter the results of a controversial meta-analysis published last year that suggested a higher risk of death for people that took vitamin E supplements.
In the new research, scientists used 300 mice bred to age rapidly that normally live for an average 61 weeks. Aged 28 weeks, half of the animals were given daily supplements of vitamin E, equivalent to a dosage of about 1200-2000mg per day in humans.
Although this amount is much higher than the RDA, it has been used without adverse effects in studies on Alzheimer's disease patients.
The mice given vitamin E supplements in the study lived an average of 85 weeks without any negative side effects being observed. The maximal lifespan increased 17 per cent to 136 weeks.
Further, the team from the University of Cadiz in Spain and the University of Buenos Aires in Argentina found that vitamin E supplements appeared to improve the ability of mice to perform in neuromuscular tests, suggesting that the vitamin also improved quality of life as well as longevity.
The vitamin E group was better than the others at crossing a 50 centimetre-high wire tightrope and negotiating a T-shaped maze. As they aged, the differences were even greater, with the mice given regular vitamin E performing up to 45 per cent better at tests.
Writing in the 14 July online issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, the researchers said the findings supported the free radical theory of ageing put forward by Gerschman and Harman in the 1950s.
For example, this theory was supported by the fact that the mice given vitamin E had lower levels of free radical mediated reactions and oxidative damage in their mitochondria, the energy source of all cells.
Normally in ageing there is an increase in products of oxidation.
The vitamin E supplements were also "able to prevent the decrease in the activities of brain enzymes that are mitochondrial markers of ageing" by substantial levels, said Alberto Boveris, professor at the University of Buenos Aires.
The researchers write that the "mitochondrial content of lipid protein oxidation products, an indication of free-radical mediated reactions and oxidative damage, was increased in the brain and liver of ageing mice, and the effect was partially [and significantly] prevented by vitamin E."
This was shown by measuring the protein carbonyl content of brain mitochondria, which increased 33 per cent to 69 per cent at 52 and 76 weeks from 28 weeks, and this increase was markedly prevented (76 per cent and 65 per cent) by vitamin E supplementation measured at the two age points.
The researchers say that further studies are needed to find the threshold for vitamin E doses that provide beneficial effects in the neurological function in ageing mammals.
Boveris and his colleagues are about to begin a new study in mice to see if they can repeat their results with smaller doses of vitamin E.