Study: Vitamin E Extends Lifespan, Improves Life Quality in Mice

9-8-2005 - Vitamin E supplements have recently been regarded as worthless after trials have indicated that they do not help patients with Alzheimer’s disease. However, a new study published in the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology found that vitamin E might extend lifespan and improve the quality of life in humans.

The study, conducted by Professor Dr. Ana Navarro and colleagues at the University of Cadiz, Spain and the University of Buenos Aires, Argentina, found that high doses of vitamin E, equivalent to 1,300 milligrams per day for human use, extended the lifespan of male mice by 40 percent. The maximal lifespan was also extended by 17 percent. Female mice gained a 14 percent increase in their lifespan, while their maximal lifespan was not increased when their diets were supplemented with high vitamin E.

Not only did vitamin E extend the lifespan of the mice, but it improved the quality of their life in terms of their neurological performance as well. The mice given high doses of vitamin E improved their neuromuscular function as indicated by a tightrope test by nine percent at the age of 52 weeks and 28 percent at the age of 78 weeks. The exploratory performance as showed in a T-maze test was improved by 24 percent at the age of 52 weeks and 45 percent at the age of 78 weeks.

In the study, researchers supplemented 5.0 grams of dl-RRR-alpha tocopherol acetate per kilogram of food in the mouse diet. The supplementation started at the age of 28 weeks to avoid any intervention in the normal development and growth of mice. 90 male mice and 90 female mice were used to test the effect of vitamin E on their lifespan or survival. Among the 90 mice, 40 were using vitamin E supplemented diets.

Neurological performance was assessed every two weeks starting at the age of 28 weeks. In addition, a host of biochemical assays were performed in male mice to understand how high doses of vitamin E affect the mice at a molecular level.

The results showed that vitamin E levels were hiked by 2.5 times in the brain issues and seven times in the liver tissues. The increase of alpha-tocopherol in the brain and the liver apparently led to reduction of oxidative damages caused by lipid and protein oxidation products.

Thiobarbituric acid-reactive substances or TBARS and protein carbonyl were indicative of oxidative damages. Normally, protein carbonyl content in brain mitochondria increased by 33 percent at 52 weeks and 69 percent at 76 weeks of age compared to that at 28 weeks. But vitamin E reduced the increase by 76 percent at 52 weeks and 65 percent at 76 weeks of age. The brain mitochondrial content of TBARS increased by 40 percent and 60 percent at week 52 and 76 respectively. But vitamin E reduced the increase by 35 percent and 37 percent at 52 weeks and 76 weeks of age respectively. Protein carbonyl and TBARS contents in liver mitochondria displayed the same pattern in the control and vitamin E supplemented mice, but the difference was less marked.

Mitochondrial enzymatic activities including those of NADH-cytochrome c reductase, cytochrome oxidase, mitochondrial nitro oxidase synthase (mtNOS), and Mn-superoxide mismutase (MnSOD) normally decreased linearly from 35 to 67 percent in the brain and 37 to 40 percent in the liver as the mice aged from 28 weeks to 76 weeks. Vitamin E supplementation reduced the decrease in enzymatic activities by 42 to 66 percent in the brain and 16 to 50 percent in the liver.

The study also found that the rates of respiration f brain mitochondria in active state 3 with malate-glutamate and succinate as substrates decreased by 21-24 percent in 52 wee old mice of the control group. Vitamin E can prevent the decrease by 48 to 50 percent. The preventive effect was also observed in liver mitochondria, but the magnitude of the prevention was smaller.

According to the authors, previous studies found that two grams of vitamin E per day improved cognitive capacity in Alzheimer's disease patients. 1.2 grams per day also benefited healthy elderly.

The evidence offered by this current study supported the concept of mitochondrial hypothesis of aging. The mitochondrial aging theory explains that aging is caused by accumulative oxidative damages and the decrease in the mitochondrial capacity of energy production in the organ and tissues, according to the authors. Vitamin E retards the aging process on both fronts.

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