Antioxidants can lengthen your life

An antioxidant enzyme that protects the energy production of the cells prolong the life of mice by 20%. A world-famous researcher presumes that the method can also be applied on humans.

Antioxidants can prolong your life. If you manipulate the genes of mice into producing excess amounts of the antioxidative enzyme katalase, the mice will live an average of 20% longer.

At the same time, they will age more slowly which can be seen from the reduced tendency to cataract and the reduced age-related weakening of the cardiac muscle. Something similar can most likely be achieved in humans, albeit without the manipulation of human genes. This is the message from one of the heavyweight researchers in biological medicine, the American Peter S. Rabinovitch, professor of pathology at University of Washington. Rabinovitch is famous for his share in the development of the so-called flow cytometry, a technique for counting and sorting cells according to their biologic abilities. Flow cytometry is used every day around the world when researchers gather up and count cancer cells, cells with particular genetic abilities, etc.

The enzyme katalase which is what this is all about is a well-known antioxidant. It neutralizes hydrogen peroxide and thereby prevents the formation of free oxygen radicals which would otherwise be able to destroy the DNA of the cells, thereby causing cancer and killing the cells.

Rabinovitch and his team manipulated the DNA of the mice in three different ways. Some of them were made capable of producing more katalase in the cell nuclei where the DNA is located. Some of them were manipulated into producing more katalase in the liquid interior of the cells, the cytoplasma. Finally, the third group was manipulated into forming more katalase in the mitochondria, i.e. the microscopic energy factories that swim around in the cytoplasma transforming oxygen and carbon into carbon dioxide and water - and energy.

Which mice lived the longest? The last group did! While the first two groups only lived insignificantly longer, the protection of the mitochondria was able to lengthen the life of the mice by 20%.

Protect the mitochondria
The dominating theory is that ageing is connected to a degeneration of these strange micro-organelles that are present in all cells. Mitochondria are present in egg cells but not in spermatozoa and for this reason, both men and women get their mitochondria from their mother. A mitochondrion has its own DNA which is quite fragile towards free radicals compared to the DNA of the cell nucleus. Unfortunately, mitochondria produce free oxygen radicals themselves. This is an inevitable side effect of their function. The formation increases as the mitochondria age which affects the entire mechanism of the cell. It is quite easy to suppose that when the mitochondria age, the cells age as well.

Rabinovitch emphasizes that the new study supports the theory that free radicals cause ageing and that this predominantly takes place in the mitochondria. To a significant degree, this can target the search for life-sustaining medicine - which is one of Rabinovitch's recommendations.

An obvious possibility that Rabinovitch does not mention is already available, i.e. the mineral selenium. Several studies, some of which have been carried out by Rabinovitch himself, have shown that selenium prevents cancer and studies initiated in order to finally settle this matter are ongoing. In countries where the soil is poor in selenium - as in the UK - a selenium supplement will result in a significantly increased production of the antioxidative enzyme glutathione peroxidase (GSHPx).

What is interesting is that GSHPx neutralizes hydrogen peroxide in the exact same way as does katalase.



  • Science (DOI 10.1126/science.1106653).

  • Rudolph RE, Vaughan TL, Kristal AR, Blount PL, Levine DS, Galipeau PC, Prevo LJ, Sanchez CA, Rabinovitch PS, Reid BJ Serum selenium levels in relation to markers of neoplastic progression among persons with Barrett's esophagus. J Natl Cancer Inst. 2003 May 21;95(10):750-7.