Protection from oxidative stress by enhanced glycolysis; a possible mechanism of cellular immortalization
H. Kondoh1, M.E. Lleonart2, D. Bernard3 and J. Gil4
1Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University, Japan, 2Department of Pathology, Hospital Vall de’Hebron, Barcelona, Spain, 3Laboratory of Molecular Virology, Faculty of Medicine, Free University of Brussels, Brussels, Belgium and 4Cell Proliferation Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Hospital, London, United Kingdom.
Offprint requests to: Hiroshi Kondoh, Department of Geriatric Medicine, Graduate Schoool of Medicine, Kyoto University, 54 Kawara-chgo, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. e-mail: email@example.com
Summary. Reactive oxygen species (ROS) play a crucial role not only in the physiological signal transduction but also in the pathogenesis of several human diseases such as atherosclerosis, neuro-degenerative diseases, metabolic disorders, aging or cancer amongst others. Oxidative stress is also responsible for cellular and organism senescence, in accordance with what Harman initially proposed in the free radical theory of aging. Recent findings support the notion that protection from oxidative stress can increase life span significantly. We reported that enhanced glycolysis could modulate cellular life span with reduction of oxidative stress. Moreover, the tumor suppressor gene p53 controls post-transcriptionally the level of the glycolytic enzyme, phosphoglycerate mutase (PGM). As enhanced glycolysis is a distinctive and prominent feature of cancer cells (termed the Warburg effect), our findings disclosed a novel aspect of the Warburg effect: the connection between senescence and oxidative stress. Histol Histopathol 22, 85-90 (2007)
Key words: Glycolysis, Senescence, the Wardburg effect, Phosphoglycerate mutase (PGM), Oxidative stress