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Health News Archive 332 - Anti-Aging and Disease
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Anti-Oxidants Reduce Free Radicals, Aging, and Disease

Scientists at Harvard Medical School have found a mechanism behind the damage that oxidative stress causes to cells which results in the deterioration associated with aging and disease. Oxidative stress is caused by highly reactive molecules known as free radicals formed as a byproduct of metabolism. Although free radicals are quenched by antioxidants, the increase in free radical production that occurs with age overwhelms the body's antioxidant defenses, resulting in damage to the cells' DNA, proteins and lipids. The findings were published in the June 1, 2006 issue of the journal Cell.

Azad Bonni, MD, PhD and colleagues discovered that exposure of brain neurons to oxidative stress signals caused by free radicals stimulates the activity of an enzyme called MST, which previous research had determined to be involved in cell death. They also found that once MST is stimulated by oxidative stress, it activates another family of molecules known as FOXO proteins, instructing them to move from the cells' cytoplasm (the body of the cell) into the cell nucleus. The researchers discovered that when FOXO enters the nucleus, it switches on genes that instruct neurons to self-destruct.

"A common molecular denominator in aging and many age-related diseases is oxidative stress," observed Dr Bonni, who is the lead author of the report and an associate professor of pathology at Harvard Medical School. Discovery of the MST-FOXO mechanism is an important piece of information in defining how oxidative stress causes a biological response in neurons. Because oxidative stress in neurons and other cells has been implicated in stroke, heart disease, diabetes, and neurodegenerative and other disorders, the FOXO mechanism could become a target for therapies for these diseases.

Summary

Oxidative stress influences cell survival and homeostasis, but the mechanisms underlying the biological effects of oxidative stress remain to be elucidated. Here, we demonstrate that the protein kinase MST1 mediates oxidative-stress-induced cell death in primary mammalian neurons by directly activating the FOXO transcription factors. MST1 phosphorylates FOXO proteins at a conserved site within the forkhead domain that disrupts their interaction with 14-3-3 proteins, promotes FOXO nuclear translocation, and thereby induces cell death in neurons. We also extend the MST-FOXO signaling link to nematodes. Knockdown of the C. elegans MST1 ortholog CST-1 shortens life span and accelerates tissue aging, while overexpression of cst-1 promotes life span and delays aging. The cst-1-induced life-span extension occurs in a daf-16-dependent manner. The identification of the FOXO transcription factors as major and evolutionarily conserved targets of MST1 suggests that MST kinases play important roles in diverse biological processes including cellular responses to oxidative stress and longevity.

Source: Maria K. Lehtinen, Zengqiang Yuan, Peter R. Boag, Yue Yang, Judit Villén, Esther B.E. Becker, Sara DiBacco, Núria de la Iglesia, Steven Gygi, T. Keith Blackwell and Azad Bonni; A Conserved MST-FOXO Signaling Pathway Mediates Oxidative-Stress Responses and Extends Life Span. Cell, Vol 125, 987-1001, 02 June 2006.

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