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Update on Catalase in the Mitochondria (Monday May 25 2009) You might recall that mice genetically engineered to generate more of the antioxidant catalase in their mitochondria live longer in good health. Similarly, ingested antioxidant compounds engineered to migrate to the mitochondria have much the same effect (but don't go looking for that in the stores - it's only in the lab so far). Other ingested antioxidants are a wash - no effects, or negative effects. Here's an update from the group working on catalase-producing mice: "Age is a major risk for cardiovascular diseases. Although mitochondrial reactive oxygen species have been proposed as one of the causes of aging, their role in cardiac aging remains unclear. We have previously shown that overexpression of catalase targeted to mitochondria (mCAT) prolongs murine median lifespan by 17% to 21% ... Cardiac aging in mice is accompanied by [a number of characteristic biochemical and structural forms of damage and change in the heart, heart tissue, and heart cells]. All of these age-related changes were significantly attenuated in mCAT mice." Much as one would expect: less damage to cells and tissues means a longer life, on average. Link to original article   Share |

Prior News No Alzheimer's in Other Primates Early Stem Stem Cell Therapy for Kidney Disease Hypoxic Response and Calorie Restriction More on Parkinson's Disease as Autophagy Failure Making Sense of Gene Expression Patterns and Aging

Later News More Anti-Cancer Viral Engineering Rapamycin, Autophagy, and Longevity Working With Neurogenesis Telomere Length and Years of Healthy Life Complicating Alzheimer's Disease

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