Rest of volume 3, Issue 1

The rest of issue 1 of 2000 consists of:

• A summary of the 52nd Annual Meeting of the Gerontological Society of America, by ADNJ de Grey. Highlighted results: Extension of fruit fly maximum lifespan by overexpression of mitochondrial superoxide dismutase. Extension of maximum lifespan in nematode by supplementation of something that has superoxide dismutase and catalase activity.
• A summary of the Oxygen Society/Free Radical Research Society Annual Meeting, by GR Buettner and FQ Schafer, which seemed to be a mixture of lectures and conference. Talks about the importance of nitric oxide in mitochondrial respiration, protein carbonyls as aging markers, various supplements, and iron(II)-dioxygen as main oxidisers.
• A four-part discussion about the paper by Kowald and Kirkwood (http://readingrejuvenationresearch.blogspot.com/2011/01/modeling-role-of-mitochondrial.html) from volume 2, issue 3, that extends de Grey's model on mutant mitochondrial amplification.
• • A letter by SR Primmer adding a selection effect to the demise of mutant mitochondria in replicating cells, by mutant mitochondria-containing cells committing apoptosis. On the other hand, it points out that aged rats have higher percentage of mitochondria with lower membrane potential. It mainly presents an alternative hypothesis to the survival of mutant mitochondria by suggesting that the mitochondrion takes an active role in destroying itself and that the mutant version probably survives by failing to perform the self-destruction. It also claims that telomere shortening will be important in-vivo quoting examples similar to the ones in the article in this issue (http://readingrejuvenationresearch.blogspot.com/2011/04/role-of-cell-senescence-in-human-aging.html)
  • A Kowald gives a short reply saying he can't see how mitochondria can be part of their own destruction given the genes they have, and that various different mutations are amplified (if most genes are needed for self-destruction, then most mutations would stop it from performing that action though)
  • de Grey gives a longer reply pointing out a difference in methodology of the study showing lower membrane potential in older cells making it irrelevant. He also tries to split the theorising of the mechanism of mitochondria destruction from the trigger/selection of which mitochondrion to destruct, (wouldn't keeping them joined lead to simpler theories?) and assigns Primmer's mitochondrial involvement in the self-destruction as part of the mechanism, not the trigger, thus being compatible with the other theory.
  • Fossel finaly editorialises about the topic. All four have different interpretations of the result that mice lacking telomerase are mostly fine until the sixth generation, and they mostly want results on the opposite case, ie when telomerase is turned on all the time on all cells.