Human Longevity: Omega-3 Fatty Acids, Bioenergetics, by R C Valentine; David L Valentine

By R C Valentine; David L Valentine

''Human cells are shielded from the ravages of getting older by way of protective platforms together with novel mechanisms opposed to membrane oxidation brought during this booklet. The booklet proposes a unified thought during which getting older cells confronted with declining strength creation via mitochondria and the fairly excessive fee of defending membranes opposed to oxidation are caused by means of power tension to turn on programmed mobile loss of life. It includes

''This booklet is outfitted at the proposition that we age as our mitochondria age. we advise a revised model of Harman's recognized speculation that includes mitochondrial oxidative and effort stresses because the root explanations of getting older. it truly is renowned that mobile demise or apoptosis is brought on by means of power tension or oxidative tension. there's convincing facts exhibiting that as mitochondria age mitochondrial DNA (mtDNA) accumulates mutations lowering strength output. preserving hugely unsaturated mitochondrial membranes opposed to oxidative rigidity additionally consumes a unprecedented volume of energy''-- Read more...

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C. 1964. Bacterial ferredoxin. Bacteriol. Rev. 28:497–517. 3 Membranes of Deep-­Sea Bacteria as Surrogates for Mitochondrial Membranes of Humans Bacteria first became prominent as model organisms for studies of fundamental aspects of aging and age-­related diseases during the last several decades of the twentieth century. During that era data from bacteria seemed to reinforce the popular (conventional) mitochondrial theory of aging featuring oxidative stress acting as a mutagen and directly driving the aging process.

In the early 1980s it was found that protons pass spontaneously across membranes at amazing rates by a novel proton (cation) tunneling mechanism (Nichols and Deamer, 1980). Controversial at first, this mechanism has been confirmed during studies of the mode of action of gramicidin A. This peptidic antibiotic kills target bacterial cells by catastrophic energy uncoupling caused by breaching of electrochemical gradients of protons essential for energizing the cell. Gramicidin A kills by forming a membrane-­spanning nanotube with a core region containing a thread of water formed by 21 water molecules arranged in single file and matching the thickness of the bilayer.

Mutations partially restoring a wild-­ type fatty acid phenotype occur in spite of the presence of strong selective pressure applied by culturing cells in the presence of high levels of the antibiotic corresponding to the antibiotic resistance gene carried by the transposon system used to construct the mutant. We have found that the presence of the EPA plasmid helped to stabilize the fabB– mutant, allowing us to maintain the EPA recombinant for several years. This involved monthly transfers to fresh media before suppressor mutations finally occurred.

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