X-Message-Number: 25555 Date: Sat, 15 Jan 2005 12:24:10 -0800 (PST) From: Doug Skrecky <> Subject: trace episodic hydrogen peroxide as a life extender? [Episodic 20 mM H2O2 increased human skin cell longevity in vitro by 60%. (ref #1) This intriguing result has not (yet) been followed up on with an in vivo rodent longevity experiment. There was one study on house flies which found that a steady state concentration of 10 mM H2O2 in drinking water increased average lifespan by 9%. (ref #2) However 5 mM H2O2 reduced lifespan by 16%, and 100 mM H2O2 reduced it by 27%. Although 10 mM increased fly's glutathione by 98%, 5 mM actually decreased this by 8%. Perhaps it is just as well that a potential antiaging medication commonly found in the house has been ignored. High doses of hydrogen peroxide accelerate cellular senescence, and anyone taking very low "hormetic" doses of it to prevent aging would be playing Russian roulette, with the philosophy that "what does not kill me makes me stronger." Try terminalia chebula instead. This is a lot safer.] (reference #1) J Cell Biochem. 2004 Oct 15;93(3):588-97. Slow-down of age-dependent telomere shortening is executed in human skin keratinocytes by hormesis-like-effects of trace hydrogen peroxide or by anti-oxidative effects of pro-vitamin C in common concurrently with reduction of intracellular oxidative stress. The cellular life-span of cultivated human skin epidermis keratinocytes NHEK-F was shown to be extended up to 150% of population doubling levels (PDLs) by repetitive addition with two autooxidation-resistant derivatives of ascorbic acid (Asc), Asc-2-O-phosphate (Asc2P), and Asc-2-O-alpha-glucoside (Asc2G), respectively, but to be not extended with Asc itself. In contrast, hydrogen peroxide (H(2)O(2)) as dilute as 20 microM which was non-cytotoxic to the keratinocytes, or at 60 microM being marginally cytotoxic achieved the cellular longevity, unexpectedly, up to 160 and 120% of PDLs, respectively, being regarded as a hormesis-like stimulatory effect. The lifespan -extended cells that were administered with Asc2P, Asc2G, or 20 microM H(2)O(2) were prevented from senescence-induced symptoms such as PDL-dependent enlargement of a cell size of 14.7 microm finally up to 17.4 microm upon Hayflick's limit-called loss of proliferation ability as estimated with a channelizer, and retained young cell morphological aspects such as thick and compact shape and intense attachment to the culture substratum even upon advanced PDLs, whereas other non-extended cells looked like thin or fibrous shape and large size upon lower PDLs. The PDL-dependent shortening of telomeric DNA of 11.5 kb finally down to 9.12-8.10 kb upon Hayflick's limit was observed in common for each additive-given cells, but was decelerated in the following order: 20 microM H(2)O(2) > Asc2P = Asc2G > 60 microM H(2)O(2) > Asc = no additive, being in accord with the order of cell longevity. Intracellular reactive oxygen species (ROS) was diminished by Asc2P, Asc2G or 20 microM H(2)O(2), but not significantly by Asc or 60 microM H(2)O(2) as estimated by fluorometry using the redox indicator dye CDCFH. There was no appreciable difference among NHEK keratinocytes that were administered with or without diverse additives in terms of telomerase activity per cell, which was 1.40 x 10(4)-4.48 x 10(4) times lower for the keratinocytes than for HeLa cells which were examined as the typical tumor cells. Thus longevity of the keratinocytes was suggested to be achieved by slowdown of age-dependent shortening of telomeric DNA rather than by telomerase; telomeres may suffer from less DNA lesions due to the continuous and thorough repression of intracellular ROS, which was realized either by pro-vitamin C such as Asc2P or Asc2G that exerted an antioxidant ability more persistent than Asc itself or by 20 microM H(2)O(2) which diminished intracellular ROS assumedly through a hormesis-like effect. (reference #2) Exp Gerontol. 1988;23(3):211-6. Effect of hydrogen peroxide administration on life span, superoxide dismutase, catalase, and glutathione in the adult housefly, Musca domestica. The general objective of this study was to further elucidate the relationship between oxidative stress and the aging process. H2O2 is known to be a progenator of reactive oxygen species, such as hydroxyl free radical, by various mechanisms involving, among others, a superoxide anion radical-driven Fenton cycle, or splitting of the 0-0 bond by hemoproteins. Effects of H2O2 administration on life span, activities of superoxide dismutase, catalase, concentrations of endogenous H2O2, and glutathione in the housefly are described. Adult male flies were given various concentrations of H2O2, ranging from 0 to 100 mM H2O2, in their drinking water. Life span was shortened by H2O2 intake except in 10 mM H2O2 administrated flies, which exhibited the longest life span. Flies administered 10 mM H2O2 also contained the highest concentration of reduced glutathione (GSH). Superoxide dismutase and catalase activities were not affected by H2O2 intake. Compensatory elevation in GSH may be responsible for the increase in life span observed in 10 mM H2O2 administered flies. 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