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      Ki-Energy (Life-Energy) Protects Isolated Rat Liver Mitochondria from Oxidative Injury

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          Abstract

          We investigated whether ‘Ki-energy’ (life-energy) has beneficial effects on mitochondria. The paradigm we developed was to keep isolated rat liver mitochondria in conditions in which they undergo heat deterioration (39°C for 10 min). After the heat treatment, the respiration of the mitochondria was measured using a Clarke-type oxygen electrode. Then, the respiratory control ratio (RC ratio; the ratio between State-3 and State-4 respiration, which is known to represent the integrity and intactness of isolated mitochondria) was calculated. Without the heat treatment, the RC ratio was >5 for NADH-linked respiration (with glutamate plus malate as substrates). The RC ratio decreased to 1.86–4.36 by the incubation at 39°C for 10 min. However, when Ki-energy was applied by a Japanese Ki-expert during the heat treatment, the ratio was improved to 2.24–5.23. We used five preparations from five different rats, and the significance of the differences of each experiment was either P < 0.05 or P < 0.01 ( n = 3–5). We analyzed the degree of lipid peroxidation in the mitochondria by measuring the amount of TBARS (thiobarbituric acid reactive substances). The amount of TBARS in heat-treated, no Ki-exposed mitochondria was greater than that of the control (no heat-treated, no Ki-exposed). However, the amount was reduced in the heat-treated, Ki-exposed mitochondria (two experiments; both P < 0.05) suggesting that Ki-energy protected mitochondria from oxidative stress. Calcium ions may play an important role in the protection by Ki-energy. Data also suggest that the observed Ki-effect involves, at least, near-infrared radiation (0.8–2.7 μm) from the human body.

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          Most cited references28

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          Mitochondria and apoptosis.

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          A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.
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            Molecular characterization of mitochondrial apoptosis-inducing factor.

            Mitochondria play a key part in the regulation of apoptosis (cell death). Their intermembrane space contains several proteins that are liberated through the outer membrane in order to participate in the degradation phase of apoptosis. Here we report the identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of isolated nuclei. AIF is a flavoprotein of relative molecular mass 57,000 which shares homology with the bacterial oxidoreductases; it is normally confined to mitochondria but translocates to the nucleus when apoptosis is induced. Recombinant AIF causes chromatin condensation in isolated nuclei and large-scale fragmentation of DNA. It induces purified mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Microinjection of AIF into the cytoplasm of intact cells induces condensation of chromatin, dissipation of the mitochondrial transmembrane potential, and exposure of phosphatidylserine in the plasma membrane. None of these effects is prevented by the wide-ranging caspase inhibitor known as Z-VAD.fmk. Overexpression of Bcl-2, which controls the opening of mitochondrial permeability transition pores, prevents the release of AIF from the mitochondrion but does not affect its apoptogenic activity. These results indicate that AIF is a mitochondrial effector of apoptotic cell death.
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                Author and article information

                Journal
                Evid Based Complement Alternat Med
                Evidence-based Complementary and Alternative Medicine
                Evidence-based Complementary and Alternative Medicine
                Oxford University Press
                1741-427X
                1741-4288
                December 2006
                08 June 2006
                : 3
                : 4
                : 475-482
                Affiliations
                1Philadelphia Biomedical Research Institute King of Prussia, PA 19406
                2Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine Philadelphia, PA 19104, USA
                3School of Nishino Breathing Method, Shibuya-ku Tokyo 150, Japan
                Author notes
                For reprints and all correspondence: S. Tsuyoshi Ohnishi, PhD, Philadelphia Biomedical Research Institute, suite 250, 100 Ross Road, King of Prussia. PA 19406, USA. Tel: +1-610-688-6276; Fax: +1-610-254-9332; E-mail: stohnishi@ 123456aol.com
                Article
                10.1093/ecam/nel032
                1697750
                17173111
                35566054-5aa5-42c2-b040-f5edebd32229
                © The Author (2006). Published by Oxford University Press. All rights reserved

                The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

                History
                : 19 October 2005
                : 11 May 2006
                Categories
                Original Articles

                Complementary & Alternative medicine
                reactive oxygen species,oxidative stress,ki-energy,mitochondria,respiratory control ratio,tbars,lipid peroxidation,infrared radiation

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