X-Message-Number: 32592
Date: Sun, 23 May 2010 10:25:22 -0700 (PDT)
From: 
Subject: hydrogen & carbon monoxide as solution additives? II

Am J Transplant. 2010 Apr;10(4):763-72. Epub 2010 Feb 25.

Ex vivo application of carbon monoxide in UW solution prevents 
transplant-induced renal ischemia/reperfusion injury in pigs.

Yoshida J, Ozaki KS, Nalesnik MA, Ueki S, Castillo-Rama M, Faleo G, Ezzelarab M,
Nakao A, Ekser B, Echeverri GJ, Ross MA, Stolz DB, Murase N. Department of 
Surgery, Thomas E. Starzl Transplantation Institute, Pittsburgh, PA, USA.
Abstract

    I/R injury is a major deleterious factor of successful kidney 
    transplantation (KTx). Carbon monoxide (CO) is an endogenous gaseous 
    regulatory molecule, and exogenously delivered CO in low concentrations 
    provides potent cytoprotection. This study evaluated efficacies of CO 
    exposure to excised kidney grafts to inhibit I/R injury in the pig KTx 
    model. Porcine kidneys were stored for 48 h in control UW or UW supplemented
    with CO (CO-UW) and autotransplanted in a 14-day follow-up study. In the 
    control UW group, animal survival was 80% (4/5) with peak serum creatinine 
    levels of 12.0 +/- 5.1 mg/dL. CO-UW showed potent protection, and peak 
    creatinine levels were reduced to 6.9 +/- 1.4 mg/dL with 100% (5/5) survival
    without any noticeable adverse event or abnormal COHb value. Control grafts
    at 14 days showed significant tubular damages, focal fibrotic changes and 
    numerous infiltrates. The CO-UW group showed significantly less severe 
    histopathological changes with less TGF-beta and p-Smad3 expression. Grafts 
    in CO-UW also showed significantly lower early mRNA levels for 
    proinflammatory cytokines and less lipid peroxidation. CO in UW provides 
    significant protection against renal I/R injury in the porcine KTx model. Ex
    vivo exposure of kidney grafts to CO during cold storage may therefore be a
    safe strategy to reduce I/R injury.
PMID: 20199500

Invest Ophthalmol Vis Sci. 2010 Jan;51(1):487-92. Epub 2009 Oct 15.

Protection of the retina by rapid diffusion of hydrogen: administration of 
hydrogen-loaded eye drops in retinal ischemia-reperfusion injury.

Oharazawa H, Igarashi T, Yokota T, Fujii H, Suzuki H, Machide M, Takahashi H, 
Ohta S, Ohsawa I. Department of Ophthalmology, Musashikosugi Hospital, Nippon 
Medical School, Kanagawa, Japan.
Abstract

    PURPOSE: Retinal ischemia-reperfusion (I/R) injury by transient elevation of
    intraocular pressure (IOP) is known to induce neuronal damage through the 
    generation of reactive oxygen species. Study results have indicated that 
    molecular hydrogen (H(2)) is an efficient antioxidant gas that selectively 
    reduces the hydroxyl radical (*OH) and suppresses oxidative stress-induced 
    injury in several organs. This study was conducted to explore the 
    neuroprotective effect of H(2)-loaded eye drops on retinal I/R injury. 
    METHODS: Retinal ischemia was induced in rats by raising IOP for 60 minutes.
    H(2)-loaded eye drops were prepared by dissolving H(2) gas into a saline to
    saturated level and administered to the ocular surface continuously during 
    the ischemia and/or reperfusion periods. One day after I/R injury, apoptotic
    cells in the retina were quantified, and oxidative stress was evaluated by 
    markers such as 4-hydroxynonenal and 8-hydroxy-2-deoxyguanosine. Seven days 
    after I/R injury, retinal damage was quantified by measuring the thickness 
    of the retina. RESULTS: When H(2)-loaded eye drops were continuously 
    administered, H(2) concentration in the vitreous body immediately increased 
    and I/R-induced *OH level decreased. The drops reduced the number of retinal
    apoptotic and oxidative stress marker-positive cells and prevented retinal 
    thinning with an accompanying activation of Muller glia, astrocytes, and 
    microglia. The drops improved the recovery of retinal thickness by >70%. 
    CONCLUSIONS: H(2) has no known toxic effects on the human body. Thus, the 
    results suggest that H(2)-loaded eye drops are a highly useful 
    neuroprotective and antioxidative therapeutic treatment for acute retinal 
    I/R injury.
PMID: 19834032

[Could hydrogen extend human lifespan by suppressing infections?]

Shock. 2009 Dec 7. [Epub ahead of print]

Protective Effects of Hydrogen Gas on Murine Polymicrobial Sepsis via Reducing 
Oxidative Stress and HMGB1 Release.

Xie K, Yu Y, Pei Y, Hou L, Chen S, Xiong L, Wang G. 1Department of 
Anesthesiology, General Hospital of Tianjin Medical University, Tianjin 300052, 
P. R. China. Tel: +86-22-60361519. 2Department of Anesthesiology, Xijing 
Hospital, Fourth Military Medical University, Xi'an 710032, Shaanxi Province, P.
R. China. Tel: +86-29-84775337.
Abstract

    Despite recent advances in antibiotic therapy and intensive care, sepsis is 
    still considered to be the most common cause of death in intensive care 
    units (ICU). Excessive production of reactive oxygen species (ROS) plays an 
    important role in the pathogenesis of sepsis. Recently, it has been 
    suggested that molecular hydrogen (H2) exerts a therapeutic antioxidant 
    activity by selectively reducing hydroxyl radicals (*OH, the most cytotoxic 
    ROS) and effectively protects against organ damage induced by 
    ischemia/reperfusion. Therefore, we hypothesized that H2 treatment had a 
    beneficial effect on sepsis. In the present study, we found that H2 
    inhalation starting at 1 and 6 hours after cecal ligation and puncture (CLP)
    or sham operation significantly improved the survival rate of septic mice 
    with moderate or severe CLP in a concentration- and time-dependent manner. 
    Furthermore, moderate or severe CLP mice showed significant multiple organ 
    damage characterized by the increases of lung myeloperoxidase (MPO) 
    activity, wet-to-dry (W/D) weight ratio, protein concentration in 
    bronchoalveolar lavage (BAL), serum biochemical parameters, and organ 
    histopathological scores at 24 hours after CLP operation, which was 
    significantly attenuated by 2% H2 treatment. In addition, we found that the 
    beneficial effects of H2 treatment on sepsis and sepsis-associated organ 
    damage were associated with the decreased levels of oxidative product, 
    increased activities of antioxidant enzymes and reduced levels of 
    high-mobility group box 1 (HMGB1) in serum and tissue. Thus, H2 inhalation 
    may be an effective therapeutic strategy for septic patients.
PMID: 19997046


[Could hydrogen inhibit cancer growth? We'd need a little more proof than this!]

Biol Pharm Bull. 2008 Jan;31(1):19-26.
Inhibitory effect of electrolyzed reduced water on tumor angiogenesis.

Ye J, Li Y, Hamasaki T, Nakamichi N, Komatsu T, Kashiwagi T, Teruya K, Nishikawa
R, Kawahara T, Osada K, Toh K, Abe M, Tian H, Kabayama S, Otsubo K, Morisawa S,
Katakura Y, Shirahata S. Graduate School of Systems Life Sciences, Kyushu 
University, Higashi-ku, Fukuoka 812-8581, Japan.
Abstract

    Vascular endothelial growth factor (VEGF) is a key mediator of tumor 
    angiogenesis. Tumor cells are exposed to higher oxidative stress compared to
    normal cells. Numerous reports have demonstrated that the intracellular 
    redox (oxidation/reduction) state is closely associated with the pattern of 
    VEGF expression. Electrolyzed reduced water (ERW) produced near the cathode 
    during the electrolysis of water scavenged intracellular H(2)O(2) and 
    decreased the release of H(2)O(2) from a human lung adenocarcinoma cell 
    line, A549, and down-regulated both VEGF transcription and protein secretion
    in a time-dependent manner. To investigate the signal transduction pathway 
    involved in regulating VEGF expression, mitogen-activated kinase (MAPK) 
    specific inhibitors, SB203580 (p38 MAPK inhibitor), PD98059 (ERK1/2 
    inhibitor) and JNKi (c-Jun N-terminal protein kinase inhibitor) were 
    applied. The results showed that only PD98059 blocks VEGF expression, 
    suggesting an important role for ERK1/2 in regulating VEGF expression in 
    A549 cells. As well, ERW inhibited the activation of extracellular 
    signal-regulated kinase (ERK) in a time-dependent manner. Co-culture 
    experiments to analyze in vitro tubule formation assay revealed that A549 
    cell-derived conditioned medium significantly stimulated the formation of 
    vascular tubules in all analyzed parameters; tubule total area, tubule 
    junction, number of tubules, and total tubule length. ERW counteracted the 
    effect of A549 cell-conditioned medium and decreased total tube length 
    (p<0.01). The present study demonstrated that ERW down-regulated VEGF gene 
    transcription and protein secretion through inactivation of ERK.
PMID: 18175936
Free text>
http://www.jstage.jst.go.jp/article/bpb/31/1/19/_pdf

J Food Sci. 2007 Jun;72(5):S298-302.
Effect of pH on the taste of alkaline electrolyzed water.

Koseki M, Tanaka Y, Noguchi H, Nishikawa T. Yamawaki Gakuen Junior College, 
4-10-36, Akasaka, Minato-ku, Tokyo 107-8371, Japan
Abstract

    The pH dependence of the taste of alkaline electrolyzed water (AEW) made by 
    electrolyzing bottled mineral waters was examined by sensory evaluation. For
    water with a calcium concentration of 79 or 93 mg/L, the taste of AEW with 
    a pH of 9.5 was considered better than that of the unelectrolyzed water. In 
    contrast, for water with a calcium concentration of 10 mg/L, the taste of 
    the unelectrolyzed water was preferred to that of AEW with a pH of 9.5. 
    Electrolysis reduced the calcium concentrations in waters with calcium 
    concentrations of 79 or 93 mg/L, but did not change the calcium 
    concentration in water with a calcium concentration of 10 mg/L. Electrolysis
    probably improved the taste of water with a higher calcium concentration by
    reducing the calcium concentration; however, the effect of electrolysis on 
    water with a calcium concentration of 10 mg/L is likely to be the result of 
    the pH increase alone.
PMID: 17995745

[If this stuff is so great why isn't everybody at the AMA guzzling it?

Appl Biochem Biotechnol. 2006 Nov;135(2):133-44.

Electrolyzed-reduced water protects against oxidative damage to DNA, RNA, and 
protein.

Lee MY, Kim YK, Ryoo KK, Lee YB, Park EJ. Department of Genetic Engineering, 
Soonchunhyang University, Asan, Chungnam 336-600, Korea.
Abstract

    The generation of reactive oxygen species is thought to cause extensive 
    oxidative damage to various biomolecules such as DNA, RNA, and protein. In 
    this study, the preventive, suppressive, and protective effects of in vitro 
    supplementation with electrolyzed-reduced water on H2O2-induced DNA damage 
    in human lymphocytes were examined using a comet assay. Pretreatment, 
    cotreatment, and posttreatment with electrolyzed-reduced water enhanced 
    human lymphocyte resistance to the DNA strand breaks induced by H2O2 in 
    vitro. Moreover, electrolyzed-reduced water was much more effective than 
    diethylpyrocarbonate-treated water in preventing total RNA degradation at 4 
    and 25 degrees C. In addition, electrolyzed-reduced water completely 
    prevented the oxidative cleavage of horseradish peroxidase, as determined 
    using sodium dodecyl sulfate-polyacrylamide gels. Enhancement of the 
    antioxidant activity of ascorbic acid dissolved in electrolyzed-reduced 
    water was about threefold that of ascorbic acid dissolved in nonelectrolyzed
    deionized water, as measured by a xanthine-xanthine oxidase superoxide 
    scavenging assay system, suggesting an inhibitory effect of electrolyzed 
    reduced water on the oxidation of ascorbic acid.
PMID: 17159237

Biochem Biophys Res Commun. 1997 May 8;234(1):269-74.

Electrolyzed-reduced water scavenges active oxygen species and protects DNA from
oxidative damage.

Shirahata S, Kabayama S, Nakano M, Miura T, Kusumoto K, Gotoh M, Hayashi H, 
Otsubo K, Morisawa S, Katakura Y. Institute of Cellular Regulation Technology, 
Graduate School of Genetic Resources Technology, Kyushu University, Fukuoka, 
Japan
Abstract

    Active oxygen species or free radicals are considered to cause extensive 
    oxidative damage to biological macromolecules, which brings about a variety 
    of diseases as well as aging. The ideal scavenger for active oxygen should 
    be 'active hydrogen'. 'Active hydrogen' can be produced in reduced water 
    near the cathode during electrolysis of water. Reduced water exhibits high 
    pH, low dissolved oxygen (DO), extremely high dissolved molecular hydrogen 
    (DH), and extremely negative redox potential (RP) values. Strongly 
    electrolyzed-reduced water, as well as ascorbic acid, (+)-catechin and 
    tannic acid, completely scavenged O.-2 produced by the hypoxanthine-xanthine
    oxidase (HX-XOD) system in sodium phosphate buffer (pH 7.0). The superoxide
    dismutase (SOD)-like activity of reduced water is stable at 4 degrees C for
    over a month and was not lost even after neutralization, repeated freezing 
    and melting, deflation with sonication, vigorous mixing, boiling, repeated 
    filtration, or closed autoclaving, but was lost by opened autoclaving or by 
    closed autoclaving in the presence of tungsten trioxide which efficiently 
    adsorbs active atomic hydrogen. Water bubbled with hydrogen gas exhibited 
    low DO, extremely high DH and extremely low RP values, as does reduced 
    water, but it has no SOD-like activity. These results suggest that the 
    SOD-like activity of reduced water is not due to the dissolved molecular 
    hydrogen but due to the dissolved atomic hydrogen (active hydrogen). 
    Although SOD accumulated H2O2 when added to the HX-XOD system, reduced water
    decreased the amount of H2O2 produced by XOD. Reduced water, as well as 
    catalase and ascorbic acid, could directly scavenge H2O2. Reduce water 
    suppresses single-strand breakage of DNA b active oxygen species produced by
    the Cu(II)-catalyzed oxidation of ascorbic acid in a dose-dependent manner,
    suggesting that reduced water can scavenge not only O2.- and H2O2, but also
    1O2 and .OH.
PMID: 9169001

Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=32592