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氫氣治療維生素C缺乏引起的神經損傷  02-77086600 

已有 3225 次閱讀 2009-2-10 20:16 |個人分類:飲用氫氣水|系統分類:科研筆記|關鍵字:論文，氫氣，抗氧化

這個研究採用基因缺陷動物模型，對這個模型不太熟悉。有研究發現這種動物在維生素C缺乏時，腦內超氧離子水準升高。看來是一個腦氧化損傷的模型。這個文章也有體外腦片的內容。不過好象不是直接效應，而是用了氫後造成的後續影響。因此說可影響超氧陰離子的說法不準確。最近我們在投稿時，有人根據這個文獻給我們提出：選擇性抗氧化的作用不能明確。有一些強詞奪理。

Hydrogen-rich pure water prevents superoxide formation in brain slices of vitamin C-depleted SMP30/GNL knockout mice

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Yasunori Sato^a, b, 1, Shizuo Kajiyama^c, 1, Akiko Amano^b, Yoshitaka Kondo^b, Toru Sasaki^d, Setsuko Handa^b, Ryoya Takahashi^a, Michiaki Fukui^e, Goji Hasegawa^e, Naoto Nakamura^e, Hikohito Fujinawa^f, Toyotaka Mori^f, Mitsuhiro Ohta^g, Hiroshi Obayashi^h, Naoki Maruyama^b and Akihito Ishigami^{a, b,  ,} 

^aDepartment of Biochemistry, Faculty of Pharmaceutical Sciences, Toho University, Chiba 274-8510, Japan

^bAging Regulation, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan

^cKajiyama Clinic, Kyoto 615-0035, Japan

^dResearch Team for Molecular Biomarker, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan

^eDepartment of Endocrinology and Metabolism, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto 602-8566, Japan

^fI’rom Pharmaceutical Co., LTD., Tokyo 141-0032, Japan

^gDepartment of Medical Biochemistry, Kobe Pharmaceutical University, Kobe 658-8566, Japan

^hInstitute of Bio-Response Informatics, Kyoto 612-8016, Japan

Received 31 July 2008. 

Available online 14 August 2008.

Abstract

Hydrogen is an established anti-oxidant that prevents acute oxidative stress. To clarify the mechanism of hydrogen’s effect in the brain, we administered hydrogen-rich pure water (H₂) to senescence marker protein-30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice, which cannot synthesize vitamin C (VC), also a well-known anti-oxidant. These KO mice were divided into three groups; recipients of H₂, VC, or pure water (H₂O), administered for 33 days. VC levels in H₂ and H₂O groups were <6% of those in the VC group. Subsequently, superoxide formation during hypoxia-reoxygenation treatment of brain slices from these groups was estimated by a real-time biography imaging system, which models living brain tissues, with Lucigenin used as chemiluminescence probe for superoxide. A significant 27.2% less superoxide formed in the H₂ group subjected to ischemia–reperfusion than in the H₂O group. Thus hydrogen-rich pure water acts as an anti-oxidant in the brain slices and prevents superoxide formation.

Keywords: Ascorbic acid; Chemiluminescence; Gluconolactonase; Hydrogen-rich pure water; Oxidative stress; ROS; Senescence marker protein-30; Superoxide; Vitamin C

Abbreviations: EDTA, ethylenediaminetetraacetic acid; GNL, gluconolactonase; HPLC, high-performance liquid chromatography; KO, knockout; ROS, reactive oxygen species; SMP30, senescence marker protein-30; SOD, superoxide dismutase; VC, vitamin C

Article Outline

Materials and methods

Results

Effect of hydrogen-rich pure water on body weight

Total vitamin C levels in the brain after ingestion of hydrogen-rich pure water

Superoxide formation during hypoxia-reoxygenation in a model of the living brain

Discussion

Acknowledgements

References

全文

关于这个动物模型的重要参考文献：Senescence marker protein-30 基因是对抗细胞内游离钙离子的重要蛋白，这个蛋白的名字说明与衰老有密切的关系，当这个蛋白缺乏的时候，细胞尽管没有表面异常，但对TNF引起的细胞碉亡非常敏感，说明这个模型非常容易发生细胞损伤，该研究有必要深入，提示氢气对碉亡的影响有比较深刻的细胞信号背景，也许是通过影响细胞内游离钙离子发挥重要作用。可惜一直没有后续研究。

文章全文可以从这里获得：http://ajp.amjpathol.org/cgi/reprint/161/4/1273

Am J Pathol. 2002 Oct;161(4):1273-81.

Senescence marker protein-30 knockout mouse liver is highly susceptible to tumor necrosis factor-alpha- and Fas-mediated apoptosis.

Ishigami A, Fujita T, Handa S, Shirasawa T, Koseki H, Kitamura T, Enomoto N, Sato N, Shimosawa T, Maruyama N.

Department of Molecular Pathology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. ishigami@tmig.or.jp

Abstract

Senescence marker protein-30 (SMP30) is a calcium-binding protein that decreases in an androgen-independent manner with aging. To elucidate the physiological role of this protein, we introduced a null mutation of the SMP30 gene into the germ line of mice. Despite the complete lack of SMP30 (SMP30-/-), these mutant mice were indistinguishable from their wild-type (SMP30+/+) littermates in terms of development and fertilization capability. We then investigated the tissue susceptibility for apoptosis induced by cytokine using primary cultured hepatocytes, because SMP30 could rescue cells from cell death caused by calcium influx, using a calcium ionophore as previously described. SMP30-/- hepatocytes were found to be more susceptible to apoptosis induced by tumor necrosis factor-alpha (TNF-alpha) plus actinomycin D (ActD) than SMP30+/+ hepatocytes. In addition, the TNF-alpha/ActD-induced caspase-8 activity in SMP30-/- hepatocytes was twofold greater than that in SMP30+/+ hepatocytes. In contrast, no significant difference was observed in the TNF-alpha/ActD-induced nuclear factor-kappa B activation of SMP30+/+ versus SMP30-/- hepatocytes, indicating that SMP30 is not related to TNF-alpha/ActD-induced nuclear factor-kappa B activation itself. Moreover, deletion of the SMP30 gene enhanced liver injury after treatment in vivo with anti-Fas antibody and the SMP30+/- mice showed intermediate susceptibility to Fas-induced apoptosis. Collectively, these results demonstrate that SMP30 acts to protect cells from apoptosis.

PMID: 12368201 [PubMed – indexed for MEDLINE]PMCID: PMC1867294Free PMC Article

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