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

Sato, Yasunori; Kajiyama, Shizuo; Amano, Akiko; Kondo, Yoshitaka; Sasaki, Toru; Handa, Shizuo; Takahashi, Ryutaro; Fukui, Michiaki; Hasegawa, Goji; Nakamura, Naoto; Fujinawa, Hikohito; Mori, Toyotaka; Ohta, Mitsuhiro; Obayashi, Hiroshi; Maruyama, Naoki; Ishigami, Akihito

doi:10.1016/j.bbrc.2008.08.020

Cited by 141 publications

(101 citation statements)

References 27 publications

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“…In addition, vitamin C depletion in SMP30/GNL knockout mice resulted in an increase of superoxide generation in the brain. 16,17) Mice, rats and many other animals can synthesize vitamin C in vivo; however, humans, monkeys and guinea pigs have lost this ability owing to evolutionary changes that yielded point mutations of the gluconolactone oxidase gene. Logically, then, SMP30/GNL must perform other physiological functions, because SMP30/ GNL proteins are produced abundantly in the liver, kidney, pancreas and adrenal cortex of humans.…”

Section: Discussionmentioning

confidence: 99%

Over-expression of Senescence Marker Protein-30 Decreases Reactive Oxygen Species in Human Hepatic Carcinoma Hep G2 Cells

Handa

Maruyama

Ishigami

2009

Biological & Pharmaceutical Bulletin

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Senescence Marker Protein-30 (SMP30) was originally identified as a novel protein in the rat liver, the expression of which decreases androgen-independently with aging. 1,2) SMP30 is a 34 kDa protein expressed mainly in hepatocytes and renal tubular epithelia, 1) and its amino acid sequences are highly conserved among vertebrates, i.e., 70 to 90%, strongly suggesting that the age-dependent decreases of SMP30 reported in the liver, kidney and lung may contribute to senescence.1,3-7) SMP30 transcripts have been detected in multiple mouse tissues including the liver, kidney, brain, lung and testis by reverse transcription-polymerase chain reaction (RT-PCR) analysis. 7) In humans, immunohistochemical staining has localized SMP30 mainly in parenchymal cells of the liver, proximal tubular cells of the kidney, acinal and ductal cells of the pancreas and fasciculata cells of the adrenal cortex.2) The human SMP30 gene, which is located in the p11.3-q11.2 segment of the X chromosome, 4) could be a candidate agent of X-linked diseases mapped to that region.To clarify the physiological functions and the relationships between age-associated decreases of SMP30 and disorders of aged organs, we established SMP30 knockout mice. 8) These knockout animals are viable and fertile but lower in body weight and shorter in life span than the wild-type. 9) Throughout our experiments in vitro and in vivo, the livers of SMP30 knockout mice were far more susceptible to tumor necrosis factor (TNF)-a-and Fas-mediated apoptosis than those from the wild-type. 8) Moreover, histological and biochemical analyses of livers from SMP30 knockout mice showed abnormal accumulations of neutral lipids and phospholipids.9) This abnormal lipid metabolism must increase the tissues' susceptibility to apoptosis. Such changes of SMP30 expression might, then, account for the deterioration of cellular functions and lowered resistance to harmful stimuli in aged tissues.We recently identified SMP30 as a gluconolactonase (GNL, EC 3.1.1.17) that is involved in the vitamin C biosynthetic pathway and found that SMP30/GNL knockout mice cannot synthesize vitamin C in vivo.10) Humans, monkeys and guinea pigs are similarly incapable of synthesizing vitamin C in vivo, because the gluconolactone oxidase gene has mutated throughout evolution; however, mice, rats and many other animals do synthesize vitamin C in vivo. With aging, SMP30/GNL content decreases in the liver, kidney and lung, and such decreases affect the normally copious amount of SMP30/GNL in the livers of younger humans.2) To discern what, if any, functions SMP30/GNL has in the human liver, we transfected the Hep G2 human liver carcinoma cell line with the human SMP30/GNL gene. In the present study, we found that the over-expression of SMP30/GNL in these Hep G2 cells contributed to the decrease of reactive oxygen species (ROS) formation, presumably increasing the cells' state of oxidative stress. MATERIALS AND METHODSCell Culture Stable transfectants expressing the human SMP30/GNL were established as described p...

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Section: Discussionmentioning

confidence: 99%

Over-expression of Senescence Marker Protein-30 Decreases Reactive Oxygen Species in Human Hepatic Carcinoma Hep G2 Cells

Handa

Maruyama

Ishigami

2009

Biological & Pharmaceutical Bulletin

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“…Koyama et al (2008) have shown that H 2 -saturated alkaline electrolyzed water, produced by an alkaline ionized water apparatus, suppresses urinary excretion of exercise-induced 8-hydroxy-2Ј-deoxyguanosine (8-OHdG) in humans compared with a placebo group. Furthermore, Sato et al (2008) have found that consumption of H 2 -saturated water prevents the formation of superoxide anion radicals (O 2 Ϫ˙) in the brain in vivo. These findings also strongly indicate that H 2 rich water is effective in suppressing oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Effect of Molecular Hydrogen Saturated Alkaline Electrolyzed Water on Disuse Muscle Atrophy in Gastrocnemius Muscle

Fujita

Tanaka

Saihara

et al. 2011

J Physiol Anthropol

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The objectives of this paper were to determine the level of oxidative stress in atrophied gastrocnemius, and to verify the effect of molecular hydrogen (H 2 ) saturated alkaline electrolyzed water (HSW) on gastrocnemius atrophy by modifying the redox status, indicated by 8-hydroxy-2Ј-deoxyguanosine (8-OHdG), malondialdehyde (MDA), and superoxide dismutase (SOD)-like activity. Female Wistar rats were divided into four groups: (1) the control (CONT); (2) the Hindlimb unloading (HU, for 3 weeks) given purified normal water (HU-NW); (3) the HU given alkaline electrolyzed reduced water (HU-AEW); and (4) the HU given HSW (HU-HSW). We showed that 8-OHdG, but not MDA, significantly increased by 149% and 145% in HU-NW and HU-AEW, respectively, when compared with CONT. In contrast, there was a trend toward suppression in 8-OHdG levels (increased by 95% compared with CONT) by treatment of HSW, though this effect was not prominent. Additionally, SOD-like activity significantly increased in both HU-NW (184%) and HU-AEW (199%) when compared with CONT. This result suggests the elevation of O 2 Ϫ˙ in the atrophied gastrocnemius. However, upregulation of SOD-like activity in the HU-HSW was increased by only 169% compared with CONT, though this difference is too small to detect statistical significance. HU led to 13% and 15% reduction of gastrocnemius wet weights in HU-NW and HU-AEW, respectively, compared with CONT. And the reduction of gastrocnemius wet weights in HU-HSW was attenuated by 7% compared with CONT. The gastrocnemius wet weights in the HU-HSW group were significantly greater than those in the HU-AEW, but not statistically significant with HU-NW. These results indicate that HU causes an increase in oxidative stress, but, in this experimental protocol, continuous consumption of HSW during HU does not demonstrate successful attenuation of oxidative stress and HU-mediated gastrocnemius atrophy.

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“…9 Although the physiological function of SMP30 is still not entirely clear, our studies using SMP30 knockout mice have revealed that a reduction in SMP30 expression may account for the age-associated deterioration of cellular function and the enhanced susceptibility to harmful stimuli in aged tissue. [10][11][12][13][14][15][16] Recently, we have reported that hepatic SMP30 is closely associated with the pathogenesis of nonalcoholic fatty liver disease in human. 17 Male SMP30 knockout (KO) mice and wild-type (WT) mice were divided into the groups at 7 weeks of age and fed a high fat diet (HFD) or a standard diet (SD) for 8 weeks.…”

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confidence: 99%

Decreased senescence marker protein-30 could be a factor that contributes to the worsening of glucose tolerance in normal aging

Hasegawa

2010

Islets

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

Cited by 141 publications

References 27 publications

Over-expression of Senescence Marker Protein-30 Decreases Reactive Oxygen Species in Human Hepatic Carcinoma Hep G2 Cells

Over-expression of Senescence Marker Protein-30 Decreases Reactive Oxygen Species in Human Hepatic Carcinoma Hep G2 Cells

Effect of Molecular Hydrogen Saturated Alkaline Electrolyzed Water on Disuse Muscle Atrophy in Gastrocnemius Muscle

Decreased senescence marker protein-30 could be a factor that contributes to the worsening of glucose tolerance in normal aging

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