27 research outputs found

    Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease

    Get PDF
    Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxidative stress evokes irreversible cell death, and propose a novel therapeutic strategy for PD using molecular hydrogen. Hydrogen has an ability to reduce oxidative damage and ameliorate the loss of nigrostriatal dopaminergic neuronal pathway in two experimental animal models. Thus, it is strongly suggested that hydrogen might provide a great advantage to prevent or minimize the onset and progression of PD

    Rice immediately adapts the dynamics of photosynthates translocation to roots in response to changes in soil water environment

    Get PDF
    Rice is susceptible to abiotic stresses such as drought stress. To enhance drought resistance, elucidating the mechanisms by which rice plants adapt to intermittent drought stress that may occur in the field is an important requirement. Roots are directly exposed to changes in the soil water condition, and their responses to these environmental changes are driven by photosynthates. To visualize the distribution of photosynthates in the root system of rice plants under drought stress and recovery from drought stress, we combined X-ray computed tomography (CT) with open type positron emission tomography (OpenPET) and positron-emitting tracer imaging system (PETIS) with 11C tracer. The short half-life of 11C (20.39 min) allowed us to perform multiple experiments using the same plant, and thus photosynthate translocation was visualized as the same plant was subjected to drought stress and then re-irrigation for recovery. The results revealed that when soil is drier, 11C-photosynthates mainly translocated to the seminal roots, likely to promote elongation of the root with the aim of accessing water stored in the lower soil layers. The photosynthates translocation to seminal roots immediately stopped after rewatering then increased significantly in crown roots. We suggest that when rice plant experiencing drought is re-irrigated from the bottom of pot, the destination of 11C-photosynthates translocation immediately switches from seminal root to crown roots. We reveal that rice roots are responsive to changes in soil water conditions and that rice plants differentially adapts the dynamics of photosynthates translocation to crown roots and seminal roots depending on soil conditions

    Short day length-induced decrease of cesium uptake without altering potassium uptake manner in poplar

    Get PDF
    Short day length-induced alteration of potassium (K) localization in perennial trees is believed to be a mechanism for surviving and adapting to severe winters. To investigate the relationship between cesium (Cs) and K localizations, a model tree poplar, hybrid aspen T89, was employed. Under short day length conditions, the amount of 137Cs absorbed through the root and translocated to the root was drastically reduced, but 42K was not. Potassium uptake from the rhizosphere is mediated mainly by KUP/HAK/KT and CNGC transporters. In poplar, however, these genes were constantly expressed under short-day conditions except for a slight increase in the expression a KUP/HAK/KT gene six weeks after the onset of the short-day treatment. These results indicated that the suppression of 137Cs uptake was triggered by short day length but not regulated by competitive Cs+ and K+ transport. We hypothesize that there are separately regulated Cs+ and K+ transport systems in poplar

    Hydrogen in Drinking Water Reduces Dopaminergic Neuronal Loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mouse Model of Parkinson's Disease

    Get PDF
    It has been shown that molecular hydrogen (H2) acts as a therapeutic antioxidant and suppresses brain injury by buffering the effects of oxidative stress. Chronic oxidative stress causes neurodegenerative diseases such as Parkinson's disease (PD). Here, we show that drinking H2-containing water significantly reduced the loss of dopaminergic neurons in PD model mice using both acute and chronic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The concentration-dependency of H2 showed that H2 as low as 0.08 ppm had almost the same effect as saturated H2 water (1.5 ppm). MPTP-induced accumulation of cellular 8-oxoguanine (8-oxoG), a marker of DNA damage, and 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation were significantly decreased in the nigro-striatal dopaminergic pathway in mice drinking H2-containing water, whereas production of superoxide (O2•−) detected by intravascular injection of dihydroethidium (DHE) was not reduced significantly. Our results indicated that low concentration of H2 in drinking water can reduce oxidative stress in the brain. Thus, drinking H2-containing water may be useful in daily life to prevent or minimize the risk of life style-related oxidative stress and neurodegeneration

    陸上植物のセシウム吸収・輸送を制御する分子機構

    No full text

    Therapeutic Approach to Neurodegenerative Diseases by Medical Gases: Focusing on Redox Signaling and Related Antioxidant Enzymes

    Get PDF
    Oxidative stress in the central nervous system is strongly associated with neuronal cell death in the pathogenesis of several neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. In order to overcome the oxidative damage, there are some protective signaling pathways related to transcriptional upregulation of antioxidant enzymes, such as heme oxygenase-1 (HO-1) and superoxide dismutase (SOD)-1/-2. Their expression is regulated by several transcription factors and/or cofactors like nuclear factor-erythroid 2 (NF-E2) related factor 2 (Nrf2) and peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α). These antioxidant enzymes are associated with, and in some cases, prevent neuronal death in animal models of neurodegenerative diseases. They are activated by endogenous mediators and phytochemicals, and also by several gases such as carbon monoxide (CO), hydrogen sulphide (H2S), and hydrogen (H2). These might thereby protect the brain from severe oxidative damage and resultant neurodegenerative diseases. In this paper, we discuss how the expression levels of these antioxidant enzymes are regulated. We also introduce recent advances in the therapeutic uses of medical gases against neurodegenerative diseases

    Alteration of <i>Arabidopsis SLAC1</i> promoter and its association with natural variation in drought tolerance

    No full text
    <div><p>Natural variation for drought tolerance is a major issue in adaptation and geographic distribution of terrestrial plants. Despite the importance, little is known about the genes and molecular mechanisms that determine its naturally occurring diversity. We analyzed the intraspecific drought tolerance variation between 2 accessions of <i>Arabidopsis thaliana</i>, Columbia (Col)-0 and Wassilewskija (Ws)-2. Measurement of weight loss in detached seedlings demonstrated a clear difference between drought-tolerant Col-0 and drought-sensitive Ws-2. They also differed in their stomatal response under drought condition. Using a quantitative genetic approach, we found a significant quantitative locus on chromosome 1. Surveying in the locus, we extrapolated that the <i>SLAC1</i> gene, which is associated with stomatal closure, was likely responsible for the difference of drought tolerance. Comparison of their nucleotide and amino acid sequences revealed that there were few differences in regions encoding <i>SLAC1</i> protein but was a large deletion in <i>SLAC1</i> promoter of Ws-2. Histochemical GUS staining showed that the <i>SLAC1</i> expressed dominantly in guard cells of Col-0, but did less in guard cells of Ws-2. Quantitative PCR analysis also showed that transcript level of <i>SLAC1</i> in guard cells was higher in Col-0 than in Ws-2. The <i>SLAC1</i> transcription analyses indicate low accumulation of <i>SLAC1</i> in guard cells of Ws-2. When taken together, our results suggest that the low drought tolerance of Ws-2 was associated with the deletion of the promoter region of Ws-2 <i>SLAC1</i>.</p></div
    corecore