Masatake Fujimura

ORCID: 0000-0002-8206-7078
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About
Contact & Profiles
Research Areas
  • Mercury impact and mitigation studies
  • Heavy Metal Exposure and Toxicity
  • Endoplasmic Reticulum Stress and Disease
  • Trace Elements in Health
  • Heme Oxygenase-1 and Carbon Monoxide
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Selenium in Biological Systems
  • Anesthesia and Neurotoxicity Research
  • Air Quality and Health Impacts
  • Neuroscience and Neuropharmacology Research
  • Redox biology and oxidative stress
  • Toxic Organic Pollutants Impact
  • Pain Mechanisms and Treatments
  • Environmental Toxicology and Ecotoxicology
  • Advanced Nanomaterials in Catalysis
  • Cancer-related gene regulation
  • Phenothiazines and Benzothiazines Synthesis and Activities
  • Wnt/β-catenin signaling in development and cancer
  • Protein Kinase Regulation and GTPase Signaling
  • Plant Disease Resistance and Genetics
  • Alzheimer's disease research and treatments
  • Sulfur Compounds in Biology
  • Genetic Neurodegenerative Diseases
  • Cardiac Valve Diseases and Treatments
  • Aortic Disease and Treatment Approaches

National Institute for Minamata Disease
2016-2025

Mitsubishi Tanabe Pharma Corporation
2013-2019

All-Russian Scientific Research Institute of Medicinal and Aromatic Plants
2019

Mitsubishi Chemical (Japan)
2013

Toyo University
2006-2008

Tokyo Women's Medical University Adachi Medical Center
2008

Tohoku University
2004

Mitsubishi Corporation (United States)
2002

University of Occupational and Environmental Health Japan
2001

Abstract Glycogen synthase kinase 3 (GSK3) has been identified as a promising target for the treatment of Alzheimer’s disease (AD), where abnormal activation this enzyme associated with hyperphosphorylation tau proteins. This study describes effects selective GSK3 inhibitor, SAR502250, in models neuroprotection and neuropsychiatric symptoms (NPS) AD. In P301L human transgenic mice, SAR502250 attenuated cortex spinal cord. prevented increase neuronal cell death rat embryonic hippocampal...

10.1038/s41598-019-54557-5 article EN cc-by Scientific Reports 2019-12-02

Botrytis cinerea field isolates collected in Japan were screened for resistance to Qo inhibitor fungicides (QoIs). Of the 198 screened, six grew well on a medium containing azoxystrobin, QoI, when salicylhydroxamic acid, an alternative oxidase inhibitor, was present. The mutation cytochrome b gene ( cytb ) characterized. All QoI‐resistant had same (GGT G C T) that led substitution of glycine by alanine at position 143 , which is known confer QoI plant pathogens. To detect this mutation,...

10.1111/j.1365-3059.2008.01909.x article EN Plant Pathology 2008-07-17

Methylmercury (MeHg) toxicity is a continuous environmental problem to human health. The critical role of oxidative stress in the pathogenesis MeHg cytotoxicity has been clarified, but molecular mechanisms underlying MeHg-mediated remain be elucidated. Here we demonstrate post-transcriptional effect on antioxidant selenoenzymes by using MeHg-susceptible cell line. MeHg-induced selenium deficiency leads failure recoding UGA codon for selenocysteine and results degradation major selenoenzyme...

10.1074/jbc.m110.168872 article EN cc-by Journal of Biological Chemistry 2010-11-25

Clinical manifestations of methylmercury (MeHg) intoxication include cerebellar ataxia, concentric constriction visual fields, and sensory auditory disturbances. The symptoms depend on the site MeHg damage, such as cerebellum occipital lobes. However, underlying mechanism MeHg-induced tissue vulnerability remains to be elucidated. In present study, we used a rat model subacute investigate possible blood-brain barrier (BBB) damage. was established by exposing rats 20-ppm for up 4 weeks;...

10.1371/journal.pone.0170623 article EN cc-by PLoS ONE 2017-01-24

Abstract Methylmercury selectively damages the central nervous system (CNS). The tumor necrosis factor (TNF) superfamily includes representative cytokines that participate in inflammatory response as well cell survival, and apoptosis. In this study, we found administration of methylmercury induced TNF-α expression brain mice. Although accumulated mercury concentration liver kidneys was greater than brain, to a extent brain. Thus, it is possible there may exist selective mechanism by which...

10.1038/srep38294 article EN cc-by Scientific Reports 2016-12-02

We provide the first data regarding maternal-to-fetal transfer of toxic trace elements (total Hg (THg) and organic (OHg), As, Cd, Pb) seven essential minerals (Mg, Cr, Mn, Fe, Cu, Zn, Se) in tissues 29 pairs small Indian mongoose that were naturally exposed to metals. The fetal mass negatively correlated with liver O/THg ratio, suggesting mineralization from form might occur during growth. maternal THg OHg concentrations THg/Se molar ratios whole blood (FB)/maternal (MB) significantly...

10.1016/j.scitotenv.2025.179108 article EN cc-by-nc-nd The Science of The Total Environment 2025-03-26

Methylmercury (MeHg), inorganic mercury (IHg), lead (Pb), amyloid-β peptide (Aβ), and rotenone (RTN) are well-known toxicants. Here, we demonstrate that these five toxicants exhibit differing effects on cerebrocortical neurons. The concentration responsible for 30% loss of viability (EC30) values 3 days after exposure was approximately 100nM MeHg, IHg, RTN 10μM Aβ. Neuritic degeneration subsequent apoptotic cell death were observed in toxicant-treated cells. In contrast, the EC30 value to Pb...

10.1093/toxsci/kfr352 article EN Toxicological Sciences 2012-01-05

Industrial pollution due to heavy metals such as mercury is a major concern for the environment and public health. Mercury, in particular methylmercury (MeHg), primarily affects brain development neuronal activity, resulting neurotoxic effects. Because chemokines can modulate functions are involved neuroinflammatory neurodegenerative diseases, we tested possibility that effect of MeHg may interfere with chemokine CCL2. We have used an original protocol young mice using MeHg-contaminated...

10.1093/toxsci/kfr252 article EN Toxicological Sciences 2011-10-05
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