Palytoxin is an emergent toxin in Europe and one of the most toxic substances know to date. The toxin disrupts the physiological functioning of the Na/K-ATPase converting the enzyme in a permeant cation channel. Human intoxications by PLTX after consumption of contaminated fishery products are a serious health issue and can be fatal. Several reports have previously investigated the oral and intraperitoneal toxicity of PLTX in mice. However, in all cases short observation periods (24 and 48 h) after toxin administration were evaluated. In this work, single oral or intraperitoneal doses of PLTX were administered to healthy mice and surviving animals were followed up for 96 h. The data obtained here allowed us to calculate the oral and intraperitoneal lethal doses 50 (LD) which were in the range of the values previously described. Surprisingly, the oral NOAEL for PLTX was more than 10 times lower than that previously described, a fact that indicates the need for the reevaluation of the levels of the toxin in edible fishery products.
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http://dx.doi.org/10.1016/j.toxicon.2020.01.010 | DOI Listing |
Alzheimers Dement
December 2024
Chiang Mai University/Neurophysiology Unit/Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai, Thailand.
Background: Our studies suggest that iron-overloaded rats developed neurotoxicity and cognitive impairment (1,2). An increase in brain mitochondrial fission and brain mitophagy have been considered as one of underlying mechanisms in brain with iron-overloaded condition (3,4). Hence, a pharmacological intervention focused on preventing brain mitochondrial pathologies is required.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Microglia play an important role in immune memory. Lipopolysaccharide (LPS) triggers immune memory and primes microglia, resulting in brain pathologies and brain dysfunction following a second stimulus (1, 2). An increase in the C1q/ PSD95 expressions within microglia and excessively synaptic pruning were observed in mouse model of Alzheimer's disease (3).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Doxorubicin (Dox), a chemotherapeutic agent, is known to cause chemobrain leading to cognitive decline and brain mitochondrial dysfunction. Ivabradine (Iva), hyperpolarization-activated cyclic nucleotide-gated channel blocker used for angina and arrhythmia, has been shown to be an anticonvulsant, antioxidant, and neuroprotective agent. However, the effects of Iva on cognitive function, and brain mitochondrial function in Dox-induced chemobrain are still not determined.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Excessive high-fat diet (HFD) consumption develops the obese pre-diabetic condition, which initiates neuroinflammation and numerous brain pathologies, resulting in cognitive decline (1). A cinnamamide derivative compound (2i-10) is recently identified as a novel myeloid differentiation factor 2 (MD-2) inhibitor, and has been shown to attenuate inflammation via toll-like receptor 4 (TLR4) signaling pathway (2). However, the effects of 2i-10 on the neuroinflammation, brain pathologies and cognitive function in the obese pre-diabetic rats have never been studied.
View Article and Find Full Text PDFFront Immunol
January 2025
Department of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, United States.
Introduction: A subtype of human mast cells (MCs) found in the skin and to a lesser extent in the lung and gut express a novel G protein-coupled receptor (GPCR) known as Mas-related GPCR-X2 (MRGPRX2, mouse counterpart MrgprB2). In addition to drug-induced pseudoallergy and cutaneous disorders, MrgprB2 contributes to ulcerative colitis, IgE-mediated lung inflammation and systemic anaphylaxis. Interestingly, most agonists activate MRGPRX2 with higher potency than MrgprB2.
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