Measurement of glutathione concentration for the study of redox status in subjects with neurological disease has been limited to peripheral markers. We recruited 19 subjects with large strokes. Using magnetic resonance spectroscopy we measured brain glutathione concentration in the stroke region and in healthy tissue to calculate a glutathione-ratio. Elevated glutathione-ratio was observed in subacute (<72 hours) subjects without hemorrhagic transformation (mean=1.19, P=0.03, n=6). No trend was seen when all subjects were considered (n=19, 3 to 754 hours, range=0.45 to 1.41). This technique can detect glutathione changes because of disease, and may be valuable in clinical trials of stroke and other neurological diseases.
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http://dx.doi.org/10.1038/jcbfm.2012.127 | DOI Listing |
Metab Brain Dis
January 2025
Department of Zoology, Faculty of Science, Alexandria University, Alexandria, 21515, Egypt.
Exaggerated neuronal excitation by glutamate is a well-known cause of excitotoxicity, a key factor in numerous neurodegenerative disorders. This study examined the neurotoxic effect of monosodium glutamate (MSG) in the brain cortex of rats and focused on assessing the potential neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFAs). Four groups of adult male rats (n = 10) were assigned as follows; normal control, ω-3 PUFAs (400 mg/kg) alone, MSG (4 mg/g) alone, and MSG plus ω-3 PUFAs (4 mg/g MSG plus 400 mg/kg ω-3 PUFAs).
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, USA.
Introduction: Iron-mediated cell death (ferroptosis) is a proposed mechanism of Alzheimer's disease (AD) pathology. While iron is essential for basic biological functions, its reactivity generates oxidants which contribute to cell damage and death.
Methods: To further resolve mechanisms of iron-mediated toxicity in AD, we analyzed post mortem human brain and ApoEFAD mice.
Cell Biol Toxicol
January 2025
Department of Environmental Toxicology, Swiss Federal Institute of Aquatic Science and Technology, Eawag, 8600, Dübendorf, Switzerland.
Advancing in vitro systems to address the effects of chemical pollution requires a thorough characterization of their functionalities, such as their repertoire of biotransformation enzymes. Currently, knowledge regarding the presence, activity magnitudes, and inducibility of different biotransformation pathways in vitro is scarce, particularly across organs. We report organ-specific kinetics for phase I and II biotransformation enzymes, under basal and induced conditions, in two in vitro systems using salmonid fish: S9 sub-cellular fractions from brown trout (Salmo trutta) and rainbow trout (Oncorhynchus mykiss) were compared with rainbow trout cell lines.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pharmacology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria.
Stress is linked to oxidative imbalance, neuroendocrine system malfunction, and cognitive dysfunction. It is a recognized cause of neuropsychiatric diseases. Natural flavonoid apigenin (API) has neuroprotective and antidepressant properties, but little is known about its potential in restoring memory function under stress-related circumstances.
View Article and Find Full Text PDFToxicol Ind Health
January 2025
Department of of Toxicology, Faculty of Pharmacy, Istanbul Okan University, Istanbul, Turkey.
Di-2-(ethylhexyl)phthalate (DEHP) is a phthalate derivative used extensively in a wide range of materials, such as medical devices, toys, cosmetics, and personal care products. Many mechanisms, including epigenetics, may be involved in the effects of phthalates on brain development. In this study, Sprague-Dawley male rats were obtained 21-23 days after their birth (post-weaning) and were exposed to DEHP during the prepubertal period with low-dose DEHP (DEHP-L, 30 mg/kg/day) and high-dose DEHP (DEHP-H, 60 mg/kg/day, 37 days) until the end of adolescence (PND 60).
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