Objective: Mercury (Hg) is a classic cumulative neurotoxicant implicated in neuronal deficit via oxidative damage and inflammatory responses. We sought to investigate whether seed methanol extract (BCSE) would modulate oxidative neurotoxicity induced by Hg in rats.
Materials And Methods: Rats were orally treated with BCSE (200 or 400 mg/kg body weight of rat) for 28 days, while Hg was administered from day 15 to day 28. After sacrifice, antioxidant enzyme activities, reduced glutathione (GSH), nitric oxide (NO), malondialdehyde (MDA), and acetylcholinesterase (AchE) and adenine deaminase (ADA) activities were evaluated in the cerebrum and cerebellum of rats.
Results: Mercury induced significant depressions in catalase (CAT) and glutathione peroxidase (GPx) activities and GSH levels, whereas levels of NO and activities of AchE and ADA markedly increased. The histopathology of the brain tissues confirmed these changes. In contrast, BCSE administration prominently modulated the brain NO production and reversed the Hg-induced biochemical alterations comparable to normal control.
Conclusion: Methanol extract of seeds protects the cerebrum and cerebellum against Hg-induced brain damage via its antioxidant and NO modulatory actions.
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http://dx.doi.org/10.22038/AJP.2021.18262 | DOI Listing |
J Hazard Mater
December 2024
College of Life Science, Henan Normal University, Xinxiang 453007, China. Electronic address:
The widespread application of quantum dots (QDs) in recent years has raised concerns about potential environmental and human health risks. Although the toxicity of cadmium telluride quantum dots (CdTe QDs) has been partially studied, their effects on stem cells, tissue regeneration, neurodevelopment, and neurobehavioral toxicity remain unclear. This study aimed to investigate the combined toxic effects and mechanisms of CdTe QDs on planarians at the individual, tissue, cellular, and molecular levels.
View Article and Find Full Text PDFChem Biol Interact
January 2025
Key Laboratory of Environmental Medicine Engineering, Ministry of Education of China, School of Public Health, Southeast University, Nanjing 210009, Jiangsu, China. Electronic address:
Copper, as a vital trace element and ubiquitous environmental pollutant, exhibits a positive correlation with the neurodegenerative diseases. Recent studies have highlighted ferroptosis's significance in heavy metal-induced neurodegenerative diseases, yet its role in copper-related neurotoxicity remains unclear. This study aimed to investigate the role of ferroptosis in copper-induced neurotoxicity.
View Article and Find Full Text PDFJ Hazard Mater
December 2024
International Research Center for Marine Biosciences at Shanghai Ocean University, Ministry of Science and Technology, Shanghai Ocean University, Shanghai 201306, China; Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources, Ministry of Education, Shanghai Ocean University, Shanghai 201306, China. Electronic address:
The aggregation state of nano-TiO in the environment is altered under marine heatwaves (MHWs), thus affecting its bioavailability and toxicity to the marine organisms. Here, we investigated the toxic mechanisms and effects of nano-TiO on gut-hepatopancreas axis health of Mytilus coruscus exposed to 25 and 250 μg/L of nano-TiO under laboratory-simulated MHW. Compared with the control conditions or post-MHW cooling phase, prolonged MHW exposure significantly inhibited digestive function, decreased immune-related enzymes activities, and caused neurotoxicity in the mussels.
View Article and Find Full Text PDFAquat Toxicol
December 2024
School of Emergency Management, School of the Environment and Safety, Jiangsu University, 301 Xuefu Rd., Zhenjiang, Jiangsu 212013, China. Electronic address:
Monoethylhexyl phthalate (MEHP) is the primary metabolite of di(2-ethylhexyl) phthalate (DEHP), the most prevalent phthalate plasticiser globally. It has been demonstrated that MEHP exerts more potent toxic effects than DEHP. Nevertheless, the full extent of the toxicity of MEHP to neurodevelopmental organisms remains unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Gladstone Institutes, UCSF, San Francisco, CA, USA.
Background: Cerebrovascular alterations and innate immune activation are key features of Alzheimer's disease (AD). However, the mechanisms that link blood-brain barrier disruption to neurodegeneration are poorly understood and well-defined druggable targets at the neurovascular interface are limited.
Method: By developing a multiomic and genetic loss-of-function pipeline, we reported the transcriptomic and global phosphoproteomic landscape of blood-induced microglia activation and the causal role for fibrin in induction of neurodegenerative genes and oxidative stress pathways in innate immune cells.
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