Impaired Mitochondrial Function and Ubiquitin Proteasome System Activate α-Synuclein Aggregation in Zinc-Induced Neurotoxicity: Effect of Antioxidants - Singh, Garima; Mittra, Namrata; Singh, Chetna (Journal of molecular neuroscience, 2025)
Keywords: Adenosine triphosphate; alpha-Synuclein - metabolism; Animals; Antioxidants; Antioxidants - pharmacology; ATP; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell death; Cell differentiation; Cell Line, Tumor; Cyclic N-Oxides - pharmacology; Cyclosporins; Dopamine; Enzymatic activity; Heat shock proteins; Humans; Impairment; Kinases; Locomotor activity; Male; Membrane permeability; Membrane potential; Membrane Potential, Mitochondrial; Mice; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondrial permeability transition pore; Neurochemistry; Neurology; Neurosciences; Neurotoxicity; Peroxisome proliferator-activated receptors; Proteasome Endopeptidase Complex - metabolism; Proteasomes; Protein interaction; Protein Kinases; Proteins; Proteomics; PTEN protein; Rats; Reactive oxygen species; Reactive Oxygen Species - metabolism; Silymarin; Silymarin - pharmacology; Spin Labels; Synuclein; Tempol; Translocation; Tyrosine; Tyrosine 3-monooxygenase; Tyrosine 3-Monooxygenase - genetics; Tyrosine 3-Monooxygenase - metabolism; Ubiquitin; Ubiquitin - metabolism; Ubiquitin-Protein Ligases - genetics; Ubiquitin-Protein Ligases - metabolism; Zinc; Zinc - toxicity; Mitochondrial dysfunction; Dopaminergic neurodegeneration; Antioxidant; α-synuclein aggregation; Ubiquitin proteasome system; Zinc