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The metabolic profile of autistic patients has been shown to be abnormal with elevated biomarkers that indicate chronic oxidative stress and evidence that GSH synthesis may be insufficient to maintain redox homeostasis [14, 15]
These structural features improve peptide stability , extend half-life , and reduce amyloid fibril formation relative to native amylin, supporting sustained activity in experimental systems
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Mitochondrial diseases are characterized by both a diminished capacity to produce ATP as well as an elevated production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) [3]
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