Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic
Web of Science
AuthorTrist, BG; Hilton, JB; Hare, DJ; Crouch, PJ; Double, KL
Source TitleAngewandte Chemie International Edition
PublisherWILEY-V C H VERLAG GMBH
AffiliationPharmacology and Therapeutics
School of BioSciences
Document TypeJournal Article
CitationsTrist, B. G., Hilton, J. B., Hare, D. J., Crouch, P. J. & Double, K. L. (2020). Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic. ANGEWANDTE CHEMIE-INTERNATIONAL EDITION, 60 (17), pp.9215-9246. https://doi.org/10.1002/anie.202000451.
Access StatusOpen Access
Open Access URLPublished version
NHMRC Grant codeNHMRC/1122981
Cu/Zn superoxide dismutase (SOD1) is a frontline antioxidant enzyme catalysing superoxide breakdown and is important for most forms of eukaryotic life. The evolution of aerobic respiration by mitochondria increased cellular production of superoxide, resulting in an increased reliance upon SOD1. Consistent with the importance of SOD1 for cellular health, many human diseases of the central nervous system involve perturbations in SOD1 biology. But far from providing a simple demonstration of how disease arises from SOD1 loss-of-function, attempts to elucidate pathways by which atypical SOD1 biology leads to neurodegeneration have revealed unexpectedly complex molecular characteristics delineating healthy, functional SOD1 protein from that which likely contributes to central nervous system disease. This review summarises current understanding of SOD1 biology from SOD1 genetics through to protein function and stability.
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