Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.

Trist, BG; Hilton, JB; Hare, DJ; Crouch, PJ; Double, KL

Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.

Trist, BG Hilton, JB Hare, DJ Crouch, PJ Double, KL

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Publisher:: Wiley
Publication Type:: Journal Article
Citation:: Angewandte Chemie, 2021, 60, (17), pp. 9215-9246
Issue Date:: 2021-01-01

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Field	Value	Language
dc.contributor.author	Trist, BG
dc.contributor.author	Hilton, JB
dc.contributor.author	Hare, DJ
dc.contributor.author	Crouch, PJ
dc.contributor.author	Double, KL
dc.date.accessioned	2022-02-14T01:25:42Z
dc.date.available	2022-02-14T01:25:42Z
dc.date.issued	2021-01-01
dc.identifier.citation	Angewandte Chemie, 2021, 60, (17), pp. 9215-9246
dc.identifier.issn	0044-8249
dc.identifier.issn	1521-3773
dc.identifier.uri	http://hdl.handle.net/10453/154476
dc.description.abstract	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.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Wiley
dc.relation.ispartof	Angewandte Chemie
dc.relation.isbasedon	10.1002/anie.202000451
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	03 Chemical Sciences
dc.subject.classification	Organic Chemistry
dc.subject.mesh	Antioxidants
dc.subject.mesh	Biocatalysis
dc.subject.mesh	Central Nervous System Diseases
dc.subject.mesh	Enzyme Stability
dc.subject.mesh	Humans
dc.subject.mesh	Superoxide Dismutase-1
dc.subject.mesh	Superoxides
dc.subject.mesh	Humans
dc.subject.mesh	Central Nervous System Diseases
dc.subject.mesh	Superoxides
dc.subject.mesh	Antioxidants
dc.subject.mesh	Enzyme Stability
dc.subject.mesh	Biocatalysis
dc.subject.mesh	Superoxide Dismutase-1
dc.title	Superoxide Dismutase 1 in Health and Disease: How a Frontline Antioxidant Becomes Neurotoxic.
dc.type	Journal Article
utslib.citation.volume	60
utslib.location.activity	Germany
utslib.for	03 Chemical Sciences
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Mathematical and Physical Sciences
utslib.copyright.status	open_access	*
pubs.consider-herdc	true
dc.date.updated	2022-02-14T01:25:36Z
pubs.issue	17
pubs.publication-status	Published
pubs.volume	60
utslib.citation.issue	17

Abstract:

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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http://hdl.handle.net/10453/154476