Maternal L-carnitine supplementation improves brain health in offspring from cigarette smoke exposed mothers

Chan, YL; Saad, S; Al-Odat, I; Oliver, BG; Pollock, C; Jones, NM; Chen, H

Maternal L-carnitine supplementation improves brain health in offspring from cigarette smoke exposed mothers

Chan, YL

Saad, S

Al-Odat, I Oliver, BG

Pollock, C Jones, NM

Chen, H

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Publication Type:: Journal Article
Citation:: Frontiers in Molecular Neuroscience, 2017, 10
Issue Date:: 2017-02-13

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Field	Value	Language
dc.contributor.author	Chan, YL https://orcid.org/0000-0002-9605-4200	en_US
dc.contributor.author	Saad, S https://orcid.org/0000-0001-8067-8046	en_US
dc.contributor.author	Al-Odat, I	en_US
dc.contributor.author	Oliver, BG https://orcid.org/0000-0002-7122-9262	en_US
dc.contributor.author	Pollock, C	en_US
dc.contributor.author	Jones, NM https://orcid.org/0000-0001-6738-6022	en_US
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.date.available	2017-01-27	en_US
dc.date.issued	2017-02-13	en_US
dc.identifier.citation	Frontiers in Molecular Neuroscience, 2017, 10	en_US
dc.identifier.issn	1662-5099	en_US
dc.identifier.uri	http://hdl.handle.net/10453/83337
dc.description.abstract	© 2017 Chan, Saad, Al-Odat, Oliver, Pollock, Jones and Chen. Maternal cigarette smoke exposure (SE) causes detrimental changes associated with the development of chronic neurological diseases in the offspring as a result of oxidative mitochondrial damage. Maternal L-Carnitine administration has been shown to reduce renal oxidative stress in SE offspring, but its effect in the brain is unknown. Here, we investigated the effects of maternal L-Carnitine supplementation on brain markers of oxidative stress, autophagy, mitophagy and mitochondrial energy producing oxidative phosphorylation (OXPHOS) complexes in SE offspring. Female Balb/c mice (8 weeks) were exposed to cigarette smoke prior to mating, during gestation and lactation with or without L-Carnitine supplementation (1.5 mM in drinking water). In 1 day old male SE offspring, brain mitochondrial damage was suggested by increased mitochondrial fusion and reduced autophagosome markers; whereas at 13 weeks, enhanced brain cell damage was suggested by reduced fission and autophagosome markers, as well as increased apoptosis and DNA fragmentation markers, which were partially reversed by maternal L-Carnitine supplementation. In female SE offspring, enhanced mitochondrial regeneration was suggested by decreased fission and increased fusion markers at day 1. At 13 weeks, there was an increase in brain energy demand, oxidative stress and mitochondrial turnover, reflected by the protein changes of OXPHOS complex, fission and autophagosome markers, as well as the endogenous antioxidant, which were also partially normalized by maternal L-Carnitine supplementation. However, markers of apoptosis and DNA fragmentation were not significantly changed. Thus L-Carnitine supplementation may benefit the brain health of the offspring from smoking mothers.	en_US
dc.relation.ispartof	Frontiers in Molecular Neuroscience	en_US
dc.relation.isbasedon	10.3389/fnmol.2017.00033	en_US
dc.title	Maternal L-carnitine supplementation improves brain health in offspring from cigarette smoke exposed mothers	en_US
dc.type	Journal Article
utslib.citation.volume	10	en_US
utslib.for	1108 Medical Microbiology	en_US
utslib.for	1109 Neurosciences	en_US
utslib.for	1103 Clinical Sciences	en_US
pubs.embargo.period	Not known	en_US
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 Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	open_access
pubs.publication-status	Published	en_US
pubs.volume	10	en_US

Abstract:

© 2017 Chan, Saad, Al-Odat, Oliver, Pollock, Jones and Chen. Maternal cigarette smoke exposure (SE) causes detrimental changes associated with the development of chronic neurological diseases in the offspring as a result of oxidative mitochondrial damage. Maternal L-Carnitine administration has been shown to reduce renal oxidative stress in SE offspring, but its effect in the brain is unknown. Here, we investigated the effects of maternal L-Carnitine supplementation on brain markers of oxidative stress, autophagy, mitophagy and mitochondrial energy producing oxidative phosphorylation (OXPHOS) complexes in SE offspring. Female Balb/c mice (8 weeks) were exposed to cigarette smoke prior to mating, during gestation and lactation with or without L-Carnitine supplementation (1.5 mM in drinking water). In 1 day old male SE offspring, brain mitochondrial damage was suggested by increased mitochondrial fusion and reduced autophagosome markers; whereas at 13 weeks, enhanced brain cell damage was suggested by reduced fission and autophagosome markers, as well as increased apoptosis and DNA fragmentation markers, which were partially reversed by maternal L-Carnitine supplementation. In female SE offspring, enhanced mitochondrial regeneration was suggested by decreased fission and increased fusion markers at day 1. At 13 weeks, there was an increase in brain energy demand, oxidative stress and mitochondrial turnover, reflected by the protein changes of OXPHOS complex, fission and autophagosome markers, as well as the endogenous antioxidant, which were also partially normalized by maternal L-Carnitine supplementation. However, markers of apoptosis and DNA fragmentation were not significantly changed. Thus L-Carnitine supplementation may benefit the brain health of the offspring from smoking mothers.

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http://hdl.handle.net/10453/83337