MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring

Sukjamnong, S; Chan, YL; Zakarya, R; Nguyen, LT; Anwer, AG; Zaky, AA; Santiyanont, R; Oliver, BG; Goldys, E; Pollock, CA; Chen, H; Saad, S

MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring

Sukjamnong, S Chan, YL

Zakarya, R

Nguyen, LT

Anwer, AG Zaky, AA Santiyanont, R Oliver, BG

Goldys, E Pollock, CA Chen, H

Saad, S

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Publication Type:: Journal Article
Citation:: Scientific Reports, 2018, 8 (1)
Issue Date:: 2018-12-01

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Field	Value	Language
dc.contributor.author	Sukjamnong, S	en_US
dc.contributor.author	Chan, YL https://orcid.org/0000-0002-9605-4200	en_US
dc.contributor.author	Zakarya, R https://orcid.org/0000-0002-9259-9369	en_US
dc.contributor.author	Nguyen, LT https://orcid.org/0000-0002-0630-4959	en_US
dc.contributor.author	Anwer, AG	en_US
dc.contributor.author	Zaky, AA	en_US
dc.contributor.author	Santiyanont, R	en_US
dc.contributor.author	Oliver, BG https://orcid.org/0000-0002-7122-9262	en_US
dc.contributor.author	Goldys, E	en_US
dc.contributor.author	Pollock, CA	en_US
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.contributor.author	Saad, S https://orcid.org/0000-0001-8067-8046	en_US
dc.date.available	2018-03-26	en_US
dc.date.issued	2018-12-01	en_US
dc.identifier.citation	Scientific Reports, 2018, 8 (1)	en_US
dc.identifier.uri	http://hdl.handle.net/10453/124051
dc.description.abstract	© 2018 The Author(s). To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many diseases. Female Balb/c mice (8 weeks) were divided into Sham (exposed to air), SE (exposed to cigarette smoke) and SEMQ (exposed to cigarette smoke with MitoQ supplemented from mating) groups. Kidneys from the mothers were collected when the pups weaned and those from the offspring were collected at 13 weeks. Maternal MitoQ supplementation during gestation and lactation significantly reversed the adverse impact of maternal SE on offspring's body weight, kidney mass and renal pathology. MitoQ administration also significantly reversed the impact of SE on the renal cellular mitochondrial density and renal total reactive oxygen species in both the mothers and their offspring in adulthood. Our results suggested that MitoQ supplementation can mitigate the adverse impact of maternal SE on offspring's renal pathology, renal oxidative stress and mitochondrial density in mice offspring.	en_US
dc.relation.ispartof	Scientific Reports	en_US
dc.relation.isbasedon	10.1038/s41598-018-24949-0	en_US
dc.subject.mesh	Kidney	en_US
dc.subject.mesh	Mitochondria	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Mice	en_US
dc.subject.mesh	Prenatal Exposure Delayed Effects	en_US
dc.subject.mesh	Organophosphorus Compounds	en_US
dc.subject.mesh	Ubiquinone	en_US
dc.subject.mesh	Inflammation Mediators	en_US
dc.subject.mesh	Fluorescent Antibody Technique	en_US
dc.subject.mesh	Smoking	en_US
dc.subject.mesh	Maternal Exposure	en_US
dc.subject.mesh	Signal Transduction	en_US
dc.subject.mesh	Oxidative Stress	en_US
dc.subject.mesh	Pregnancy	en_US
dc.subject.mesh	Dietary Supplements	en_US
dc.subject.mesh	Female	en_US
dc.subject.mesh	Male	en_US
dc.subject.mesh	Biomarkers	en_US
dc.subject.mesh	Receptor for Advanced Glycation End Products	en_US
dc.title	MitoQ supplementation prevent long-term impact of maternal smoking on renal development, oxidative stress and mitochondrial density in male mice offspring	en_US
dc.type	Journal Article
utslib.citation.volume	1	en_US
utslib.citation.volume	8	en_US
utslib.for	1102 Cardiorespiratory Medicine and Haematology	en_US
utslib.for	0601 Biochemistry and Cell Biology	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.issue	1	en_US
pubs.publication-status	Published	en_US
pubs.volume	8	en_US

Abstract:

© 2018 The Author(s). To investigate the effect of maternal MitoQ treatment on renal disorders caused by maternal cigarette smoke exposure (SE). We have demonstrated that maternal SE during pregnancy increases the risk of developing chronic kidney disease (CKD) in adult offspring. Mitochondrial oxidative damage contributes to the adverse effects of maternal smoking on renal disorders. MitoQ is a mitochondria-targeted antioxidant that has been shown to protect against oxidative damage-related pathologies in many diseases. Female Balb/c mice (8 weeks) were divided into Sham (exposed to air), SE (exposed to cigarette smoke) and SEMQ (exposed to cigarette smoke with MitoQ supplemented from mating) groups. Kidneys from the mothers were collected when the pups weaned and those from the offspring were collected at 13 weeks. Maternal MitoQ supplementation during gestation and lactation significantly reversed the adverse impact of maternal SE on offspring's body weight, kidney mass and renal pathology. MitoQ administration also significantly reversed the impact of SE on the renal cellular mitochondrial density and renal total reactive oxygen species in both the mothers and their offspring in adulthood. Our results suggested that MitoQ supplementation can mitigate the adverse impact of maternal SE on offspring's renal pathology, renal oxidative stress and mitochondrial density in mice offspring.

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http://hdl.handle.net/10453/124051