A Mitochondrial specific antioxidant reverses metabolic dysfunction and fatty liver induced by maternal cigarette smoke in mice

Li, G; Chan, YL; Sukjamnong, S; Anwer, AG; Vindin, H; Padula, M; Zakarya, R; George, J; Oliver, BG; Saad, S; Chen, H

A Mitochondrial specific antioxidant reverses metabolic dysfunction and fatty liver induced by maternal cigarette smoke in mice

Li, G Chan, YL

Sukjamnong, S Anwer, AG Vindin, H Padula, M

Zakarya, R

George, J Oliver, BG

Saad, S

Chen, H

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Publication Type:: Journal Article
Citation:: Nutrients, 2019, 11 (7)
Issue Date:: 2019-07-01

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Field	Value	Language
dc.contributor.author	Li, G	en_US
dc.contributor.author	Chan, YL https://orcid.org/0000-0002-9605-4200	en_US
dc.contributor.author	Sukjamnong, S	en_US
dc.contributor.author	Anwer, AG	en_US
dc.contributor.author	Vindin, H	en_US
dc.contributor.author	Padula, M https://orcid.org/0000-0002-8283-0643	en_US
dc.contributor.author	Zakarya, R https://orcid.org/0000-0002-9259-9369	en_US
dc.contributor.author	George, J	en_US
dc.contributor.author	Oliver, BG https://orcid.org/0000-0002-7122-9262	en_US
dc.contributor.author	Saad, S https://orcid.org/0000-0001-8067-8046	en_US
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.date.available	2019-07-18	en_US
dc.date.issued	2019-07-01	en_US
dc.identifier.citation	Nutrients, 2019, 11 (7)	en_US
dc.identifier.uri	http://hdl.handle.net/10453/134715
dc.description.abstract	© 2019 by the authors. Licensee MDPI, Basel, Switzerland. Maternal smoking leads to glucose and lipid metabolic disorders and hepatic damage in the offspring, potentially due to mitochondrial oxidative stress. Mitoquinone mesylate (MitoQ) is a mitochondrial targeted antioxidant with high bioavailability. This study aimed to examine the impact of maternal cigarette smoke exposure (SE) on offspring’s metabolic profile and hepatic damage, and whether maternal MitoQ supplementation during gestation can affect these changes. Female Balb/c mice (eight weeks) were either exposed to air or SE for six weeks prior to mating and throughout gestation and lactation. A subset of the SE dams were supplied with MitoQ in the drinking water (500 μmol/L) during gestation and lactation. Intraperitoneal glucose tolerance test was performed in the male offspring at 12 weeks and the livers and plasma were collected at 13 weeks. Maternal SE induced glucose intolerance, hepatic steatosis, mitochondrial oxidative stress and related damage in the adult offspring. Maternal MitoQ supplementation reduced hepatic mitochondrial oxidative stress and improved markers of mitophagy and mitochondrial biogenesis. This may restore hepatic mitochondrial health and was associated with an amelioration of glucose intolerance, hepatic steatosis and pathological changes induced by maternal SE. MitoQ supplementation may potentially prevent metabolic dysfunction and hepatic pathology induced by intrauterine SE.	en_US
dc.relation	http://purl.org/au-research/grants/nhmrc/APP1110368
dc.relation.ispartof	Nutrients	en_US
dc.relation.isbasedon	10.3390/nu11071669	en_US
dc.subject.mesh	Mitochondria, Liver	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Mice, Inbred BALB C	en_US
dc.subject.mesh	Mice	en_US
dc.subject.mesh	Fatty Liver	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	Antioxidants	en_US
dc.subject.mesh	Tobacco Smoke Pollution	en_US
dc.subject.mesh	Maternal Exposure	en_US
dc.subject.mesh	Oxidative Stress	en_US
dc.subject.mesh	Lactation	en_US
dc.subject.mesh	Pregnancy	en_US
dc.subject.mesh	Female	en_US
dc.subject.mesh	Male	en_US
dc.subject.mesh	Metabolic Syndrome	en_US
dc.subject.mesh	Lipidomics	en_US
dc.title	A Mitochondrial specific antioxidant reverses metabolic dysfunction and fatty liver induced by maternal cigarette smoke in mice	en_US
dc.type	Journal Article
utslib.citation.volume	7	en_US
utslib.citation.volume	11	en_US
utslib.for	1108 Medical Microbiology	en_US
utslib.for	0605 Microbiology	en_US
utslib.for	0908 Food Sciences	en_US
utslib.for	1111 Nutrition and Dietetics	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	7	en_US
pubs.publication-status	Published	en_US
pubs.volume	11	en_US

Abstract:

© 2019 by the authors. Licensee MDPI, Basel, Switzerland. Maternal smoking leads to glucose and lipid metabolic disorders and hepatic damage in the offspring, potentially due to mitochondrial oxidative stress. Mitoquinone mesylate (MitoQ) is a mitochondrial targeted antioxidant with high bioavailability. This study aimed to examine the impact of maternal cigarette smoke exposure (SE) on offspring’s metabolic profile and hepatic damage, and whether maternal MitoQ supplementation during gestation can affect these changes. Female Balb/c mice (eight weeks) were either exposed to air or SE for six weeks prior to mating and throughout gestation and lactation. A subset of the SE dams were supplied with MitoQ in the drinking water (500 μmol/L) during gestation and lactation. Intraperitoneal glucose tolerance test was performed in the male offspring at 12 weeks and the livers and plasma were collected at 13 weeks. Maternal SE induced glucose intolerance, hepatic steatosis, mitochondrial oxidative stress and related damage in the adult offspring. Maternal MitoQ supplementation reduced hepatic mitochondrial oxidative stress and improved markers of mitophagy and mitochondrial biogenesis. This may restore hepatic mitochondrial health and was associated with an amelioration of glucose intolerance, hepatic steatosis and pathological changes induced by maternal SE. MitoQ supplementation may potentially prevent metabolic dysfunction and hepatic pathology induced by intrauterine SE.

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http://hdl.handle.net/10453/134715