L-carnitine reverses maternal cigarette smoke exposure-induced renal oxidative stress and mitochondrial dysfunction in mouse offspring

Nguyen, LT; Stangenberg, S; Chen, H; Al-Odat, I; Chan, YL; Gosnell, ME; Anwer, AG; Goldys, EM; Pollock, CA; Saad, S

L-carnitine reverses maternal cigarette smoke exposure-induced renal oxidative stress and mitochondrial dysfunction in mouse offspring

Nguyen, LT

Stangenberg, S Chen, H

Al-Odat, I Chan, YL

Gosnell, ME Anwer, AG Goldys, EM Pollock, CA Saad, S

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Publication Type:: Journal Article
Citation:: American Journal of Physiology - Renal Physiology, 2015, 308 (7), pp. F689 - F696
Issue Date:: 2015-01-01

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Field	Value	Language
dc.contributor.author	Nguyen, LT https://orcid.org/0000-0002-0630-4959	en_US
dc.contributor.author	Stangenberg, S	en_US
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.contributor.author	Al-Odat, I	en_US
dc.contributor.author	Chan, YL https://orcid.org/0000-0002-9605-4200	en_US
dc.contributor.author	Gosnell, ME	en_US
dc.contributor.author	Anwer, AG	en_US
dc.contributor.author	Goldys, EM	en_US
dc.contributor.author	Pollock, CA	en_US
dc.contributor.author	Saad, S https://orcid.org/0000-0001-8067-8046	en_US
dc.date.available	2020-05-25T19:02:42Z
dc.date.issued	2015-01-01	en_US
dc.identifier.citation	American Journal of Physiology - Renal Physiology, 2015, 308 (7), pp. F689 - F696	en_US
dc.identifier.issn	0363-6127	en_US
dc.identifier.uri	http://hdl.handle.net/10453/33433
dc.description.abstract	© 2015 the American Physiological Society. Maternal smoking is associated with metabolic disorders, renal underdevelopment, and a predisposition to chronic kidney disease in offspring, yet the underlying mechanisms are unclear. By exposing female Balb/c mice to cigarette smoke for 6 wk premating and during gestation and lactation, we showed that maternal smoke exposure induced glucose intolerance, renal underdevelopment, inflammation, and albuminuria in male offspring. This was associated with increased renal oxidative stress and mitochondrial dysfunction at birth and in adulthood. Importantly, we demonstrated that dietary supplementation of L-carnitine, an amino acid shown to increase antioxidant defenses and mitochondrial function in numerous diseases, in smoke-exposed mothers during pregnancy and lactation significantly reversed the detrimental maternal impacts on kidney pathology in these male offspring. It increased SOD2 and glutathione peroxidase 1, reduced ROS accumulation, and normalized levels of mitochondrial preprotein translocases of the outer membrane, and oxidative phosphorylation complexes I–V in the kidneys of mouse progeny after intrauterine cigarette smoke exposure. These findings support the hypothesis that oxidative stress and mitochondrial dysfunction are closely linked to the adverse effects of maternal smoking on male offspring renal pathology. The results of our study suggest that L-carnitine administration in cigarette smokeexposed mothers mitigates these deleterious renal consequences	en_US
dc.relation.ispartof	American Journal of Physiology - Renal Physiology	en_US
dc.relation.isbasedon	10.1152/ajprenal.00417.2014	en_US
dc.subject.classification	Urology & Nephrology	en_US
dc.subject.mesh	Kidney	en_US
dc.subject.mesh	Mitochondria	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Mice, Inbred BALB C	en_US
dc.subject.mesh	Animals, Newborn	en_US
dc.subject.mesh	Prenatal Exposure Delayed Effects	en_US
dc.subject.mesh	Vitamin B Complex	en_US
dc.subject.mesh	Carnitine	en_US
dc.subject.mesh	Smoking	en_US
dc.subject.mesh	Maternal Exposure	en_US
dc.subject.mesh	Oxidation-Reduction	en_US
dc.subject.mesh	Oxidative Stress	en_US
dc.subject.mesh	Pregnancy	en_US
dc.subject.mesh	Female	en_US
dc.subject.mesh	Male	en_US
dc.title	L-carnitine reverses maternal cigarette smoke exposure-induced renal oxidative stress and mitochondrial dysfunction in mouse offspring	en_US
dc.type	Journal Article
utslib.citation.volume	7	en_US
utslib.citation.volume	308	en_US
utslib.for	1116 Medical Physiology	en_US
utslib.for	0606 Physiology	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.issue	7	en_US
pubs.publication-status	Published	en_US
pubs.volume	308	en_US

Abstract:

© 2015 the American Physiological Society. Maternal smoking is associated with metabolic disorders, renal underdevelopment, and a predisposition to chronic kidney disease in offspring, yet the underlying mechanisms are unclear. By exposing female Balb/c mice to cigarette smoke for 6 wk premating and during gestation and lactation, we showed that maternal smoke exposure induced glucose intolerance, renal underdevelopment, inflammation, and albuminuria in male offspring. This was associated with increased renal oxidative stress and mitochondrial dysfunction at birth and in adulthood. Importantly, we demonstrated that dietary supplementation of L-carnitine, an amino acid shown to increase antioxidant defenses and mitochondrial function in numerous diseases, in smoke-exposed mothers during pregnancy and lactation significantly reversed the detrimental maternal impacts on kidney pathology in these male offspring. It increased SOD2 and glutathione peroxidase 1, reduced ROS accumulation, and normalized levels of mitochondrial preprotein translocases of the outer membrane, and oxidative phosphorylation complexes I–V in the kidneys of mouse progeny after intrauterine cigarette smoke exposure. These findings support the hypothesis that oxidative stress and mitochondrial dysfunction are closely linked to the adverse effects of maternal smoking on male offspring renal pathology. The results of our study suggest that L-carnitine administration in cigarette smokeexposed mothers mitigates these deleterious renal consequences

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http://hdl.handle.net/10453/33433