Oxidative stress, mitochondrial perturbations and fetal programming of renal disease induced by maternal smoking

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

Oxidative stress, mitochondrial perturbations and fetal programming of renal disease induced by maternal smoking

Stangenberg, S Nguyen, LT

Chen, H

Al-Odat, I Killingsworth, MC Gosnell, ME Anwer, AG Goldys, EM Pollock, CA Saad, S

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Publication Type:: Journal Article
Citation:: International Journal of Biochemistry and Cell Biology, 2015, 64 pp. 81 - 90
Issue Date:: 2015-07-01

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Field	Value	Language
dc.contributor.author	Stangenberg, S	en_US
dc.contributor.author	Nguyen, LT https://orcid.org/0000-0002-0630-4959	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	Killingsworth, MC	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	2020-05-25T19:07:03Z
dc.date.issued	2015-07-01	en_US
dc.identifier.citation	International Journal of Biochemistry and Cell Biology, 2015, 64 pp. 81 - 90	en_US
dc.identifier.issn	1357-2725	en_US
dc.identifier.uri	http://hdl.handle.net/10453/37249
dc.description.abstract	© 2015 Elsevier Ltd. An adverse in-utero environment is increasingly recognized to predispose to chronic disease in adulthood. Maternal smoking remains the most common modifiable adverse in-utero exposure leading to low birth weight, which is strongly associated with chronic kidney disease (CKD) in later life. In order to investigate underlying mechanisms for such susceptibility, female Balb/c mice were sham or cigarette smoke-exposed (SE) for 6 weeks before mating, throughout gestation and lactation. Offspring kidneys were examined for oxidative stress, expression of mitochondrial proteins, mitochondrial structure as well as renal functional parameters on postnatal day 1, day 20 (weaning) and week 13 (adult age). From birth throughout adulthood, SE offspring had increased renal levels of mitochondrial-derived reactive oxygen species (ROS), which left a footprint on DNA with increased 8-hydroxydeoxyguanosin (8-OHdG) in kidney tubular cells. Mitochondrial structural abnormalities were seen in SE kidneys at day 1 and week 13 along with a reduction in oxidative phosphorylation (OXPHOS) proteins and activity of mitochondrial antioxidant Manganese superoxide dismutase (MnSOD). Smoke exposure also resulted in increased mitochondrial DNA copy number (day 1-week 13) and lysosome density (day 1 and week 13). The appearance of mitochondrial defects preceded the onset of albuminuria at week 13. Thus, mitochondrial damage caused by maternal smoking may play an important role in development of CKD at adult life.	en_US
dc.relation.ispartof	International Journal of Biochemistry and Cell Biology	en_US
dc.relation.isbasedon	10.1016/j.biocel.2015.03.017	en_US
dc.subject.classification	Biochemistry & Molecular Biology	en_US
dc.subject.mesh	Kidney	en_US
dc.subject.mesh	Lysosomes	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	Kidney Diseases	en_US
dc.subject.mesh	Prenatal Exposure Delayed Effects	en_US
dc.subject.mesh	Electron Transport Chain Complex Proteins	en_US
dc.subject.mesh	Superoxide Dismutase	en_US
dc.subject.mesh	DNA, Mitochondrial	en_US
dc.subject.mesh	Smoking	en_US
dc.subject.mesh	Oxidative Phosphorylation	en_US
dc.subject.mesh	Oxidative Stress	en_US
dc.subject.mesh	Pregnancy	en_US
dc.subject.mesh	Female	en_US
dc.title	Oxidative stress, mitochondrial perturbations and fetal programming of renal disease induced by maternal smoking	en_US
dc.type	Journal Article
utslib.citation.volume	64	en_US
utslib.for	0601 Biochemistry and Cell Biology	en_US
utslib.for	1101 Medical Biochemistry and Metabolomics	en_US
utslib.for	1116 Medical Physiology	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	64	en_US

Abstract:

© 2015 Elsevier Ltd. An adverse in-utero environment is increasingly recognized to predispose to chronic disease in adulthood. Maternal smoking remains the most common modifiable adverse in-utero exposure leading to low birth weight, which is strongly associated with chronic kidney disease (CKD) in later life. In order to investigate underlying mechanisms for such susceptibility, female Balb/c mice were sham or cigarette smoke-exposed (SE) for 6 weeks before mating, throughout gestation and lactation. Offspring kidneys were examined for oxidative stress, expression of mitochondrial proteins, mitochondrial structure as well as renal functional parameters on postnatal day 1, day 20 (weaning) and week 13 (adult age). From birth throughout adulthood, SE offspring had increased renal levels of mitochondrial-derived reactive oxygen species (ROS), which left a footprint on DNA with increased 8-hydroxydeoxyguanosin (8-OHdG) in kidney tubular cells. Mitochondrial structural abnormalities were seen in SE kidneys at day 1 and week 13 along with a reduction in oxidative phosphorylation (OXPHOS) proteins and activity of mitochondrial antioxidant Manganese superoxide dismutase (MnSOD). Smoke exposure also resulted in increased mitochondrial DNA copy number (day 1-week 13) and lysosome density (day 1 and week 13). The appearance of mitochondrial defects preceded the onset of albuminuria at week 13. Thus, mitochondrial damage caused by maternal smoking may play an important role in development of CKD at adult life.

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http://hdl.handle.net/10453/37249