Oxidative stress, mitochondrial perturbations and fetal programming of renal disease induced by maternal smoking
Autor: | Hui Chen, Carol A. Pollock, Ayad G. Anwer, Ewa M. Goldys, Long T. Nguyen, Murray C. Killingsworth, Ibrahim Al-Odat, Martin E. Gosnell, Stefanie Stangenberg, Sonia Saad |
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Rok vydání: | 2014 |
Předmět: |
Biochemistry & Molecular Biology
medicine.medical_specialty Mitochondrial DNA Offspring Oxidative phosphorylation Biology medicine.disease_cause Kidney Biochemistry DNA Mitochondrial Oxidative Phosphorylation Pregnancy Internal medicine medicine Animals Mice Inbred BALB C Superoxide Dismutase Smoking Maternal effect Cell Biology medicine.disease 3. Good health Mitochondria Oxidative Stress medicine.anatomical_structure Endocrinology Electron Transport Chain Complex Proteins Prenatal Exposure Delayed Effects Albuminuria Female Kidney Diseases medicine.symptom Lysosomes Oxidative stress Kidney disease |
Zdroj: | The international journal of biochemistrycell biology. 64 |
ISSN: | 1878-5875 |
Popis: | © 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. |
Databáze: | OpenAIRE |
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