Original ContributionSustained hypoxia modulates mitochondrial DNA content in the neonatal rat brain
Section snippets
Sustained hypoxia model in the neonatal rat
An adaptation of a neonatal hypoxia model [7], [8], [9] was used: individually caged dams with litters (n = 8 pups/litter, Fisher 344) were maintained in airtight Plexiglas chambers (PROOX, Redfield, NY, USA) at reduced respiratory oxygen (9.5 ± 1.0% O2) generated by air replacement with nitrogen using an oxygen regulator (PROOX) [25], [26] or ambient air (∼ 21% O2, normoxia) for either 1 or 11 days. Chambers were equipped with fans and appropriate filters to remove excess CO2. Rats were maintained
Hypoxic rearing of pups from P3 through P14 induces oxidative stress in the brain
Significantly lower body and brain weights were recorded for P14 and P7 pups after sustained hypoxia initiated on postnatal day 3 (9.5% ± 1.0% O2), whereas no significant differences in brain and body weights were detected after a short 24-h hypoxic exposure (P3 through P4) (Table 2). Similarly reduced brain weight gains, suggestive of inability to meet energetic demands of normal growth and neurodevelopment, were reported previously in settings of sustained neonatal hypoxia in mouse [7], [8] and
Discussion
Sustenance of normal growth and development relies on perinatal oxygen and nutrient availability. To improve the understanding of neurodevelopmental deficits associated with placental insufficiency or preterm birth in humans [1], [2], [3], rodent models of sublethal neonatal hypoxia have been established [4], [5], [7], [8]. Although commonly neurodevelopmental problems dominate the outcomes in these models, in some cases ameliorations of deficits have been observed and occasionally linked to
Acknowledgments
This work was supported by the March of Dimes Birth Defects Foundation, NIH NINDS 39449, and Shriners 8670 grants.
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2014, International Journal of Biochemistry and Cell BiologyCitation Excerpt :Interestingly, it has also been reported that a subpopulation of HSCs that divide infrequently are in a dormant reversible cell state (Wilson et al., 2008). Latil et al. showed that, satellite cells isolated from 4 days PM muscle displayed reduced mitochondrial mass, reduced transcription of mitochondrial and antioxidant genes and increased mtDNA content, as a consequence of decreased oxygen tension and generation of ROS (Aly et al., 2011; Hoppeler et al., 2003; Lee et al., 2008). Interestingly, low-oxygen tension equivalent to hypoxia is prevalent in muscle, hematopoietic, mesenchymal and neural stem cell niches (Mohyeldin et al., 2010; Shi and Garry, 2006).