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Our previous data also suggests that maternal SE impairs brain mitochondrial levels of oxidative phosphorylation (OXPHOS) complexes in male offspring with reduced endogenous antioxidant capacity from birth (Chan et al., Furthermore, as SE offspring have reduced brain antioxidants and increased cellular oxidative damage (Chan et al., 2015) and can provide neuroprotection by elevating brain antioxidant capacity in aging rats (Juliet et al., 2015)

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