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Through studies of 33 human autopsy brains, we determined that early PWMI was related to oxidative damage that particularly targeted the oligodendrocyte lineage, whereas other neuronal and glial cell types were markedly more resistant. F<jats:sub>2<\/jats:sub>\u2010isoprostanes, an arachidinate metabolite\/lipid peroxidation marker of oxidative damage, were significantly increased in early PWMI lesions but not in cerebral cortex. That deleterious lipid peroxidation accompanied early PWMI was supported by similar increases in F<jats:sub>2<\/jats:sub>\u2010isoprostanes levels in the cerebral cortex from term infants with hypoxic\u2010ischemic cortical injury. Detection of F<jats:sub>4<\/jats:sub>\u2010neuroprostanes, a neuronal\u2010specific oxidative damage marker, confirmed that neuroaxonal elements were resistant to injury in cerebral cortex and white matter. Significant protein nitration was not detected in PWMI lesions by 3\u2010nitrotyrosine staining. Significant cellular degeneration was confirmed in early PWMI lesions by terminal deoxynucleotidyltransferase\u2013mediated dUTP nick end labeling and a marked depletion of oligodendrocyte progenitors of 71 \u00b1 8%. Hence, the predilection of preterm infants for PWMI is related to selective lipid peroxidation\u2013mediated injury of cerebral white matter and targeted death of oligodendrocyte progenitors. 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