Maternal prenatal omega-3 fatty acid supplementation attenuates hyperoxia-induced apoptosis in the developing rat brain

Supraphysiologic amounts of oxygen negatively influences brain maturation and development. The aim of the present study was to evaluate whether maternal ω-3 long-chain polyunsaturated fatty acid (ω-3 FA) supplementation during pregnancy protects the developing brain against hyperoxic injury. Thirty-six rat pups from six different dams were divided into six groups according to the diet modifications and hyperoxia exposure. The groups were: a control group (standard diet + room air), a hyperoxia group (standard diet + 80% O2 exposure), a hyperoxia + high-dose ω-3 FA-supplemented group, a hyperoxia + low-dose ω-3 FA-supplemented group, a room air + low-dose ω-3 FA-supplemented + group, and a room air + high dose ω-3 FA-supplemented group. The ω-3 FA's were supplemented as a mixture of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) from the second day of pregnancy until birth. Rat pups in the hyperoxic groups were exposed to 80% oxygen from birth until postnatal day 5 (P5). At P5, all animals were sacrificed. Neuronal cell death and apoptosis were evaluated by cell count, TUNEL, and active Caspase-3 immunohistochemistry. Histopathological examination showed that maternally ω-3 FA deficient diet and postnatal hyperoxia exposure were associated with significantly lower neuronal counts and significantly higher apoptotic cell death in the selected brain regions. Ω-3 FA treatment significantly diminished apoptosis, in the selected brain regions, in a dose dependent manner. Our results suggest that the maternal ω-3 FA supply may protect the developing brain against hyperoxic injury.

► Maternal omega 3 fatty acid deprivation and early postnatal hyperoxia exposure negatively influences brain maturation and development.
► Severe prenatal omega 3 fatty acid depletion may increase vulnerability to oxidative brain damage.
► Maternal DHA supply appears to confer neuroprotective effects on the developing brain against hyperoxic brain injury.