RESUMO
Prenatal exposure to lipopolysaccharide (LPS) has been exploited to simulate brain disorder in animal model. Prenatal LPS-exposure has shown elevated levels of pro-inflammatory cytokines in the early stages of the postnatal period. This study determines the effect of prenatal LPS-exposure on oxidative stress (OS) in the distinct brain regions in the early postnatal stages. LPS (50 µg/kg, i.p.) and water for injection (100 µl, i.p.) were given to the experimental (n=5) and control (n=5) group of pregnant Swiss albino mice respectively on gestational day (GD)-16 and 17. Animals were decapitated on postnatal day (PnD) - 1, 7, 14 and 21 to assay levels of oxidative markers from 6 distinct brain regions. When compared with the control, prenatal LPS-exposure alters levels of OS markers: (i) on PnD-1, glutathione (GSH) level is raised and superoxide dismutase (SOD) activity is dropped, (ii) on PnD-7, advanced oxidation of protein product (AOPP) level is elevated, (iii) on PnD-14, lipid peroxidation (MDA) and activity of catalase (CAT) are enhanced, (iv) on PnD-21, increased MDA continued. The hippocampus (HC) and cerebellum (CB) were mostly susceptible to OS in the early postnatal development. Levels of MDA and activity of CAT enzyme were increased on PnD-14 in the cortex, HC and CB. Except MDA, all OS markers recovered and returned to the level of control animals on PnD-21. Taken together, these results suggest that prenatal LPS-exposure induces age- and region-specific OS in the early postnatal stage.
