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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Acute maternal oxidant exposure causes susceptibility of the fetal brain to inflammation and oxidative stress

Fig. 2

Ethanol and glutathione depletion generate oxidative stress in fetal and maternal brain. Twenty-four hours after dams were subcutaneously administered ethanol (2.5 g/kg), following 1 h intraperitoneal pretreatment with either NAC (4 mg/dose) or BSO (1.5 g/kg), total GSH levels were determined by HPLC in fetal (a) and maternal (b) brain lysates. 2,4-Dinitrophenylhydrazine (DNP) derivatized protein carbonylation levels in lysates were quantified spectrophotometrically in fetal (c) and maternal (d) brains. Expression of 4-Hydroxynonenal adduct formation was used to determine lipid peroxidation in the brain. A representative immunoblot against 4HNE in fetal (e) and maternal (f) lysates. Values are mean ± SEM (*p ≤ 0.05, **p ≤ 0.005 vs control; #p ≤ 0.05, ##p ≤ 0.005 vs ethanol), (n = 6 per group)

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