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Abstract
Previous studies have shown that hypoxia increases production of oxygen free radicals in fetal guinea pig brain. The present study tests the hypothesis that pretreatment with Mg++, a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor-ion channel, will prevent the hypoxia-induced increase in oxygen free radicals. Term guinea pig fetuses were divided into 4 groups: normoxic (n=7), hypoxic (n=7), Mg++ treated normoxic (n=6) and Mg++ treated hypoxic (n=6). The normoxic and the hypoxic groups were exposed for 60 min to 21% or 7% oxygen, respectively. An initial bolus of MgSO4 (600/mg/kg, i.p.) was administered to the mothers of the Mg treated group 1 hr prior to hypoxia and 30 min later by a second dose(300 mg/kg). Fetal cerebral cortical tissue was homogenized in N2-bubbled ice-cold 100 mM μ -phenyl-N-tert-butylnitrone (PBN) to trap oxygen free radicals. PBN spin adducts were extracted in toluene and free radicals were measured by electron spin resonance spectroscopy (ESR) at -20C. Peak height of the spin adduct signal was used as an index of the intensity of free radical formation, expressed as units/g dry tissue. Fetal brain hypoxia was documented biochemically by decreased tissue levels of ATP and phosphocreatine. Without Mg++ treatment, cortical tissue from hypoxic fetuses showed a significant increase in spin adducts (normoxic: 33.8±9.3 MM/g tissue vs. hypoxic: 57.9±9.2 MM/g tissue, 71% increase, p<0.01). In Mg++ treated groups spin adduct levels in cortical tissue from hypoxic fetuses did not significantly differ from the normoxic fetuses (30.2±9.9 MM/g tissue, Mg++ normoxic vs. 30.6±8.1MM/g tissue, Mg++ hypoxic). The results demonstrate that Mg++ administration significantly attenuates the hypoxia-induced increase in oxygen free radicals in fetal guinea pig brain. Since intracellular Ca++ is known to increase activity of several oxygen free radicalgenerating pathways, blockade of Ca++ entry via thereceptor-ion channel may be the mechanism by which Mg++ pretreatment prevents hypoxia-induced free radical generation.
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