title: Post-hypoxic magnesium decreases nuclear oxidative damage in the fetal guinea pig brain.
abstract: This study was to determine if administration of MgSO(4) after the hypoxic insult (post-hypoxia) would attenuate neuronal damage in the fetal guinea pig brain. Pregnant guinea pigs (45-60 days gestation) were exposed to hypoxia (7% O2) for 1 h. Following hypoxia, one group recovered for 24 h with no additional treatment (post-hypoxia) and another group received MgSO(4), 300 mg/kg i.p., followed by 100 mg/kg i.p., each hour for three doses (post-hypoxia+Mg) and allowed to recover for 24 h. Fetal brain magnesium content was decreased (P<0.05) 4 h post-hypoxia which was prevented by treatment with MgSO(4). High energy phosphates were significantly lower (P<0.05) in the post-hypoxia group which was partially prevented by post-hypoxic magnesium. Na+,K+-ATPase activity was significantly lower (P<0.05) and nuclear membrane fluorescent compounds were significantly higher (P<0.05) in the post-hypoxia group but were not significantly changed in the post-hypoxia+Mg group compared with the normoxic control group. DNA fragmentation was observed to be lower in the Mg-treated post-hypoxic group. This study demonstrates that maternal MgSO(4) administration following in utero hypoxia prevents associated decreases in fetal brain magnesium and suppresses alterations in both the neuronal and nuclear membranes and genomic fragmentation in the fetal guinea pig brain.
authors.affiliation: Department of Obstetrics and Gynecology, Winthrop University Hospital, 259 First Street, Mineola, NY 11501, USA. Devmaulik@aol.com
authors.forename: D
authors.initials: D
authors.lastname: Maulik
authors.forename: I
authors.initials: I
authors.lastname: Qayyum
authors.forename: S R
authors.initials: SR
authors.lastname: Powell
authors.forename: M
authors.initials: M
authors.lastname: Karantza
authors.forename: O P
authors.initials: OP
authors.lastname: Mishra
authors.forename: M
authors.initials: M
authors.lastname: Delivoria-Papadopoulos
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000201:enzymology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D053938:DNA Fragmentation; D005260:Female; D005333:Fetus / Q000378:metabolism; D006168:Guinea Pigs; D002534:Hypoxia, Brain / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000187:drug effects; D008278:Magnesium Sulfate / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D011247:Pregnancy; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D008278:Magnesium Sulfate; D000255:Adenosine Triphosphate; D000254:Sodium-Potassium-Exchanging ATPase