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Acta Neurochir Suppl. 2010;106:351-7. doi: 10.1007/978-3-211-98811-4_64.

A new antioxidant compound H-290/51 attenuates nanoparticle induced neurotoxicity and enhances neurorepair in hyperthermia.

Author information

  • 1Laboratory of Cerebrovascular Research, Department of Surgical Sciences, Anesthesiology and Intensive Care Medicine, University Hospital, Uppsala, Sweden. Sharma@surgsci.uu.se

Abstract

Previous reports from our laboratory show that animals treated with engineered nanoparticles derived from metals for 1 week and subjected to hyperthermia showed enhanced neurotoxicity in terms of blood-brain barrier (BBB) disruption, brain edema formation and cell injury. It appears that nanoparticle induced enhanced oxidative stress leads to increased lipid peroxidation and over-production of hydroxyl radicals are responsible for exacerbation of neurotoxicity in hyperthermia. Therefore, in this investigation, rats (after 1 week administration of Ag or Cu nanoparticles) were treated with a new antioxidant compound H-290/51 (an inhibitor of lipid peroxidation, 50 mg/kg, p.o.) before subjecting them to hyperthermia. One group of nanoparticle treated rat received H-290/51 and were kept at room temperature for comparison. Our results show that H-290/51 significantly attenuated heat stress induced BBB impairment, brain edema formation and neurotoxicity in nanoparticle treated rats. However, no significant diminution of nanoparticle induced BBB breakdown, or neurotoxicity was observed in H-290/51 treated rats kept at room temperature. These observations suggest that nanoparticles aggravate oxidative stress following hyperthermia leading to exacerbation of neurotoxicity through oxidative stress-related mechanisms, not reported earlier.

PMID:
19812976
[PubMed - indexed for MEDLINE]
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