Volume 63 (2013) Issue: 2013 No#2-3

Oxido-reductive brain status after acute aluminium poisoning – the role of free radicals

Author(s): Milovanović Anđela, Milovanović J, Konstatinović Ljubica, Vićentić S, Pavlović B, Kojić A, Marmut Z, ^emerikić D, Galjak M, Milovanović A

Keywords:acute aluminium poisoning, brain, free radicals, oxido-reductive stress

Free radicals induce oxidative processes which damage and inactivate many intracellular components and may cause cell death. This paper presents the results of experiments performed on desert mice (gerbils), adults of both sexes. After acute intraperitoneal administration of aluminium, the oxido-reductive brain state was investigated in the cerebral cortex, hippocampus and nucleus caudatus brain structures. We observed a decrease in defense capacities of the brain – decrease of superoxide dismutase and glutathione reductase activity, with a simultaneous increase in the quantity of malondialdehyde, which indicates that under the influence of aluminium the brain capacity to neutralize superoxide radicals is significantly decreased, and that the consequence is increased generation of free radicals which damage the membrane and results in the formation of malondialdehyde from membrane lipids thus breaking the functional integrity of the cell. Acute Al3+ administration caused a dose-dependent increase in the quantity of malondialdehyde in the cerebral cortex and hippocampus, while in the nucleus caudatus this effect was somewhat less pronounced. Mitochondrial superoxide dismutase was more sensitive to the administration of Al3+ than tissue superoxide dismutase.


My account

Search


Info

ISSN: 0567-8315

eISSN: 1820-7448

Journal Impact Factor 2017: 0.604

5-Year Impact Factor: 0.439

Indexing: Thomson Reuters/Science Citation Index Expanded, Zoological Record, Biosis Previews, Web of Science, Journal Citation Reports, Google Scholar, SCIndeks, KoBSON, Genamics, Journal Seek, Research Gate, DOAJ, Journal Rate, SJR – SCImago Journal & Country Rank, WorldCat, Academic Journals Database, Medical Journals Links, MedSci, Pubget

Contribute