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Oxidative stress precedes mitochondrial dysfunction in gerbil brain after aluminum ingestion.

Abstract
Several studies suggest that aluminum (Al) intake might increase an individual's risk of developing Alzheimer disease. The dynamic of changes in acetylcholinesterase (AChE), cytochrome c oxidase (COX), Complex I, superoxide dismutase (SOD) and catalase (CAT) activities, and the lipid peroxide (MDA), superoxide anion (O₂(-)) and thiol (SH) group levels in gerbil's brain after aluminum ingestion were analyzed. Gerbils that orally received aluminum chloride (LD₂₅ or LD₅₀) were sacrificed 2, 6 or 24 h later. Another group was subacutely treated (21 days; LD10). Controls received saline. Biochemical parameters were measured in cortex, hippocampus, thalamus and nucleus caudatus. Two hours after acute Al exposure AChE activity and SH group content were decreased and MDA and O₂(-) levels were elevated in all investigated brain structures. The changes of COX and CAT were structure specific. SOD was increased after 6 h. Changes of investigated parameters were also seen after subacute Al treatment. These results might suggest the presence of additional source of free radicals in early phase of Al poisoning.
AuthorsSvetlana Vučetić-Arsić, Nevena V Radonjić, Marina Jovanović, Vesna Selaković, Tatjana Nikolić, Milica Velimirović, Tihomir Stojković, Andjela Milovanović, Jovica Milovanović, Nataša D Petronijević
JournalEnvironmental toxicology and pharmacology (Environ Toxicol Pharmacol) Vol. 36 Issue 3 Pg. 1242-52 (Nov 2013) ISSN: 1872-7077 [Electronic] Netherlands
PMID24211763 (Publication Type: Journal Article)
CopyrightCopyright © 2013 Elsevier B.V. All rights reserved.
Chemical References
  • Aluminum Compounds
  • Chlorides
  • Sulfhydryl Compounds
  • Superoxides
  • Aluminum Chloride
  • Malondialdehyde
  • Catalase
  • Prostaglandin-Endoperoxide Synthases
  • Superoxide Dismutase
  • Electron Transport Complex I
Topics
  • Aluminum Chloride
  • Aluminum Compounds (toxicity)
  • Animals
  • Brain Chemistry (drug effects)
  • Brain Diseases (chemically induced, metabolism)
  • Catalase (metabolism)
  • Chlorides (toxicity)
  • Electron Transport Complex I (metabolism)
  • Gerbillinae
  • Lethal Dose 50
  • Lipid Peroxidation (drug effects)
  • Male
  • Malondialdehyde (metabolism)
  • Mitochondrial Diseases (chemically induced, metabolism)
  • Oxidative Stress (drug effects)
  • Prostaglandin-Endoperoxide Synthases (metabolism)
  • Sulfhydryl Compounds (metabolism)
  • Superoxide Dismutase (metabolism)
  • Superoxides (metabolism)

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