Anti‐neurotoxic evaluation of synthetic and characterized metal complexes of thiosemicarbazone derivatives

Quinoline‐2‐caboxyaldehyde thiosemicarbazone (HL1) and quinoline ‐2‐caboxyaldehyde N‐dimethyl thiosemicarbazone (HL2) metal complexes were prepared and characterized using analytical and spectroscopic techniques. The measurements showed that ligands behave as monovalent or neutral tridentate ligands...

Full description

Saved in:
Bibliographic Details
Published in:Applied organometallic chemistry 2018-04, Vol.32 (4), p.n/a
Main Authors: El‐Saied, Fathy A., Salem, Tarek A., Shakdofa, Mohamad M.E., Al‐Hakimi, Ahmed N.
Format: Article
Language:English
Subjects:
Aluminum
Alzheimer's disease
anti‐neurotoxic
Brain
Chelation
Chemical bonds
Chemistry
Coordination compounds
Excretion
Ligands
metal complexes
Metals
Neurotoxicity
Nitrogen atoms
Quinoline
thiosemicarbazone
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Quinoline‐2‐caboxyaldehyde thiosemicarbazone (HL1) and quinoline ‐2‐caboxyaldehyde N‐dimethyl thiosemicarbazone (HL2) metal complexes were prepared and characterized using analytical and spectroscopic techniques. The measurements showed that ligands behave as monovalent or neutral tridentate ligands bonding via azomethine, quinoline ring nitrogen atoms and sulfur atoms in thiol or thion forms. The anti‐neurotoxic effect of ligands and their complexes showed that, exposure to aluminum increase oxidative stress in the brain, an effect that could be offset by concomitant thiosemicarbazone complexes. Complexes could be having an effect on absorption or excretion of aluminum, due to their chelating activity. These findings may shed light on the potential clinical importance of thiosemicarbazone complexes in Alzheimer's disease. Anti‐oxidative and chelating activity of quinoline‐2‐caboxyaldehyde thiosemicarbazone (HL1) and quinoline ‐2‐caboxyaldehyde N‐dimethyl thiosemicarbazone (HL2)
ISSN:0268-2605
1099-0739
DOI:10.1002/aoc.4215