Association Between Oxidative Stress and Altered Cholesterol Metabolism in Alzheimer's Disease Patients.
Alzheimer's disease
antioxydant enzymes
cholesterol
lipid peroxidation
oxidative stress
oxysterols
Journal
Current Alzheimer research
ISSN: 1875-5828
Titre abrégé: Curr Alzheimer Res
Pays: United Arab Emirates
ID NLM: 101208441
Informations de publication
Date de publication:
2020
2020
Historique:
received:
13
02
2020
revised:
10
09
2020
accepted:
22
09
2020
pubmed:
5
12
2020
medline:
12
10
2021
entrez:
4
12
2020
Statut:
ppublish
Résumé
Oxidative stress is the main feature of several diseases including Alzheimer's disease (AD). The involvement of oxysterols derivates has been recently reported. The aim of this study was to evaluate the implication of oxidative stress in cholesterol impairment in AD patients. A case-control study was conducted on 56 AD patients and 97 controls. Levels of oxidative biomarkers, including lipid peroxidation products and antioxidant enzyme activities were measured with spectrophotometric methods on red blood cells (RBCs) and plasma. Cholesterol precursors and oxysterols (7-Ketocholeterol (7KC), 7α-hydroxycholesterol (7α-OHC), 7β-hydroxycholesterol (7β-OHC), 24Shydroxycholesterol (24S-OH), 25-hyroxycholesterol (25-OHC), and 27-hydroxycholesterol (27-OHC), in plasma were quantified by gas chromatography coupled with mass spectrometry. In RBCs and plasma of AD patients, a significant decrease of glutathione peroxidase (GPx) activity was detected associated with raised levels of malondialdehyde (MDA). A decreased level of lanosterol and an accumulation of 7β-OHC, 24S-OHC, 27-OHC, and 25-OHC that were higher in plasma of AD patients, compared to controls, were also observed in AD patients. Mini-Mental State Examination (MMSE) score was correlated with MDA and conjugated dienes (CD) levels in plasma. Besides, the MDA level in RBCs was correlated with 7β-OHC. Binary logistic regression revealed an association between GPx activity and AD (OR=0.895, 95%CI: 0.848-0.945. P<0.001). Our data consolidate the relationship between the rupture of redox homeostasis and lipid and cholesterol oxidation in AD.
Sections du résumé
BACKGROUND
Oxidative stress is the main feature of several diseases including Alzheimer's disease (AD). The involvement of oxysterols derivates has been recently reported.
OBJECTIVE
The aim of this study was to evaluate the implication of oxidative stress in cholesterol impairment in AD patients.
METHODS
A case-control study was conducted on 56 AD patients and 97 controls. Levels of oxidative biomarkers, including lipid peroxidation products and antioxidant enzyme activities were measured with spectrophotometric methods on red blood cells (RBCs) and plasma. Cholesterol precursors and oxysterols (7-Ketocholeterol (7KC), 7α-hydroxycholesterol (7α-OHC), 7β-hydroxycholesterol (7β-OHC), 24Shydroxycholesterol (24S-OH), 25-hyroxycholesterol (25-OHC), and 27-hydroxycholesterol (27-OHC), in plasma were quantified by gas chromatography coupled with mass spectrometry.
RESULTS
In RBCs and plasma of AD patients, a significant decrease of glutathione peroxidase (GPx) activity was detected associated with raised levels of malondialdehyde (MDA). A decreased level of lanosterol and an accumulation of 7β-OHC, 24S-OHC, 27-OHC, and 25-OHC that were higher in plasma of AD patients, compared to controls, were also observed in AD patients. Mini-Mental State Examination (MMSE) score was correlated with MDA and conjugated dienes (CD) levels in plasma. Besides, the MDA level in RBCs was correlated with 7β-OHC. Binary logistic regression revealed an association between GPx activity and AD (OR=0.895, 95%CI: 0.848-0.945. P<0.001).
CONCLUSION
Our data consolidate the relationship between the rupture of redox homeostasis and lipid and cholesterol oxidation in AD.
Identifiants
pubmed: 33272182
pii: CAR-EPUB-112022
doi: 10.2174/1567205017666201203123046
doi:
Substances chimiques
Cholesterol
97C5T2UQ7J
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
823-834Informations de copyright
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