Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7 β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes.

Biotin attenuation of oxidative stress, mitochondrial dysfunction, lipid metabolism alteration and 7β-hydroxycholesterol-induced cell death in 158N murine oligodendrocytes. Free Radic Res. 2019 May 01;:1-11 Authors: Sghaier R, Zarrouk A, Nury T, Ilham B, O'Brien N, Mackrill JJ, Vejux A, Samadi M, Nasser B, Caccia C, Leoni V, Moreau T, Cherkaoui-Malki M, Salhedine Masmoudi A, Lizard G Abstract Mitochondrial dysfunction and oxidative stress are involved in neurodegenerative diseases associated with an enhancement of lipid peroxidation products such as 7β- hydroxycholesterol (7β-OHC). It is therefore important to study the ability of 7β-OHC to trigger mitochondrial defects, oxidative stress, metabolic dysfunctions and cell death, which are hallmarks of neurodegeneration, and to identify cytoprotective molecules. The effects of biotin were evaluated on 158N murine oligodendrocytes, which are myelin synthesizing cells, exposed to 7β-OHC (50 µM) with or without biotin (10 and 100 nM) or α-tocopherol (positive control of cytoprotection). The effects of biotin on 7β-OHC activities were determined using different criteria: cell adhesion; plasma membrane integrity; redox status. The impact on mitochondria was characterized by the measurement of transmembrane mitochondrial potential (ΔΨm), reactive oxygen species (ROS) overproduction, mitochondrial mass, quantification of cardiolipins and organic acids. Sterols and fatty acids were ...
Source: Free Radical Research - Category: Research Tags: Free Radic Res Source Type: research