Induction of Mitochondrial Changes Associated with Oxidative Stress on Very Long Chain Fatty Acids (C22:0, C24:0, or C26:0)-Treated Human Neuronal Cells (SK-NB-E)
Figure 8
Evaluation by transmission electron microscopy of the ultrastructural characteristics of human neuronal cells (SK-NB-E) treated with C22:0, C24:0, or C26:0 and of their mitochondrial characteristics. Transmission electron microscopy of SK-NB-E cells cultured for 48 h in the absence (control cells) (a, f) or presence of α-cyclodextrin (1 mg/mL) (vehicle) (b, g), C22:0 (10 μM) (c, h), C24:0 (10 μM) (d, i), or C26:0 (10 μM) (e, j). The insets in Figures (a, b, c, d, and e) correspond to Figures (f, g, h, i, and j), respectively. No differences were observed between control (a, f) and vehicle-treated cells (b, g). In C22:0-, C24:0- and C26:0-treated cells, no signs of apoptosis (cells with perinuclear chromatin, with condensed and/or fragmented nuclei) were detected [47, 48], but some mitochondrial modifications were observed. In C22:0- (h), C24:0- (i), and C26:0- (j) treated SK-NB-E cells, when compared to control and vehicle-treated cells, higher numbers of mitochondria, often larger in size, were found.
