Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic <i>β</i>-cells

<div>Respiration induced by palmitic acid in nontransgenic <i>vs</i>. UCP2-silenced INS-1E cells. Respiration was estimated in 10–14 and 3 independent experiments for nontransgenic (ntg) and UCP2-silenced INS-1E cells. The ntg cells were transfected with miRNA of a scrambled sequence. When indicated (+PA), palmitic acid in bovine serum albumin solution was added to reach a total amount of 75 nmol palmitic acid <i>per</i> l0<sup>6</sup> cells. As indicated, either 3 mmol·l<sup>-1</sup> glucose (Glc3) or 25 mmol·l<sup>-1</sup> glucose (Glc25) was present in the assay medium. The error bars represent the standard deviations. 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Oxidative Medicine and Cellular Longevity

fig6

Figure 6

Figure 6: Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic <i>β</i>-cells 

Oxidative Medicine and Cellular Longevity

Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic β-cells

Figure 6