Mild depolarization of the mitochondrial potential by PBE does not involve the constituent catechin as revealed in the present study.
As shown in Figure 8(b), PBE caused dose-dependent but mild depolarization of the brain mitochondrial potential (ΔΨ m) which only becomes statistically significant at the highest concentration of 100 μg/mL (P < 0.01) whereas catechin at the evaluated concentrations showed no effect on the brain mitochondrial potential).
To verify that the observed respiratory elevations represent a mild mitochondrial uncoupling, we monitored the IMM potential decrease (δTBHPΔΨm) at various glucose concentrations, after TBHP addition to UCP2- (Fig. 1C) and iPLA2γ-silenced INS-1E cells (Fig. 1D).
Superoxide production by mitochondria isolated from mammals (Liu, 1997; Korshunov et al., 1997) or Drosophila (Miwa et al., 2003) can be acutely sensitive to membrane potential, so if mitochondrial superoxide production contributes to ageing, mild mitochondrial uncoupling might extend lifespan.
Together, these findings suggest that mitochondria are partially uncoupled in MetR cells and raise the possibility that extended lifespan of MetR cells is due to mild mitochondrial uncoupling, consistent with earlier findings that mild uncoupling of mitochondria has the potential to extend lifespan of human fibroblasts (Passos et al., 2007).
However, mild mitochondrial depolarization is also known to trigger mitophagy: PINK1 is constitutively degraded so long as mitochondrial membrane potential is high.
Across eukaryotic species, mild mitochondrial stress can have beneficial effects on the lifespan of organisms.
Our findings indicate that ROS inhibition through mitochondrial-targeted antioxidant or mild mitochondrial uncoupling is beneficial for sperm cryopreservation in yellow catfish.
The influence on mitochondrial potential and induction of mitochondrial permeability transition also have been studied.
The results indicated a natural match for hypoxia environments in Tibetan highlands and mild mitochondrial dysfunction caused by mtDNA deleterious mutation, which provide functional evidence for our work.
