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Abstract

Mitochondrial dysfunction has been shown to participate in the induction of apoptosis and has even been suggested to be central to the apoptotic pathway. Indeed, opening of the mitochondrial permeability transition pore has been demonstrated to induce depolarization of the transmembrane potential (deltapsi(m)), release of apoptogenic factors and loss of oxidative phosphorylation. In some apoptotic systems, loss of deltapsi(m) may be an early event in the apoptotic process. However, there are emerging data suggesting that, depending on the model of apoptosis, the loss of deltapsi(m) may not be an early requirement for apoptosis, but on the contrary may be a consequence of the apoptotic-signaling pathway. Furthermore, to add to these conflicting data, loss of deltapsi(m) has been demonstrated to not be required for cytochrome c release, whereas release of apoptosis inducing factor AIF is dependent upon disruption of deltapsi(m) early in the apoptotic pathway. Together, the existing literature suggests that depending on the cell system under investigation and the apoptotic stimuli used, dissipation of deltapsi(m) may or may not be an early event in the apoptotic pathway. Discrepancies in this area of apoptosis research may be attributed to the fluorochromes used to detect deltapsi(m). Differential degrees of sensitivity of these fluorochromes exist, and there are also important factors that contribute to their ability to accurately discriminate changes in deltapsi(m).

Contribution of Mitophagy to Cell‐Mediated Mineralization: Revisiting a 50‐Year‐Old Conundrum

“…Maintaining normal Δ Ψ m is critical for mitochondrial functions 14, 22. As mentioned previously, liquid‐like ACP precursors accumulated within the mitochondria during osteogenic differentiation of hDPSCs.…”

“…Accumulation of PINK1 sends a “eat‐me” signal that induces translocation of PARKIN from the cytosol to dysfunctioned mitochondria and targets the mitochondria for lysosomal degradation 19, 20. Accordingly, immunogold labeling of PINK1, lysosomal‐associated membrane protein 1 (LAMP1, lysosome marker21), and microtubule‐associated protein‐1 light chain‐3 (LC3, autophagosome marker22) was performed to confirm the identity of the organelles previously identified by TEM. In mitochondria derived from undifferentiated hDPSCs, granules were absent and PINK1 was located inside the mitochondria (Figure 2H).…”

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

“…Mitochondria have an essential role in life and death decision of neuronal cells. Mitochondria dysfunction induced cell apoptosis and was represented by the loss of mitochondrial membrane potential (Ly et al ., 2003). Although glutamate-induced Ca 2+ influx decreased mitochondrial membrane potential (Duchen, 2000), SFC significantly recovered the mitochondrial membrane potential to 97.88 ± 9.60% of control ( p <0.05) at a concentration of 500 μg/ml (Fig.…”

Role of mitochondrial membrane permeabilization in apoptosis and cancer

“…Cooperation among these proteins leads to the formation of a conductance channel which is responsible for the sudden increase in the permeability of the IMM to small molecular weight solutes and a collapse in the mitochondrial membrane potential DC m (reviewed in Ly et al, 2003). The entry of solutes leads to a swelling of the mitochondrial matrix and a rupture of the OMM thereby releasing, in a nonspecific manner, soluble proteins from the intermembrane space.…”

“…The biochemical hallmarks include the loss of sialic acid, fragmentation of the nuclear DNA and a translocation of phosphatidylserine to the outer plasma membrane; while physical manifestations include vacuolization, chromatin condensation, blebbing of the plasma membrane and the eventual organized disintegration of the cell into packaged 'apoptotic bodies'. In the physiological setting these discrete cellular packages are subsequently targeted and cleared by phagosomes (for a recent review see Ly et al, 2003).…”