Cytochrome c as an amplifier of ROS release in mitochondria

Акопова, О. В.; Kolchinskaya, L. I.; Nosar, V. I.; Bouryi, V. A.; Mankovska, Irina N.; Sagach, V. F.

doi:10.15407/fz58.01.003

Cited by 17 publications

(11 citation statements)

References 20 publications

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“…Mitochondria play a crucial part in the cell growth and death and possess the function of ROS generation and detoxification ( 40 , 41 ). It has been demonstrated that at high concentration, ROS might lead to severe injury to cells, which referred to the ‘oxidative stress’ ( 42 – 44 ).…”

Section: Discussionmentioning

confidence: 99%

Aucubin suppresses Titanium particles‑mediated apoptosis of MC3T3‑E1 cells and facilitates osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway

et al. 2018

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Aucubin represents an iridoid glucoside separated from multiple Chinese herbs, which has been demonstrated to possess numerous pharmacological activities. In the present study, the aim was to investigate the roles and mechanisms of aucubin in the suppression of mouse MC3T3-E1 osteoblast apoptosis induced by Titanium particles and the promotion of bone formation. MTT assay and flow cytometry were performed to analyze cell viability and apoptosis, respectively. ELISA and para-nitrophenyl phosphate colorimetry were carried out to evaluate the oxidative stress markers and alkaline phosphatase (ALP). Western blotting and reverse transcription-quantitative polymerase chain reaction assays were used to evaluate the associated mRNA and protein expression. The results revealed that aucubin enhanced the cell activity of MC3T3-E1 cells treated with Ti particles. Aucubin suppressed the apoptosis of Ti particles-induced MC3T3-E1 cells and facilitated osteogenesis by affecting the B-cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein, ALP and associated osteogenic factors expression. Aucubin reduced the oxidative stress in Ti particles-induced MC3T3-E1 cells. In addition, aucubin upregulated the bone morphogenetic protein 2 (BMP2)/Smads/runt related transcription factor 2 (RunX2) pathway in Ti particles-induced MC3T3-E1 cells. In conclusion, the present study confirmed that aucubin suppressed the Ti particles-mediated apoptosis of MC3T3-E1 cells and facilitated osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Aucubin suppresses Titanium particles‑mediated apoptosis of MC3T3‑E1 cells and facilitates osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway

et al. 2018

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“…For instance, cytochrome C can transfer electron directly to p66 Shc , a redox enzyme, to generate ROS [47]. The heme center of cytochrome C may also act to enhance ROS production [48].…”

Section: Discussionmentioning

confidence: 99%

Enterovirus 71 Induces Mitochondrial Reactive Oxygen Species Generation That is Required for Efficient Replication

et al. 2014

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Redox homeostasis is an important host factor determining the outcome of infectious disease. Enterovirus 71 (EV71) infection has become an important endemic disease in Southeast Asia and China. We have previously shown that oxidative stress promotes viral replication, and progeny virus induces oxidative stress in host cells. The detailed mechanism for reactive oxygen species (ROS) generation in infected cells remains elusive. In the current study, we demonstrate that mitochondria were a major ROS source in EV71-infected cells. Mitochondria in productively infected cells underwent morphologic changes and exhibited functional anomalies, such as a decrease in mitochondrial electrochemical potential ΔΨm and an increase in oligomycin-insensitive oxygen consumption. Respiratory control ratio of mitochondria from infected cells was significantly lower than that of normal cells. The total adenine nucleotide pool and ATP content of EV71-infected cells significantly diminished. However, there appeared to be a compensatory increase in mitochondrial mass. Treatment with mito-TEMPO reduced eIF2α phosphorylation and viral replication, suggesting that mitochondrial ROS act to promote viral replication. It is plausible that EV71 infection induces mitochondrial ROS generation, which is essential to viral replication, at the sacrifice of efficient energy production, and that infected cells up-regulate biogenesis of mitochondria to compensate for their functional defect.

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“…As we have shown earlier, in low-conductance states mPTP releases Ca 2+ in exchange for protons [18], takes part in Ca 2+ cycling and oxygen consumption without much affecting ΔΨ m in rat liver mitochondria [19]. Based on our previous studies, reversible mPTP opening in low conductance states in liver mitochondria contributed to ROS production and caused mild uncoupling of Oxphos [19,20].…”

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confidence: 58%

Functional activity of permeability transition pore in energized and deenergized rat liver mitochondria

Акопова¹,

Kolchinskaya²,

Kolchinskaya³

2020

Ukr.Biochem.J

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permeability transition pore (mpTp) opening was studied under energized and deenergized conditions in rat liver mitochondria, and the effect of membrane depolarization on mPTP activity was evaluated. To assess mpTp activity, cyclosporine-sensitive swelling and cyclosporine sensitive ca 2+ efflux from mitochondria was studied using light absorbance techniques. In energized mitochondria, mpTp opening in subconductance states, at [ca 2+ ] ≤ K a , contributed positively to the rate of respiration, without affecting ΔΨ m . Threshold ca 2+ concentrations were found, which excess resulted in fast mitochondrial depolarization upon mpTp opening. An estimate of mpTp activity by cyclosporine-sensitive ca 2+ transport under energized and deenergized conditions showed that membrane depolarization by protonophore cccp essentially increased initial rate (V 0 ), at simultaneous decrease of the half-time (t 1/2 ) of ca 2+ efflux, which indicated mPTP activation, as compared to energized mitochondria. however, only partial release of ca 2+ via mpTp upon membrane depolarization was observed. With the use of selective blockers of ca 2+ uniporter and mpTp, ruthenium red (rr) and cyclosporine A (csA), partial contribution of ca 2+ uniporter and mpTp in ca 2+ transport was found. "Titration" of ca 2+ transport by adding RR at different times from the onset of depolarization showed that depolarization dramatically reduced "life span" of mpTp as compared to energized mitochondria, which agreed with the kinetic characteristics of csA-sensitive ca 2+ transport after the abolition of ΔΨ m . ca 2+ added from the outer side of mitochondrial membrane produced dual effect on mPTP activity: activation at the onset of depolarization, but consequent promotion of mPTP closure. Based on the experiments, it was concluded that mitochondrial energization was required for prolonged mpTp functioning in sub-conductance states, whereas membrane depolarization promoted the transition of mpTp to inactive state during calcium release from mitochondria. k e y w o r ds: rat liver mitochondria, calcium, permeability transition pore, ca 2+ transport, membrane potential.

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Cytochrome c as an amplifier of ROS release in mitochondria

Cited by 17 publications

References 20 publications

Aucubin suppresses Titanium particles‑mediated apoptosis of MC3T3‑E1 cells and facilitates osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway

Aucubin suppresses Titanium particles‑mediated apoptosis of MC3T3‑E1 cells and facilitates osteogenesis by affecting the BMP2/Smads/RunX2 signaling pathway

Enterovirus 71 Induces Mitochondrial Reactive Oxygen Species Generation That is Required for Efficient Replication

Functional activity of permeability transition pore in energized and deenergized rat liver mitochondria

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