Plasma Cytochrome c Detection Using a Highly Sensitive Electrochemiluminescence Enzyme-Linked Immunosorbent Assay

Radhakrishnan, Jeejabai; Origenes, Rovi; Littlejohn, Gina; Nikolich, Sanja; Choi, Eun-Jung; Smite, Sharon; Lamoureux, Lorissa; Baetiong, Alvin; Shah, Manoj; Gazmuri, Raúl J.

doi:10.1177/1177271917746972

Cited by 11 publications

(7 citation statements)

References 31 publications

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“…Although the detection of Cyt C was not based on the total protein, it was noted that detecting total Cyt C protein has been reported in several studies; for example, Eleftheriadis et al ( 40 ) demonstrated that serum Cyt C levels may be a biomarker for mitochondrial and cellular damage. In addition, Li et al ( 41 ) measured Cyt C levels via an optical microfiber, and a study by Radhakrishnan et al ( 42 ) used an ELISA approach to determine plasma Cyt C levels. Overall, although the qualification of total Cyt C levels cannot reflect programmed cell death, it is only the way for reflecting the early event of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Mitochondria-targeted antioxidant therapy for an animal model of PCOS-IR

et al. 2018

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Polycystic ovary syndrome (PCOS) is a common endocrine disorder with unknown etiology and unsatisfactory clinical treatment. Considering the ethical limitations of studies involving humans, animal models that reflect features of PCOS and insulin resistance (IR) are crucial resources in investigating this syndrome. Our previous study showed that mitochondrial dysfunction resulted from pathogenic mutations of mitochondrial DNA (mtDNA), and that oxidative stress had an active role in the phenotypic manifestation of PCOS-IR. Therefore, it was hypothesized that limiting oxidative stress and mitochondrial damage may be useful and effective for the clinical treatment of PCOS-IR. For this purpose, the present study examined the therapeutic effects of the mitochondria-targeted antioxidant MitoQ10 for PCOS-IR. Furthermore, the histopathology was used to analysis the ovarian morphological changes. The endocrine and reproductive related parameters were analyzed by ELISA approach. A PCOS-IR model was successfully established by subcutaneous injection of rats with testosterone propionate and feeding a high-fat diet. The 30 female Sprague-Dawley rats were then divided into three groups, comprising a control (n=10), animal model (PCOS-IR, n=10) and MitoQ10 treatment (n=10) group. It was found that MitoQ10 significantly improved the IR condition and reversed the endocrine and reproductive conditions of PCOS. In addition, the impaired mitochondrial functions were improved following MitoQ10 administration. Notably, western blot results suggested that this antioxidant reduced the expression levels of apoptosis-related proteins cytochrome c and B-cell lymphoma-2 (Bcl-2)-associated X protein, whereas the anti-apoptotic protein Bcl-extra large was increased following MitoQ10 treatment. Taken together, the data indicated that the MitoQ10 may have a beneficial favorable therapeutic effect on animals with PCOS-IR, most likely via the protection of mitochondrial functions and regulation of programmed cell death-related proteins.

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Section: Discussionmentioning

confidence: 99%

Mitochondria-targeted antioxidant therapy for an animal model of PCOS-IR

et al. 2018

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“…In fact, cytochrome C oxidase is a plasma biomarker of anti-apoptotic activity during chronic glaucoma. Thus, its plasma activity and concentration vary with the chronic evolution of apoptosis towards cellular necrosis, or conversely towards its disappearance [14] [15] [17] [83]. The positive correlation found between HIF-1 alpha and cytochrome C on the one hand, and on the other hand, the variations of concentrations observed within the two groups confirm the hypothesis that, during chronic glaucoma, hypoxia is responsible of anti-hypoxic mediators such as HIF-1α.…”

Section: Relationship Between Cmngb Cmcyt C and Cmgpx In Cg +mentioning

confidence: 80%

“…Indeed, it has been shown that during chronic glaucoma, the apoptosis, hypoxia and oxidative stress phenomena were correlated with the progression of the disease [17] [19] [78]. These would intensify to give way to the necrosis of the retinal cells ganglion, then in fine, those of the head of the optic nerve [12] [83]. However, the presence of higher CmNgb and CmCyt C in CG + compared to CG − made us accept the hypothesis that the absence of correlation found between CmCyt C and CmNgb is would be due to the anti-apoptotic activity of the Ngb.…”

Section: Relationship Between Cmngb Cmcyt C and Cmgpx In Cg +mentioning

confidence: 99%

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Contribution at the Study of Neuroprotective Properties of Neuroglobin during Severe Chronic Glaucoma

Essone¹,

Angue²,

Belmalih³

et al. 2020

WJNS

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Introduction: The mechanisms of overexpression of neuroglobin in patients with severe glaucoma (CG +) remain hypothetical. Objective: To study the anti-apoptotic, anti-hypoxic and anti-oxidant properties of neuroglobin in CG +. Population and Methods: The visual field, as well as plasma dosage of neuroglobin (CmNgb, ng/ml), hypoxia inductible factor-1alpha (CmHIF-1α, pg/ml), glutathione peroxidase (CmGpx, pg/ml), and cytochrome C oxidase (CmCyt C, pg/ml) were carried out in 45 CG + and 45 controls (CG −). The chi-2 test compared the proportions, and Spearman's test studied the correlations between quantitative variables (p < 5%). Results: CmNgb was 4.1 in CG + , versus 2.3 in CG − (p = 1.52 × 10 −5). CmGpx was 1144.7 in CG + , versus 752.8 in GC − (p = 0.0199). CmHIF-1α was 4.1 in CG + , versus 3.5 in CG − (p = 0.4530). CmCyt C was 2303.26 in CG + , versus 1750.44 in CG − (p = 0.0450). In CG + , there was a correlation between CmNgb and CmGpx (r = 0.417; p = 0.004), CmNgb and CmHIF-1α (r = 0.644; p = 1.8 × 10 −6), and between CmHIF-1α and CmGpx (r = 0.447; p = 0.002), CmHIF-1α and CmCyt C (r = 0.371; p = 0.012). None correlation was found between CmNgb and CmCyt C (r = 0.126; p = 0.370), as well as CmGpx and CmCyt C (r = 0.102; p = 0.505). Conclusion: The variations of apoptosis, hypoxic, and oxidative stress bio-How to cite this paper: Nnang Essone,

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“…There was also a prominent increase in plasma cytochrome c , which is a mitochondrial protein responsible for the transfer of electrons from complex III to complex IV of the electron transport chain. Its release to the plasma is associated with the severity of myocardial injury after cardiac arrest [43,59]. Buffer administration was also associated with lactatemia attaining levels substantially higher than expected from cardiac arrest.…”

Section: Cellular Mechanisms Of the Observed Functional Benefitsmentioning

confidence: 99%

Sodium-Hydrogen Exchanger Isoform-1 Inhibition: A Promising Pharmacological Intervention for Resuscitation from Cardiac Arrest

2019

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Out-of-hospital sudden cardiac arrest is a major public health problem with an overall survival of less than 5%. Upon cardiac arrest, cessation of coronary blood flow rapidly leads to intense myocardial ischemia and activation of the sarcolemmal Na+-H+ exchanger isoform-1 (NHE-1). NHE-1 activation drives Na+ into cardiomyocytes in exchange for H+ with its exchange rate intensified upon reperfusion during the resuscitation effort. Na+ accumulates in the cytosol driving Ca2+ entry through the Na+-Ca2+ exchanger, eventually causing cytosolic and mitochondrial Ca2+ overload and worsening myocardial injury by compromising mitochondrial bioenergetic function. We have reported clinically relevant myocardial effects elicited by NHE-1 inhibitors given during resuscitation in animal models of ventricular fibrillation (VF). These effects include: (a) preservation of left ventricular distensibility enabling hemodynamically more effective chest compressions, (b) return of cardiac activity with greater electrical stability reducing post-resuscitation episodes of VF, (c) less post-resuscitation myocardial dysfunction, and (d) attenuation of adverse myocardial effects of epinephrine; all contributing to improved survival in animal models. Mechanistically, NHE-1 inhibition reduces adverse effects stemming from Na+–driven cytosolic and mitochondrial Ca2+ overload. We believe the preclinical work herein discussed provides a persuasive rationale for examining the potential role of NHE-1 inhibitors for cardiac resuscitation in humans.

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Plasma Cytochrome c Detection Using a Highly Sensitive Electrochemiluminescence Enzyme-Linked Immunosorbent Assay

Cited by 11 publications

References 31 publications

Mitochondria-targeted antioxidant therapy for an animal model of PCOS-IR

Mitochondria-targeted antioxidant therapy for an animal model of PCOS-IR

Contribution at the Study of Neuroprotective Properties of Neuroglobin during Severe Chronic Glaucoma

Sodium-Hydrogen Exchanger Isoform-1 Inhibition: A Promising Pharmacological Intervention for Resuscitation from Cardiac Arrest

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