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Oxygen Transport
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
P.N. Chatzinikolaou, N.V. Margaritelis, A.N. Chatzinikolaou, V. Paschalis, A.A. Theodorou, I.S. Vrabas, A. Kyparos, M.G. Nikolaidis
Once inside the muscle cell, oxygen flow to mitochondria is achieved by two ways: (i) as dissolved oxygen and (ii) via myoglobin-mediated delivery (Pias, 2020). Intracellular oxygen bound to myoglobin exceeds free oxygen by a ratio of 30:1, leaving an approximate sarcoplasmic free oxygen of ≈3.2 μM at 37°C (Pias, 2020). The role of myoglobin has been debated over the years, with the prevailing theories being that it serves as a (1) short-term oxygen storage (e.g., at rest), (2) oxygen transporter to mitochondria (e.g., during exercise) and (3) redox catalyst (Meyer, 2004). Oxygen binding to myoglobin during exercise could decrease the intramyocellular oxygen pressure gradient and enhance oxygen diffusion (Clanton, Hogan and Gladden, 2013). On the other, exercise-induced muscle damage increases serum myoglobin concentration (Balnave and Thompson, 1993) limiting oxygen availability intracellularly. Another molecule with the ability to store oxygen inside muscle is cytoglobin, which is found in micromolar concentrations (Fago et al., 2004). Despite the limited information in exercise conditions, cytoglobin has been reported to buffer intracellular oxygen (Clanton, Hogan and Gladden, 2013), regulate NO• availability (Mathai et al., 2020) and serve a role in muscle repair in mice (Singh et al., 2014).
The involvement of Nrf2/HO-1/cytoglobin and Ang-II/NF-κB signals in the cardioprotective mechanism of lansoprazole against cisplatin-induced heart injury
Published in Toxicology Mechanisms and Methods, 2023
Emad H. M. Hassanein, Fares E. M. Ali, Zuhair M. Mohammedsaleh, Ahmed M. Atwa, Mohamed Elfiky
Interestingly, the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signal is a strategic signal responsible for cellular injury detoxification (Chen and Maltagliati 2018). Recent studies found that Nrf2 signaling was inhibited in CIS-treated hearts and the restoration of myocardial Nrf2 remarkably reduced the severity of heart injury (Zhao 2019; Lin et al. 2021). It was previously documented that PPAR-γ enhances the antioxidant status (Kim and Yang 2013) and suppresses the production of inflammatory genes by interfering with nuclear factor-κB (NF-κB) transcriptional activity (Mateu et al. 2015). Notably, it has been reported that PPAR-γ activation effectively protects against CIS-induced organ toxicities (Badawy et al. 2019; Michel and Menze 2019). Moreover, cytoglobin is a type of intracellular respiratory globin found in almost all tissues (Lüdemann et al. 2019), and it’s upregulation plays a crucial role in the protection against chemotherapy-associated adverse effects (Hassanein et al. 2020; Abd El-Ghafar et al. 2021; Ali et al. 2021a).
Dietary natural flavonoids treating cancer by targeting aryl hydrocarbon receptor
Published in Critical Reviews in Toxicology, 2019
Tian Yang, Ya-Long Feng, Lin Chen, Nosratola D. Vaziri, Ying-Yong Zhao
This indicates that Phortress has a selective tumor suppressor effect in tumor cells, and its anti-tumor activity is linked to CYP1A1 activity. In addition, some new ideas about the role of 5 F 203 in cancer treatment have been reported recently. Luzzani et al. demonstrated that 5 F 203 can inhibit c-Met receptor phosphorylation in human renal cancer cell lines (TK-10 cells). And c-Met receptor signaling is important in the migration and metastasis of tumor cells (Luzzani et al. 2017). And McLean et al. demonstrate that 5 F 203 induces reactive oxygen species mediated DNA damage at least in part via AhR, c-Jun-N-terminal kinase, or p38 mitogen-activated protein kinase activation and modulates the expression of oxidative stress-responsive genes such as cytoglobin to confer its anticancer effect (McLean et al. 2015). In addition, Rowland et al. previously demonstrated that 5 F 203 induce the expression of tumor suppressor gene cell albumin in breast cancer cells. And they recently discovered that 5 F 203 not only induces apoptosis but also induces caspase-3 activation in triple negative breast cancer (TNBC) cells and breast cancer cells. It is suggested that 5 F 203 has the potential to restore cytoglobin expression as a novel strategy for the treatment of TNBC (Rowland et al. 2019).
Targeting glucose-dependent insulinotropic polypeptide receptor for neurodegenerative disorders
Published in Expert Opinion on Therapeutic Targets, 2018
Mahip K. Verma, Rajan Goel, Nandakumar Krishnadas, Kumar V. S. Nemmani
Modulation of the neuronal redox status by GIP is a significant contributing factor toward the reported neuroprotective effects. GIP-mediated rescue to CGNs was found to be associated with upregulation of cytoglobin (Cygb) gene, providing superoxide dismutase (SOD) inducing capability and antioxidant effects [48]. 4-hydroxy-2-nonenal (4-HNE) is a reactive aldehyde mediating oxidative stress, leading to protein modification in several neurodegenerative disorders and cancers. Neuroprotective effects of GIP analog, D-Ala2GIP-glu-PAL, on the dopaminergic neurons of SNpc could potentially be linked to the observed reduction in mid-brain 4-HNE levels [49]. Whole brain levels of malondialdehyde were found to be reduced with treatment with GIPR agonist, D-Ala2GIP in a murine PD model. Moreover, the treatment was also associated with restoration of reduced glutathione levels compared to diseased controls [50]. Accumulation of 8-oxoguanine as a result of oxidative stress in the mitochondrial DNA leads to mitochondrial dysfunction and resultant impairments in the neuritogenesis in several neurodegenerative conditions [51]. In the APP/PS1 model of AD, chronic administration of GIP analog, D-Ala2GIP, for 12–19 months was associated with significant reduction in the 8-oxoguanine in the mouse hippocampus [45].