Intracellular catalase activity instead of glutathione level dominates the resistance of cells to reactive oxygen species

Zhao, Mengxin; Wen, Junlin; Wang, Lu; Wang, Xiaoping; Chen, Tongsheng

doi:10.1007/s12192-019-00993-1

Cited by 41 publications

(32 citation statements)

References 53 publications

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“…Along with GSH metabolism and the Warburg effect, there are enzymes and antioxidant factors that are largely modulated in cancer cells, such as Superoxide Dismutases (SODs), Catalase (CAT), NADP oxidases (NOXs), Nuclear Factor Erythroid 2-related Factor 2 (NRF2), COX-2, Nitric Oxide Synthase-2 (NOS2), and Hypoxia-Inducible Factor 1 alpha (HIF1α) [ 131 , 132 , 133 , 134 ]. HIF1α, which is also overexpressed in the Warburg effect, increases the expression of Glucose Transporters (GLUTs), glycolytic enzymes, and Pyruvate Dehydrogenase Kinase, isoenzyme 1 (PDK1), which blocks the entry of pyruvate into the Tricarboxylic Acid (TCA) cycle [ 128 ].…”

Section: Flavonoids and Redox Metabolismmentioning

confidence: 99%

The Hallmarks of Flavonoids in Cancer

Ponte

Pavan

et al. 2021

Molecules

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Flavonoids represent an important group of bioactive compounds derived from plant-based foods and beverages with known biological activity in cells. From the modulation of inflammation to the inhibition of cell proliferation, flavonoids have been described as important therapeutic adjuvants against several diseases, including diabetes, arteriosclerosis, neurological disorders, and cancer. Cancer is a complex and multifactor disease that has been studied for years however, its prevention is still one of the best known and efficient factors impacting the epidemiology of the disease. In the molecular and cellular context, some of the mechanisms underlying the oncogenesis and the progression of the disease are understood, known as the hallmarks of cancer. In this text, we review important molecular signaling pathways, including inflammation, immunity, redox metabolism, cell growth, autophagy, apoptosis, and cell cycle, and analyze the known mechanisms of action of flavonoids in cancer. The current literature provides enough evidence supporting that flavonoids may be important adjuvants in cancer therapy, highlighting the importance of healthy and balanced diets to prevent the onset and progression of the disease.

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Section: Flavonoids and Redox Metabolismmentioning

confidence: 99%

The Hallmarks of Flavonoids in Cancer

Ponte

Pavan

et al. 2021

Molecules

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“…An alternative approach to study the role of peroxisomal H 2 O 2 metabolism in cellular thiol-disulfide homeostasis is to interfere with CAT activity. Here it is interesting to mention that (i) CAT activity, and not the cellular glutathione levels, appear to dominate the resistance of cells to ROS [102], (ii) treatment of Chang liver cells with 3-amino-1,2,4-triazole, an irreversible inhibitor of CAT activity, increases the protein disulfide levels by 20% [103], and (iii) cardiac-specific overexpression of CAT in mice decreases oxidative cysteine modification of cardiac proteins [104]. Whether the observed changes in cysteine oxidation are caused by alterations in the release of peroxisome-derived H 2 O 2 or by changes in the capacity of peroxisomes to scavenge extra-peroxisomal H 2 O 2 (Figure 2), remains to be determined.…”

Section: The Emerging Roles Of Peroxisomes In Cellular H2o2 Signalingmentioning

confidence: 99%

Peroxisomal Hydrogen Peroxide Metabolism and Signaling in Health and Disease

Lismont

Revenco

Fransen

2019

IJMS

130

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Hydrogen peroxide (H2O2), a non-radical reactive oxygen species generated during many (patho)physiological conditions, is currently universally recognized as an important mediator of redox-regulated processes. Depending on its spatiotemporal accumulation profile, this molecule may act as a signaling messenger or cause oxidative damage. The focus of this review is to comprehensively evaluate the evidence that peroxisomes, organelles best known for their role in cellular lipid metabolism, also serve as hubs in the H2O2 signaling network. We first briefly introduce the basic concepts of how H2O2 can drive cellular signaling events. Next, we outline the peroxisomal enzyme systems involved in H2O2 metabolism in mammals and reflect on how this oxidant can permeate across the organellar membrane. In addition, we provide an up-to-date overview of molecular targets and biological processes that can be affected by changes in peroxisomal H2O2 metabolism. Where possible, emphasis is placed on the molecular mechanisms and factors involved. From the data presented, it is clear that there are still numerous gaps in our knowledge. Therefore, gaining more insight into how peroxisomes are integrated in the cellular H2O2 signaling network is of key importance to unravel the precise role of peroxisomal H2O2 production and scavenging in normal and pathological conditions.

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“…The cells were then harvested and washed in PBS three times and oxidation-induced DCF uorescence was assayed by uorescence microscopy. 26…”

Section: Detection Of Intracellular Rosmentioning

confidence: 99%

Homocysteine Promotes Migration of Adventitial Fibroblasts via Angiotensin II type 1 Receptor Activation to Aggravate Atherosclerosis

Zhu¹,

Hao²,

Li³

et al. 2020

Preprint

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BackgroundHyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. However, the mechanisms of HHcy-induced arteriosclerosis are largely unknown. Objective:To clarify the effect of Hcy on adventitial fibroblasts (AFs) and its relation with angiotensin II type 1 receptor (AT1R).Method:The apolipoprotein E gene-deficient mice (Apoe−/−) were used as the murine model for atherosclerosis. HHcy was induced and treated by feeding them 1.5% methionine and telmisartan (gavage 10 mg/kg/d) for 12 weeks, respectively. The AFs and HEK293A cells transfected with the AT1R plasmid were used to investigate the interaction between Hcy and AT1R. All data were expressed as mean ± SEM. The data were analyzed by one-way ANOVA or repeated measurement ANOVA.Results:HHcy aggravated the plaque area of the aortic root and increased the expression of IL-6, MCP-1, and the macrophage marker Mac3 in the plaque and adventitia of the aorta, whereas telmisartan improved this effect. Hyperhomocysteinemia induced the occurrence of the AFs marker protein ER-TR7 in the plaque and the entire layer of the aorta, whereas telmisartan also improved this effect, indicating that hyperhomocysteinemia induced AFs migration and that AT1R mediated this process. Hcy increased the production of AFs H2O2, ROS, and IL-6 of AFs, indicating that Hcy activated the oxidative stress and inflammatory reactions, which may induce cell migration. The subsequent scratch and transwell experiments confirmed that Hcy induced the AFs migration and that telmisartan inhibited this effect. Hcy increased the expression of AFs AT1R and the phosphorylation levels of PKC and ERK1/2 in the AF and HEK293A cells transfected with the AT1R plasmid, whereas telmisartan inhibited this effect, indicating that Hcy activated AT1R intracellular signaling pathway.Conclusion:Hcy promoted adventitial inflammation, induced AFs migration, and aggravated atherosclerosis by activating AT1R.

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Intracellular catalase activity instead of glutathione level dominates the resistance of cells to reactive oxygen species

Cited by 41 publications

References 53 publications

The Hallmarks of Flavonoids in Cancer

The Hallmarks of Flavonoids in Cancer

Peroxisomal Hydrogen Peroxide Metabolism and Signaling in Health and Disease

Homocysteine Promotes Migration of Adventitial Fibroblasts via Angiotensin II type 1 Receptor Activation to Aggravate Atherosclerosis

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