Changing Perspectives from Oxidative Stress to Redox Signaling—Extracellular Redox Control in Translational Medicine

Palacio, Paola Loreto; Godoy, José R.; Aktaş, Orhan; Hanschmann, Eva-Maria

doi:10.3390/antiox11061181

Cited by 14 publications

(5 citation statements)

References 208 publications

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“…While ROS play essential roles in various cellular processes, excessive levels can have detrimental effects on cells and contribute to carcinogenesis. High concentrations of ROS can cause damage to cellular components, including DNA, proteins, and lipids [21]. This oxidative damage can lead to mutations in critical genes, including tumor suppressor genes, which normally help regulate cell growth and prevent the development of cancer.…”

Section: Oxidative Stress Elevated Ros Level and Carcinogenesis: Conn...mentioning

confidence: 99%

“…The detrimental effects of ROS on cellular components and signaling pathways can create an environment conducive to carcinogenesis. Accumulation of DNA damage and genetic mutations, dysregulation of cellular signaling, and impaired antioxidant defense systems contribute to the initiation and progression of cancer [21]. It is important to note that ROS can also have physiological roles in cellular processes and signaling pathways under normal conditions.…”

Section: Oxidative Stress Elevated Ros Level and Carcinogenesis: Conn...mentioning

confidence: 99%

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Interplay of oxidative stress, cellular communication and signaling pathways in cancer

Iqbal,

Kabeer,

Abbas

et al. 2024

Cell Commun Signal

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Cancer remains a significant global public health concern, with increasing incidence and mortality rates worldwide. Oxidative stress, characterized by the production of reactive oxygen species (ROS) within cells, plays a critical role in the development of cancer by affecting genomic stability and signaling pathways within the cellular microenvironment. Elevated levels of ROS disrupt cellular homeostasis and contribute to the loss of normal cellular functions, which are associated with the initiation and progression of various types of cancer. In this review, we have focused on elucidating the downstream signaling pathways that are influenced by oxidative stress and contribute to carcinogenesis. These pathways include p53, Keap1-NRF2, RB1, p21, APC, tumor suppressor genes, and cell type transitions. Dysregulation of these pathways can lead to uncontrolled cell growth, impaired DNA repair mechanisms, and evasion of cell death, all of which are hallmark features of cancer development. Therapeutic strategies aimed at targeting oxidative stress have emerged as a critical area of investigation for molecular biologists. The objective is to limit the response time of various types of cancer, including liver, breast, prostate, ovarian, and lung cancers. By modulating the redox balance and restoring cellular homeostasis, it may be possible to mitigate the damaging effects of oxidative stress and enhance the efficacy of cancer treatments. The development of targeted therapies and interventions that specifically address the impact of oxidative stress on cancer initiation and progression holds great promise in improving patient outcomes. These approaches may include antioxidant-based treatments, redox-modulating agents, and interventions that restore normal cellular function and signaling pathways affected by oxidative stress. In summary, understanding the role of oxidative stress in carcinogenesis and targeting this process through therapeutic interventions are of utmost importance in combating various types of cancer. Further research is needed to unravel the complex mechanisms underlying oxidative stress-related pathways and to develop effective strategies that can be translated into clinical applications for the management and treatment of cancer.

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Section: Oxidative Stress Elevated Ros Level and Carcinogenesis: Conn...mentioning

confidence: 99%

Section: Oxidative Stress Elevated Ros Level and Carcinogenesis: Conn...mentioning

confidence: 99%

Interplay of oxidative stress, cellular communication and signaling pathways in cancer

Iqbal,

Kabeer,

Abbas

et al. 2024

Cell Commun Signal

View full text Add to dashboard Cite

show abstract

“…Oxidative stress stems from the imbalance between pro-oxidants and antioxidants in favor of the oxidants, leading to a disruption of physiological redox signaling and control, which damages cellular functions [ 1 , 2 ]. Notably, a great number of reactive oxygen species (ROS) and reactive nitrogen species (RNS) often accompany each other [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Suppresses LPS-Induced Oxidative Stress in Dendritic Cells for Inflammatory Regulation via the Nrf2/HO-1 Axis

et al. 2022

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Melatonin, an indoleamine synthesized in the pineal gland of mammals, is a natural bioactive compound with powerful antioxidant and anti-inflammatory properties. Here, we evaluated whether melatonin has the capacity to moderate the oxidative stress of dendritic cells (DCs) for inflammatory control in an acute lung injury (ALI) model. Our findings showed that melatonin remarkably inhibited total nitric oxide synthase (T-NOS) activity, nitric oxide (NO) production, intracellular reactive oxygen species (ROS) levels, and lipid peroxidation (MDA detection) levels in both an LPS-induced murine ALI model and LPS-induced DCs. Meanwhile, the reduced glutathione (GSH) level and the GSH/GSSG ratio were recovered. In addition, antioxidant enzymes, such as glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), were increased in these processes. Moreover, melatonin also inhibited the LPS-induced secretions of IL-1β, IL-6, and TGF-β in vivo and in vitro. Finally, we found that the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) axis was required in the inhibition of LPS-induced oxidative stress in DCs by melatonin. Altogether, these data indicate that melatonin strongly suppresses the LPS-induced oxidative stress in DCs, which is a promising DC-targeted strategy via inflammatory control for ALI treatment.

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“…Oxidative stress results from the imbalance between pro-oxidant and antioxidant mechanisms in the body in favor of the former. It is characterized by the accumulation of highly reactive oxygen reactive species (ROS) and reactive nitrogen species (RNS) that can react with the nucleic acids, lipids, and proteins to oxidize them, causing irreversible cell damage and leading to tissue destruction [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia Enhances Oxidative Stress in Neutrophils from ZZ Alpha-1 Antitrypsin Deficiency Patients

et al. 2023

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Alpha-1 antitrypsin deficiency (AATD) is a neutrophilic inflammatory disorder that may result in local hypoxia, reactive oxygen and nitrogen species (ROS/RNS) production, and increased damage in adjacent tissues. This study aims to determine the impact of hypoxia on neutrophil oxidative stress profile in AATD patients. Neutrophils were isolated from AATD patients and control volunteers and exposed to hypoxia (1% O2 for 4 h), ROS/RNS, mitochondrial parameters, and non-enzymatic antioxidant defenses measured by flow cytometry. The expression of enzymatic antioxidant defenses was determined by qRT-PCR. Our results indicate that ZZ-AATD neutrophils produce higher amounts of hydrogen peroxide, peroxynitrite, and nitric oxide and decreased levels of the antioxidant enzymes catalase, superoxide dismutase, and glutathione reductase. Likewise, our results show a decrease in mitochondrial membrane potential, indicating that this organelle could be involved in the production of the reactive species observed. No decrease in glutathione and thiol levels were observed. The accumulation of substances with high oxidative capacity would explain the greater oxidative damage observed in proteins and lipids. In conclusion, our results indicate that, compared to MM control individuals, ZZ-AATD neutrophils show increased ROS/RNS production under hypoxic conditions opening a new rationale for using antioxidant therapies to treat the disease.

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Changing Perspectives from Oxidative Stress to Redox Signaling—Extracellular Redox Control in Translational Medicine

Cited by 14 publications

References 208 publications

Interplay of oxidative stress, cellular communication and signaling pathways in cancer

Interplay of oxidative stress, cellular communication and signaling pathways in cancer

Melatonin Suppresses LPS-Induced Oxidative Stress in Dendritic Cells for Inflammatory Regulation via the Nrf2/HO-1 Axis

Hypoxia Enhances Oxidative Stress in Neutrophils from ZZ Alpha-1 Antitrypsin Deficiency Patients

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