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Molecular Research in Redox Balance in Pathological and Physiological Conditions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 835

Special Issue Editor


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Guest Editor
Department of Medical Biology and Biochemistry, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 85-092 Bydgoszcz, Poland
Interests: oxidant-antioxidant status; redox signaling; inflammation

Special Issue Information

Dear Colleagues,

Oxidation and reduction represent the most important molecular transformations that occur within an organism. They regulate the correct functions of the cell, its growth, and its division. However, the condition is the maintenance of physiological equilibrium between the two. The oxidant–antioxidant balance, in turn, depends on the antioxidant capacity and the production level of reactive oxygen and nitrogen species. A disturbance to the balance leads to a number of pathological changes. The most commonly observed is oxidative stress, which leads to inflammation. This is defined as a high concentration of reactive oxygen and/or nitrogen species, the consequences of which the body cannot cope with. An excess of antioxidants, which may result in antioxidant stress, has also been noted.

The objective of this Special Issue is to provide a comprehensive and systematic account of the current molecular knowledge on the redox balance in humans, while also seeking to identify and disseminate the latest original research in this field. I therefore encourage the submission of both reviews and original papers, including those pertaining to in vitro studies with reference to human organisms at the molecular level.

Dr. Pawel Sutkowy
Guest Editor

Manuscript Submission Information

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Keywords

  • oxidative stress
  • nitrosative stress
  • antioxidative stress
  • redox signaling
  • inflammation
  • antioxidants
  • reactive oxygen species
  • reactive nitrogen species
  • pathological states
  • physiological condition

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Published Papers (1 paper)

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Research

14 pages, 2375 KiB  
Article
Hypoxia Modulates Transmembrane Prostatic Acid Phosphatase (TM-PAP) in MCF-7 Breast Cancer Cells
by Marco Antonio Lacerda-Abreu, Luiz Fernando Carvalho-Kelly and José Roberto Meyer-Fernandes
Int. J. Mol. Sci. 2025, 26(5), 1918; https://doi.org/10.3390/ijms26051918 - 23 Feb 2025
Viewed by 406
Abstract
In MCF-7 breast cancer cells, transmembrane prostatic acid phosphatase (TM-PAP) plays a critical role in tumor progression, particularly under hypoxic conditions. In this study, the impact of hypoxia on ectophosphatase activity in MCF-7 cells was examined, and the underlying biological mechanisms that influence [...] Read more.
In MCF-7 breast cancer cells, transmembrane prostatic acid phosphatase (TM-PAP) plays a critical role in tumor progression, particularly under hypoxic conditions. In this study, the impact of hypoxia on ectophosphatase activity in MCF-7 cells was examined, and the underlying biological mechanisms that influence the breast cancer microenvironment were explored. Compared with normoxic cells, hypoxic cells presented significant reductions in ectophosphatase activity, indicating that hypoxia altered dephosphorylation processes critical for tumor growth and metastasis. Specific decreases in the hydrolysis of substrates, such as p-nitrophenylphosphate (pNPP) and adenosine monophosphate (AMP), were observed under hypoxic conditions, suggesting that hypoxia impaired TM-PAP activity. Further investigation revealed that hypoxia induced an increase in the concentration of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2), which inhibited ectophosphatase activity. This effect was reversed by the introduction of ROS scavengers. Additionally, hypoxia activated protein kinase C (PKC), further modulating ectophosphatase activity in MCF-7 cells. Collectively, these findings enhanced the understanding of the mechanisms through which hypoxia could influence enzyme activity associated with cancer progression and provide valuable insights into the development of targeted therapeutic strategies. Full article
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