Special Issue "Free Radical Research in Cancer"

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 October 2019.

Special Issue Editor

Dr. Ana Čipak Gašparović
E-Mail Website
Guest Editor
Laboratory for Oxidative Stress, Institute Ruder Boskovic, Zagreb, Croatia

Special Issue Information

Dear Colleagues,

It is a pleasure to invite you to contribute to this Special Issue of Antioxidants by submitting original research papers or review articles focusing on “Free Radical Research in Cancer”.

Cancer is a great challenge to efficient therapy due to biological diversity. Disturbed oxidative homeostasis in cancer cells certainly contributes to differential therapy response. One of the hallmarks of cancer cells is adaptation, which includes fine tuning of the cellular metabolic and signalling pathways, as well as transcription profiles. One of the factors causing rapid adaptation are changes in oxygen levels due to hypoxia/reoxygenation during growth changing antioxidative patterns as a consequence. Finally, these events sum up and create challenges for efficient cancer therapy.

The aim of this Special Issue is to present recent findings and to describe the state-of-the-art on the mechanisms by which free radicals contribute to cancer development and change response to therapy.

We look forward to receiving many contributions and stimulating a productive discussion on this exciting thematic of role of free radicals in cancer development, progression and treatment.

Best regards,

Dr. Ana Čipak Gašparović
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • free radicals
  • oxidative stress
  • ROS
  • RNS
  • cancer
  • cancer stem cells
  • cancer therapy
  • cell signalling
  • antioxidative transcription factors
  • drug delivery system

Published Papers (3 papers)

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Research

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Open AccessArticle
Cancer Chemotherapy and Chemiluminescence Detection of Reactive Oxygen Species in Human Semen
Antioxidants 2019, 8(10), 449; https://doi.org/10.3390/antiox8100449 - 01 Oct 2019
Abstract
Advanced treatments have improved the prognosis of cancer survivors. Anticancer drugs generate large amounts of cellular reactive oxygen species (ROS), but their direct effects on sperm ROS production are unclear. We examined 64 semen samples of men who had received cancer chemotherapy, 467 [...] Read more.
Advanced treatments have improved the prognosis of cancer survivors. Anticancer drugs generate large amounts of cellular reactive oxygen species (ROS), but their direct effects on sperm ROS production are unclear. We examined 64 semen samples of men who had received cancer chemotherapy, 467 semen samples of men consulting for idiopathic infertility, and 402 semen samples of partners of female patients as a control group. ROS production was calculated as the integrated chemiluminescence between 0 and 200 seconds after the addition of luminol to unwashed semen. We found that their ROS-positive rate of semen samples in the chemotherapy group was significantly higher than that in the control group. We compared the sperm parameters (concentration and motility) and the ROS production levels between chemotherapy subgroups and one of the remaining subgroups with positive ROS, and we found that only sperm motility was significantly lower in the samples in the postchemotherapy subgroup than in the idiopathic infertility subgroup, and that both sperm parameters were significantly lower in those from postchemotherapy subgroup than in the control subgroup. The ROS production level per million spermatozoa in the postchemotherapy subgroup was significantly higher than that in the control subgroup. Additionally, we compared variables, such as age, sperm features, and the duration from the end of the treatment to the first consultation between ROS-positive and ROS-negative subgroups in samples from men in the postchemotherapy group, but we found no significant differences. Of the men in the postchemotherapy group, three underwent a long-term antioxidant therapy, and all of them had low ROS semen levels after that. In conclusion, the production of ROS in semen detected by chemiluminescence from men who undergo cancer chemotherapy is similar to that of men with idiopathic infertility, and long-term oral antioxidant therapy may reduce the amount of ROS in the semen. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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Open AccessArticle
Cancer Cell Sensitivity to Redox-Cycling Quinones is Influenced by NAD(P)H: Quinone Oxidoreductase 1 Polymorphism
Antioxidants 2019, 8(9), 369; https://doi.org/10.3390/antiox8090369 - 02 Sep 2019
Abstract
Background: Cancer cell sensitivity to drugs may be associated with disturbed antioxidant enzymes expression. We investigated mechanisms of resistance by using oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). Since nicotinamide adenine dinucleotide phosphate (NAD(P)H): quinone oxidoreductase-1 (NQO1) is modified in tumors and [...] Read more.
Background: Cancer cell sensitivity to drugs may be associated with disturbed antioxidant enzymes expression. We investigated mechanisms of resistance by using oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). Since nicotinamide adenine dinucleotide phosphate (NAD(P)H): quinone oxidoreductase-1 (NQO1) is modified in tumors and oxidative stress-resistant cells, we studied its role in cells exposed to β-lapachone, menadione, and doxorubicin. Methods: Normal mammary epithelial 250MK, MCF-7, and Resox cells were employed. NQO1 expression and enzyme activity were determined by quantitative polymerase chain reaction (RT-PCR), immunoblotting, and biochemical assays. Dicoumarol and gene silencing (siRNA) were used to modulate NQO1 expression and to assess its potential drug-detoxifying role. MTT (3-(4,5-dimethylthia-zolyl-2)-2,5-diphenyltetrazolium bromide) or clonogenic assays were used to investigate cytotoxicity. NQO1 variants, NQO1*1 (wt), and NQO1*2 (C609T), were obtained by transfecting NQO1-null MDA-MB-231 cell line. Results: Resox cells have higher NQO1 expression than MCF-7 cells. In 250MK cells its expression was low but enzyme activity was higher suggesting a variant NQO1 form in MCF-7 cells. MCF-7 and Resox cells are heterozygous NQO1*1 (wt)/NQO1*2 (C609T). Both NQO1 polymorphism and NQO1 overexpression are main determinants for cell resistance during oxidative stress. NQO1 overexpression increases cell sensitivity to β-lapachone whereas NQO1*2 polymorphism triggers quinone-based chemotherapies-sensitivity. Conclusions: NQO1 influences cancer cells redox metabolism and their sensitivity to drugs. We suggest that determining NQO1 polymorphism may be important when considering the use of quinone-based chemotherapeutic drugs. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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Review

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Open AccessReview
Redox-Mediated Mechanism of Chemoresistance in Cancer Cells
Antioxidants 2019, 8(10), 471; https://doi.org/10.3390/antiox8100471 - 10 Oct 2019
Abstract
Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. [...] Read more.
Cellular reactive oxygen species (ROS) status is stabilized by a balance of ROS generation and elimination called redox homeostasis. ROS is increased by activation of endoplasmic reticulum stress, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family members and adenosine triphosphate (ATP) synthesis of mitochondria. Increased ROS is detoxified by superoxide dismutase, catalase, and peroxiredoxins. ROS has a role as a secondary messenger in signal transduction. Cancer cells induce fluctuations of redox homeostasis by variation of ROS regulated machinery, leading to increased tumorigenesis and chemoresistance. Redox-mediated mechanisms of chemoresistance include endoplasmic reticulum stress-mediated autophagy, increased cell cycle progression, and increased conversion to metastasis or cancer stem-like cells. This review discusses changes of the redox state in tumorigenesis and redox-mediated mechanisms involved in tolerance to chemotherapeutic drugs in cancer. Full article
(This article belongs to the Special Issue Free Radical Research in Cancer)
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