Research

17 pages, 7736 KiB

Open AccessArticle

β-Caryophyllene Inhibits Oxaliplatin-Induced Peripheral Neuropathy in Mice: Role of Cannabinoid Type 2 Receptors, Oxidative Stress and Neuroinflammation

by Jonathan Paulo Agnes, Barbara dos Santos, Raquel Nascimento das Neves, Vitória Maria Marques Luciano, Larissa Benvenutti, Fernanda Capitanio Goldoni, Roberta Giusti Schran, José Roberto Santin, Nara Lins Meira Quintão and Alfeu Zanotto-Filho

Antioxidants 2023, 12(10), 1893; https://doi.org/10.3390/antiox12101893 - 22 Oct 2023

Cited by 1 | Viewed by 1525

Abstract

Peripheral neuropathy is an important adverse effect caused by some chemotherapeutic agents, including oxaliplatin (OXA). OXA-induced peripheral neuropathy (OIPN) is a challenging condition due to diagnostic complexities and a lack of effective treatment. In this study, we investigated the antiallodynic effect of β-caryophyllene [...] Read more.

Peripheral neuropathy is an important adverse effect caused by some chemotherapeutic agents, including oxaliplatin (OXA). OXA-induced peripheral neuropathy (OIPN) is a challenging condition due to diagnostic complexities and a lack of effective treatment. In this study, we investigated the antiallodynic effect of β-caryophyllene (BCP), a cannabinoid type 2 (CB2) receptor agonist, in a mouse model of OIPN. BCP treatment inhibited OXA-induced mechanical and cold allodynia in both preventive and therapeutic drug treatment regimens. Experiments with the CB2 receptor agonist GW405833 confirmed the role of CB2 receptors in OIPN. The CB2 antagonist SR144528 abrogated the anti-nociceptive effect of BCP on mechanical allodynia, without impacting OXA-induced sensitivity to cold. BCP decreased neuroinflammation, as inferred from TNF, IL-1β, IL-6, and IL-10 profiling, and also reduced ROS production, lipid peroxidation, and 4-hydroxynonenal protein adduct formation in the spinal cords of OXA-treated mice. BCP did not affect the antitumor response to OXA or its impact on blood cell counts, implying that the cytotoxicity of OXA was preserved. These results underscore BCP as a candidate drug for OIPN treatment via CB2 receptor-dependent mechanisms, and anti-inflammatory and antioxidant responses in the spinal cord. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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21 pages, 3110 KiB

Open AccessArticle

First Generation of Antioxidant Precursors for Bioisosteric Se-NSAIDs: Design, Synthesis, and In Vitro and In Vivo Anticancer Evaluation

by Sandra Ramos-Inza, Cesar Aliaga, Ignacio Encío, Asif Raza, Arun K. Sharma, Carlos Aydillo, Nuria Martínez-Sáez, Carmen Sanmartín and Daniel Plano

Antioxidants 2023, 12(9), 1666; https://doi.org/10.3390/antiox12091666 - 24 Aug 2023

Cited by 1 | Viewed by 937

Abstract

The introduction of selenium (Se) into organic scaffolds has been demonstrated to be a promising framework in the field of medicinal chemistry. A novel design of nonsteroidal anti-inflammatory drug (NSAID) derivatives based on a bioisosteric replacement via the incorporation of Se as diacyl [...] Read more.

The introduction of selenium (Se) into organic scaffolds has been demonstrated to be a promising framework in the field of medicinal chemistry. A novel design of nonsteroidal anti-inflammatory drug (NSAID) derivatives based on a bioisosteric replacement via the incorporation of Se as diacyl diselenide is reported. The antioxidant activity was assessed using the DPPH radical scavenging assay. The new Se-NSAID derivatives bearing this unique combination showed antioxidant activity in a time- and dose-dependent manner, and also displayed different antiproliferative profiles in a panel of eight cancer cell lines as determined by the MTT assay. Ibuprofen derivative 5 was not only the most antioxidant agent, but also selectively induced toxicity in all the cancer cell lines tested (IC₅₀ < 10 µM) while sparing nonmalignant cells, and induced apoptosis partially without enhancing the caspase 3/7 activity. Furthermore, NSAID derivative 5 significantly suppressed tumor growth in a subcutaneous colon cancer xenograft mouse model (10 mg/kg, TGI = 72%, and T/C = 38%) without exhibiting any apparent toxicity. To our knowledge, this work constitutes the first report on in vitro and in vivo anticancer activity of an unprecedented Se-NSAID hybrid derivative and its rational use for developing precursors for bioisosteric selenocompounds with appealing therapeutic applications. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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18 pages, 5213 KiB

Open AccessArticle

Bradykinin B1 Receptor Affects Tumor-Associated Macrophage Activity and Glioblastoma Progression

by Ching-Kai Shen, Bor-Ren Huang, Vichuda Charoensaensuk, Liang-Yo Yang, Cheng-Fang Tsai, Yu-Shu Liu, Dah-Yuu Lu, Wei-Lan Yeh and Chingju Lin

Antioxidants 2023, 12(8), 1533; https://doi.org/10.3390/antiox12081533 - 31 Jul 2023

Cited by 2 | Viewed by 1471

Abstract

Bradykinin is a small active peptide and is considered an inflammatory mediator in several pathological conditions. Bradykinin exerts its effects by coupling to its receptors, including bradykinin B1 (B1R) and bradykinin B2. B1R has been implicated in the development of various cancers. Our [...] Read more.

Bradykinin is a small active peptide and is considered an inflammatory mediator in several pathological conditions. Bradykinin exerts its effects by coupling to its receptors, including bradykinin B1 (B1R) and bradykinin B2. B1R has been implicated in the development of various cancers. Our previous study reported that B1R promoted glioblastoma (GBM) development by supporting the migration and invasion of GBM cells. However, the mechanisms underlying the effects of B1R on tumor-associated macrophages (TAMs) and GBM progression remain unknown. Accordingly, to explore the regulatory effects of B1R overexpression (OE) in GBM on tumor-associated immune cells and tumor progression, we constructed a B1R wild-type plasmid and developed a B1R OE model. The results reveal that B1R OE in GBM promoted the expression of ICAM-1 and VCAM-1—cell adhesion molecules—in GBM. Moreover, B1R OE enhanced GBM cell migration ability and monocyte attachment. B1R also regulated the production of the protumorigenic cytokines and chemokines IL-6, IL-8, CXCL11, and CCL5 in GBM, which contributed to tumor progression. We additionally noted that B1R OE in GBM increased the expression of CD68 in TAMs. Furthermore, B1R OE reduced the level of reactive oxygen species in GBM cells by upregulating heme oxygenase-1, an endogenous antioxidant protein, thereby protecting GBM cells from oxidative stress. Notably, B1R OE upregulated the expression of programmed death-ligand 1 in both GBM cells and macrophages, thus providing resistance against T-cell response. B1R OE in GBM also promoted tumor growth and reduced survival rates in an intracranial xenograft mouse model. These results indicate that B1R expression in GBM promotes TAM activity and modulates GBM progression. Therefore, B1R could be an effective target for therapeutic methods in GBM. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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14 pages, 2202 KiB

Open AccessArticle

Sedum middendorffianum Maxim Induces Apoptosis and Inhibits the Invasion of Human Ovarian Cancer Cells via Oxidative Stress Regulation

by Ju-Yeon Choi, Miran Jeong, Kijun Lee, Jin-Ok Kim, Wan Hee Lee, InWha Park, Hak Cheol Kwon and Jung-Hye Choi

Antioxidants 2023, 12(7), 1386; https://doi.org/10.3390/antiox12071386 - 05 Jul 2023

Viewed by 1140

Abstract

Sedum middendorffianum Maxim (SMM) is a Korean endemic plant belonging to the Crassulaceae family. This study aimed to investigate the antitumor effects of the SMM extract on human ovarian cancer cells. Among five endemic plants grown in Korea, the SMM extract showed the [...] Read more.

Sedum middendorffianum Maxim (SMM) is a Korean endemic plant belonging to the Crassulaceae family. This study aimed to investigate the antitumor effects of the SMM extract on human ovarian cancer cells. Among five endemic plants grown in Korea, the SMM extract showed the most potent cytotoxicity in ovarian cancer cells and had little effect on normal ovarian surface epithelial cells. Furthermore, we revealed that the SMM extract dose-dependently induced apoptosis in human ovarian cancer A2780 and SKOV3 cells. The SMM extract markedly stimulated the activation of caspase-3/8, while the broad-spectrum caspase inhibitor and caspase-8 selective inhibitor significantly reversed SMM extract-induced apoptosis. In addition, the SMM extract significantly inhibited cell invasion and the expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 in ovarian cancer cells. Notably, the SMM extract increased the generation of intracellular ROS, and pretreatment with antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed SMM-induced cytotoxicity and anti-invasive activity. Moreover, NAC treatment reversed the SMM-induced inhibition of MMP-2/9 expression. Taken together, these data suggest that the SMM extract induces caspase-dependent apoptotic cell death and inhibits MMP-dependent invasion via ROS regulation. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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23 pages, 4405 KiB

Open AccessArticle

Novel Acylselenourea Derivatives: Dual Molecules with Anticancer and Radical Scavenging Activity

by Nora Astrain-Redin, Asif Raza, Ignacio Encío, Arun K. Sharma, Daniel Plano and Carmen Sanmartín

Antioxidants 2023, 12(7), 1331; https://doi.org/10.3390/antiox12071331 - 23 Jun 2023

Cited by 4 | Viewed by 1264

Abstract

Oxidative stress surrounding cancer cells provides them with certain growth and survival advantages necessary for disease progression. In this context, Se-containing molecules have gained attention due to their anticancer and antioxidant activity. In our previous work, we synthesized a library of 39 selenoesters [...] Read more.

Oxidative stress surrounding cancer cells provides them with certain growth and survival advantages necessary for disease progression. In this context, Se-containing molecules have gained attention due to their anticancer and antioxidant activity. In our previous work, we synthesized a library of 39 selenoesters containing functional groups commonly present in natural products (NP), which showed potent anticancer activity, but did not demonstrate high radical scavenger activity. Thus, 20 novel Se derivatives resembling NP have been synthesized presenting acylselenourea functionality in their structures. Radical scavenger activity was tested using DPPH assay and in vitro protective effects against ROS-induced cell death caused by H₂O₂. Additionally, antiproliferative activity was evaluated in prostate, colon, lung, and breast cancer cell lines, along with their ability to induce apoptosis. Compounds 1.I and 5.I showed potent cytotoxicity against the tested cancer cell lines, along with high selectivity indexes and induction of caspase-mediated apoptosis. These compounds exhibited potent and concentration-dependent radical scavenging activity achieving DPPH inhibition similar to ascorbic acid and trolox. To conclude, we have demonstrated that the introduction of Se in the form of acylselenourea into small molecules provides strong radical scavengers in vitro and antiproliferative activity, which may lead to the development of promising dual compounds. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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12 pages, 1010 KiB

Open AccessArticle

Changes in Dietary Inflammatory Index Score over Time and Cancer Development in Rural Post-Menopausal Women

by Mariah Kay Jackson, Joan Lappe, Jihyun Ma, Megan Timmerman, Elizabeth R. Lyden, Nitin Shivappa, James R. Hébert, Dianne Travers Gustafson, Laura Graeff-Armas and Corrine Hanson

Antioxidants 2023, 12(4), 946; https://doi.org/10.3390/antiox12040946 - 18 Apr 2023

Cited by 2 | Viewed by 1771

Abstract

Inflammation plays a key role in cancer development. As an important modulator of inflammation, the role of diet should be explored. The purpose of this study was to determine the association between diets with a higher inflammatory potential, as measured by the Dietary [...] Read more.

Inflammation plays a key role in cancer development. As an important modulator of inflammation, the role of diet should be explored. The purpose of this study was to determine the association between diets with a higher inflammatory potential, as measured by the Dietary Inflammatory Index (DII^®), and cancer development in a cohort of rural post-menopausal women. Dietary intake from a randomized controlled trial cohort of rural, post-menopausal women in Nebraska was used to compute energy-adjusted DII (E-DII^TM) scores at baseline and four years later (visit 9). A linear mixed model analysis and multivariate logistic regression evaluated the association between E-DII scores (baseline, visit 9, change score) and cancer status. Of 1977 eligible participants, those who developed cancer (n = 91, 4.6%) had a significantly larger, pro-inflammatory change in E-DII scores (Non-cancer: Δ 0.19 ± 1.43 vs. Cancer: Δ 0.55 ± 1.43, p = 0.02). After adjustment, odds of cancer development were over 20% higher in those with a larger change (more pro-inflammatory) in E-DII scores than those with smaller E-DII changes (OR = 1.21, 95% CI [1.02, 1.42], p = 0.02). Shifting to a more pro-inflammatory diet pattern over four years was associated with increased odds of cancer development, but not with E-DII at baseline or visit 9 alone. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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16 pages, 11166 KiB

Open AccessArticle

Doxorubicin-Loaded Iron Oxide Nanoparticles Induce Oxidative Stress and Cell Cycle Arrest in Breast Cancer Cells

by Elisa Parcero Hernandes, Danielle Lazarin-Bidóia, Raquel Dosciatti Bini, Celso Vataru Nakamura, Luiz Fernando Cótica and Sueli de Oliveira Silva Lautenschlager

Antioxidants 2023, 12(2), 237; https://doi.org/10.3390/antiox12020237 - 20 Jan 2023

Cited by 14 | Viewed by 3097

Abstract

Cancer is one of the most common diseases nowadays and derives from the uncontrollable growth of a single cell. Magnetic nanoparticles (NpMag) offer various possibilities for use in the biomedical area, including drug delivery mediated by magnetic fields. In the current study, we [...] Read more.

Cancer is one of the most common diseases nowadays and derives from the uncontrollable growth of a single cell. Magnetic nanoparticles (NpMag) offer various possibilities for use in the biomedical area, including drug delivery mediated by magnetic fields. In the current study, we evaluated the in vitro effects of iron-oxide magnetic nanoparticles conjugated with the antitumor drug doxorubicin (Dox) on human breast cancer cells. Our results revealed that magnetic nanoparticles with Dox (NpMag+Dox) induce cellular redox imbalance in MCF-7 cells. We also demonstrate that iron-oxide nanoparticles functionalized with Dox induce oxidative stress evidenced by DNA damage, lipid peroxidation, cell membrane disruption, and loss of mitochondria potential. As a result, NpMag+Dox drives MCF-7 cells to stop the cell cycle and decrease cell migration. The association of NpMg+Dox induced a better delivery of Dox to MCF cells, mainly in the presence of a magnetic field, increasing the death of MCF cells which might reduce the toxicity for healthy cells providing a better efficacy for the treatment. Thus, iron-oxide nanoparticles and doxorubicin conjugated may be candidate for anticancer therapy. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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Review

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18 pages, 2817 KiB

Open AccessReview

The Contribution of Oxidative Stress to NF1-Altered Tumors

by Elisabetta Kuhn, Federica Natacci, Massimo Corbo, Luigi Pisani, Stefano Ferrero, Gaetano Bulfamante and Donatella Gambini

Antioxidants 2023, 12(8), 1557; https://doi.org/10.3390/antiox12081557 - 04 Aug 2023

Cited by 1 | Viewed by 2027

Abstract

The neurofibromatosis-1 gene (NF1) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated NF1 as one of the most [...] Read more.

The neurofibromatosis-1 gene (NF1) was initially characterized because its germline mutation is responsible for an inherited syndromic disease predisposing tumor development, in particular neurofibromas but also various malignancies. Recently, large-scale tumor sequencing efforts have demonstrated NF1 as one of the most frequently mutated genes in human cancer, being mutated in approximately 5–10% of all tumors, especially in malignant peripheral nerve sheath tumors and different skin tumors. NF1 acts as a tumor suppressor gene that encodes neurofibromin, a large protein that controls neoplastic transformation through several molecular mechanisms. On the other hand, neurofibromin loss due to NF1 biallelic inactivation induces tumorigenic hyperactivation of Ras and mTOR signaling pathways. Moreover, neurofibromin controls actin cytoskeleton structure and the metaphase–anaphase transition. Consequently, neurofibromin deficiency favors cell mobility and proliferation as well as chromosomal instability and aneuploidy, respectively. Growing evidence supports the role of oxidative stress in NF1-related tumorigenesis. Neurofibromin loss induces oxidative stress both directly and through Ras and mTOR signaling activation. Notably, innovative therapeutic approaches explore drug combinations that further increase reactive oxygen species to boost the oxidative unbalance of NF1-altered cancer cells. In our paper, we review NF1-related tumors and their pathogenesis, highlighting the twofold contribution of oxidative stress, both tumorigenic and therapeutic. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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16 pages, 1963 KiB

Open AccessReview

Pyroptosis Modulators: New Insights of Gasdermins in Health and Disease

by Imane Allali-Boumara, Ana Dácil Marrero, Ana R. Quesada, Beatriz Martínez-Poveda and Miguel Ángel Medina

Antioxidants 2023, 12(8), 1551; https://doi.org/10.3390/antiox12081551 - 03 Aug 2023

Viewed by 1072

Abstract

Pyroptosis is an inflammation-dependent type of cell death that has been in the spotlight for the scientific community in the last few years. Crucial players in the process of pyroptosis are the members of the gasdermin family of proteins, which have been parallelly [...] Read more.

Pyroptosis is an inflammation-dependent type of cell death that has been in the spotlight for the scientific community in the last few years. Crucial players in the process of pyroptosis are the members of the gasdermin family of proteins, which have been parallelly studied. Upon induction of pyroptosis, gasdermins suffer from structural changes leading to the formation of pores in the membrane that subsequently cause the release of pro-inflammatory contents. Recently, it has been discovered that oxidation plays a key role in the activation of certain gasdermins. Here, we review the current knowledge on pyroptosis and human gasdermins, focusing on the description of the different members of the family, their molecular structures, and their influence on health and disease directly or non-directly related to inflammation. Noteworthy, we have focused on the existing understanding of the role of this family of proteins in cancer, which could translate into novel promising strategies aimed at benefiting human health. In conclusion, the modulation of pyroptosis and gasdermins by natural and synthetic compounds through different mechanisms, including modification of the redox state of cells, has been proven effective and sets precedents for future therapeutic strategies. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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20 pages, 2160 KiB

Open AccessReview

Understanding the Photodynamic Therapy Induced Bystander and Abscopal Effects: A Review

by Kave Moloudi, Paromita Sarbadhikary, Heidi Abrahamse and Blassan P. George

Antioxidants 2023, 12(7), 1434; https://doi.org/10.3390/antiox12071434 - 16 Jul 2023

Cited by 2 | Viewed by 1522

Abstract

Photodynamic therapy (PDT) is a clinically approved minimally/non-invasive treatment modality that has been used to treat various conditions, including cancer. The bystander and abscopal effects are two well-documented significant reactions involved in imparting long-term systemic effects in the field of radiobiology. The PDT-induced [...] Read more.

Photodynamic therapy (PDT) is a clinically approved minimally/non-invasive treatment modality that has been used to treat various conditions, including cancer. The bystander and abscopal effects are two well-documented significant reactions involved in imparting long-term systemic effects in the field of radiobiology. The PDT-induced generation of reactive oxygen and nitrogen species and immune responses is majorly involved in eliciting the bystander and abscopal effects. However, the results in this regard are unsatisfactory and unpredictable due to several poorly elucidated underlying mechanisms and other factors such as the type of cancer being treated, the irradiation dose applied, the treatment regimen employed, and many others. Therefore, in this review, we attempted to summarize the current knowledge regarding the non-targeted effects of PDT. The review is based on research published in the Web of Science, PubMed, Wiley Online Library, and Google Scholar databases up to June 2023. We have highlighted the current challenges and prospects in relation to obtaining clinically relevant robust, reproducible, and long-lasting antitumor effects, which may offer a clinically viable treatment against tumor recurrence and metastasis. The effectiveness of both targeted and untargeted PDT responses and their outcomes in clinics could be improved with more research in this area. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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15 pages, 1636 KiB

Open AccessReview

Unleashing Ferroptosis in Human Cancers: Targeting Ferroptosis Suppressor Protein 1 for Overcoming Therapy Resistance

by Jaewang Lee and Jong-Lyel Roh

Antioxidants 2023, 12(6), 1218; https://doi.org/10.3390/antiox12061218 - 05 Jun 2023

Cited by 6 | Viewed by 1903

Abstract

Ferroptosis, a recently identified form of regulated cell death characterized by the iron-dependent accumulation of lethal lipid peroxidation, has gained increasing attention in cancer therapy. Ferroptosis suppressor protein 1 (FSP1), an NAD(P)H-ubiquinone oxidoreductase that reduces ubiquinone to ubiquinol, has emerged as a critical [...] Read more.

Ferroptosis, a recently identified form of regulated cell death characterized by the iron-dependent accumulation of lethal lipid peroxidation, has gained increasing attention in cancer therapy. Ferroptosis suppressor protein 1 (FSP1), an NAD(P)H-ubiquinone oxidoreductase that reduces ubiquinone to ubiquinol, has emerged as a critical player in the regulation of ferroptosis. FSP1 operates independently of the canonical system xc^–/glutathione peroxidase 4 pathway, making it a promising target for inducing ferroptosis in cancer cells and overcoming ferroptosis resistance. This review provides a comprehensive overview of FSP1 and ferroptosis, emphasizing the importance of FSP1 modulation and its potential as a therapeutic target in cancer treatment. We also discuss recent progress in developing FSP1 inhibitors and their implications for cancer therapy. Despite the challenges associated with targeting FSP1, advances in this field may provide a strong foundation for developing innovative and effective treatments for cancer and other diseases. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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25 pages, 2454 KiB

Open AccessReview

Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence

by Zohra Nausheen Nizami, Hanan E. Aburawi, Abdelhabib Semlali, Khalid Muhammad and Rabah Iratni

Antioxidants 2023, 12(6), 1159; https://doi.org/10.3390/antiox12061159 - 26 May 2023

Cited by 9 | Viewed by 2254

Abstract

Reactive oxygen species (ROS) are metabolic byproducts that regulate various cellular processes. However, at high levels, ROS induce oxidative stress, which in turn can trigger cell death. Cancer cells alter the redox homeostasis to facilitate protumorigenic processes; however, this leaves them vulnerable to [...] Read more.

Reactive oxygen species (ROS) are metabolic byproducts that regulate various cellular processes. However, at high levels, ROS induce oxidative stress, which in turn can trigger cell death. Cancer cells alter the redox homeostasis to facilitate protumorigenic processes; however, this leaves them vulnerable to further increases in ROS levels. This paradox has been exploited as a cancer therapeutic strategy with the use of pro-oxidative drugs. Many chemotherapeutic drugs presently in clinical use, such as cisplatin and doxorubicin, induce ROS as one of their mechanisms of action. Further, various drugs, including phytochemicals and small molecules, that are presently being investigated in preclinical and clinical studies attribute their anticancer activity to ROS induction. Consistently, this review aims to highlight selected pro-oxidative drugs whose anticancer potential has been characterized with specific focus on phytochemicals, mechanisms of ROS induction, and anticancer effects downstream of ROS induction. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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12 pages, 651 KiB

Open AccessSystematic Review

Antioxidant Use after Diagnosis of Head and Neck Squamous Cell Carcinoma (HNSCC): A Systematic Review of Application during Radiotherapy and in Second Primary Cancer Prevention

by Piero Giuseppe Meliante, Carla Petrella, Marco Fiore, Antonio Minni and Christian Barbato

Antioxidants 2023, 12(9), 1753; https://doi.org/10.3390/antiox12091753 - 12 Sep 2023

Viewed by 1088

Abstract

Approximately 5–20% of HNSCC patients experience second primary cancers within the first 5 years of treatment, contributing to high mortality rates. Epidemiological evidence has linked a low dietary intake of antioxidants to an increased risk of cancer, especially squamous cell carcinoma, prompting research [...] Read more.

Approximately 5–20% of HNSCC patients experience second primary cancers within the first 5 years of treatment, contributing to high mortality rates. Epidemiological evidence has linked a low dietary intake of antioxidants to an increased risk of cancer, especially squamous cell carcinoma, prompting research into their potential in neoplasm chemoprevention. Cigarette smoking is the primary risk factor for HNSCC, and a diet rich in antioxidants offers protective effects against head and neck cancer. Paradoxically, smokers, who are at the highest risk, tend to consume fewer antioxidant-rich fruits and vegetables. This has led to the hypothesis that integrating antioxidants into the diet could play a role in both primary and secondary prevention for at-risk individuals. Furthermore, some HNSCC patients use antioxidant supplements during chemotherapy or radiotherapy to manage side effects, but their impact on cancer outcomes remains uncertain. This systematic review explores the evidence for the potential use of antioxidants in preventing second primary cancers in HNSCC patients. In conclusion, none of the antioxidants tested so far (α-tocopherol, β-carotene, JP, Isotretinoin, interferon α-2a, vitamin E, retinyl palmitate, N-acetylcysteine) was effective in preventing second primary tumors in HNSCC patients, and they could only be used in reducing the side effects of radiotherapy. Further research is needed to better understand the interplay between antioxidants and cancer outcomes in this context. Full article

(This article belongs to the Special Issue Oxidative Stress in Tumor Genesis, Progression and Therapy)

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