free radicals research paper

A Comprehensive Review of Free Radicals, Antioxidants, and Their Relationship with Human Ailments

Affiliations.

• 1 School of Pharmaceutical Sciences, Jaipur National University, Jagatpura, Jaipur, 302017 India.
• 2 School of Pharmaceutical Sciences, Jaipur National University, Jagatpura, Jaipur, India.
• 3 Maharishi Arvind College of Pharmacy, Ambabari, Jaipur (Raj), 302023 India.
• PMID: 30055541
• DOI: 10.1615/CritRevEukaryotGeneExpr.2018022258

The role of free radicals in various human ailments is well established. Still, the researchers continue to emphasize the involvement of free radicals in these disorders. Antioxidants are being used as an effective tool as a defense against disorders caused by free radicals. This review presents brief detail regarding the nature, types, and sources of free radicals that are of pharmacological interest. A summary of the antioxidants, along with possible mechanisms, has also been incorporated. The role of free radicals and antioxidants in various human disease are also presented.

Publication types

• Antioxidants / chemistry
• Antioxidants / metabolism*
• Digestive System / chemistry
• Digestive System / metabolism*
• Free Radicals / chemistry
• Free Radicals / metabolism*
• Oxidative Stress / genetics*
• Antioxidants
• Free Radicals

Free Radicals and Antioxidants

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Free Radicals and Antioxidants publishes full research papers presenting original, high quality research, critical review articles providing comprehensive analysis of research development within a defined area and editorial commentaries on key topical issues in Free Radical and Antioxidant Biology.

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Antioxidant properties of honey: mechanisms and clinical applications, original article, quantitative analysis of phytochemical constituents and antioxidant efficiency of cucumis prophetarum l., orientin protects bv-2 microglial cells against hypoxia reoxygenation injury through inhibiting oxidative stress, phenolic content, flavonoid content and antioxidant efficacy of opuntia elatior mill. phytochemical and antioxidant efficacy of opuntia elatior mill., anti-parkinson potential of indian ocimum species in relation to active components as revealed using metabolites profiling, in vitro and in silico enzyme inhibition studies, the rat ovaries after erythropoietin process, short communication, phytopharmacological updates on mentha longifolia: a comprehensive review.

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Breaking free from free radicals: harnessing the power of natural antioxidants for health and disease prevention

• Published: 24 November 2023
• Volume 78 , pages 2061–2077, ( 2024 )

Cite this article

• Priya Chaudhary 1 ,
• Pracheta Janmeda 1 ,
• William N. Setzer 2 , 3 ,
• Afaf Ahmed Aldahish 4 ,
• Javad Sharifi-Rad   ORCID: orcid.org/0000-0002-7301-8151 5 &
• Daniela Calina 6  

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Massive production of the free radicals disrupts the system of antioxidant defense in the animal body thereby causing damage to cellular molecules (nucleic acid, lipids, protein, and cell membrane) which results to cell death or mutation that may give rise to abnormal cell division. Synthetic antioxidants such as butylated hydroxyanisole and butylated hydroxytoluene have been determined to be toxic to the health of human beings. Thus, the finding for nontoxic, effective, and safe natural compounds with potent antioxidant activities has been increasing in the last few years. Antioxidants are most frequently utilized in the control and management of oxidative stress-associated cancer and other diseases. The present review presents brief information on free radicals, their types, oxidative stress-directed effects and the function of natural and synthetic antioxidants in the control of cancer and other diseases.

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Chaudhary, P., Janmeda, P., Setzer, W.N. et al. Breaking free from free radicals: harnessing the power of natural antioxidants for health and disease prevention. Chem. Pap. 78 , 2061–2077 (2024). https://doi.org/10.1007/s11696-023-03197-1

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Journal of Materials Chemistry A

Functional group substitution strongly influences the performances of covalent organic frameworks in the photocatalytic metal-free oxidase reaction †.

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a Department of Chemistry, Shanghai Normal University, 100 Guilin Rd., Shanghai, China E-mail: [email protected] , [email protected]

The exceptional performance of covalent organic frameworks (COFs) serving as metal-free photocatalysts has been demonstrated in numerous oxidation reactions. However, the intricate structure–activity relationship between the components, structures and reactivity of COFs remains poorly understood. This is due to their photocatalytic activity being influenced by various factors, including light absorption, charge carrier generation, separation, transport, and surface adsorption. In this study, a series of COFs with different functional group substitutions but similar topological structures were employed to investigate the relationship between the molecular structure and catalytic activity. The results reveal an activity trend in the representative superoxide radical-mediated Aza–Henry reaction, with COF-Br > COF-Cl > COF-H > COF-OMe > COF-H. Both the experimental results and density functional theory calculations confirm that the catalytic activities of COFs are closely linked to the band gap and electron affinity of the initial monomers. This study of the relationship offers a rational, time- and energy-saving strategy for developing effective COF-based photocatalysts. This approach involves evaluating the physical properties of COF monomers rather than conducting catalytic screenings on final solid COFs.

• This article is part of the themed collection: Journal of Materials Chemistry A HOT Papers

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Functional group substitution strongly influences the performances of covalent organic frameworks in the photocatalytic metal-free oxidase reaction

H. Chen, Q. Zhou, J. Hai, M. Zhu and F. Zhang, J. Mater. Chem. A , 2024, Advance Article , DOI: 10.1039/D4TA00473F

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Free Radical Research in Cancer

It can be challenging to find efficient therapy for cancer due to its biological diversity. One of the factors that contribute to its biological diversity are free radicals. Evolutionary, aerobic organisms evolve in an oxygen atmosphere, improving the energy production system by using oxygen. Oxygen is beneficial, but it can also be detrimental if free radicals are formed [ 1 ]. Free radicals, as well as some non-radical species that have oxygen, are reactive oxygen species (ROS). ROS can damage DNA leading to mutations, single, or double-strand breaks [ 2 ]. These events, if the cell is unable to repair the damage, are deleterious. If not fatal, these changes in genetic material result in tumor development by losing cell cycle control. Further, these mutations create genetic instability that result in tumor heterogeneity, and thereby increase the possibility of surviving stress conditions. In addition to direct interaction with DNA, proteins, and lipids, ROS are also signaling molecules that take an active part in regulating cellular processes [ 3 , 4 ]. It was previously thought that ROS only damage cells, but we now know that some enzymes primarily produce ROS, and they are not by-products [ 3 ]. These are NAD(P)H oxidases (NOX) and they produce ROS in response to inflammatory signaling. This planned production of ROS may play a role in proliferation, as ROS are able to activate signaling pathways, such as mitogen activated-protein kinase (MAPK)/extracellular-regulated kinase 1/2 (ERK1/2), phosphoinositide-3-kinase (PI3K)/protein kinase (Akt), and more, thoroughly reviewed in [ 3 ]. An important factor in surviving ROS is the antioxidant system of the cell. The main role of this complex system is to remove the excess ROS. As there are many ROS, there are many different parts of this system acting in a similar or unique way in removing ROS, such as the glutathione system, superoxide dismutase-catalase catalase, thioredoxin system, and small molecules (e.g. vitamin C, vitamin E). In order to ensure the right levels of these enzymes and small molecules, ROS activate several antioxidative transcription factors, such as Nrf2 and the FoxO family. These transcription factors are responsible for activating the majority of antioxidative genes [ 5 , 6 , 7 ]. Generally, cancer cells have increased amounts of ROS; consequently, they adapt by increasing the antioxidative defense system [ 8 ], thereby, strongly linking ROS and antioxidative research.

Nevertheless, ROS were at first considered detrimental, and this was used as a therapeutic strategy in fighting cancer. Most of the conventional types of chemotherapy, as well as radiotherapy, are based on ROS production. Unfortunately, this strategy has to eradicate the tumor completely, otherwise the surviving cells adapt and build up their antioxidant systems, as well as other mechanisms (e.g., drug transporters) making themselves resistant. Strategies involving activation/inhibition of signaling pathways (and here, Nrf2 was certainly an attractive target) turned out to be a double-edged sword [ 9 ].

This Special Issue aims to provide different approaches to study the role of free radicals in cancer. Recent findings are presented within eight original papers and four review papers, spanning from cancer therapy and resistance development to side effects of cancer therapy, with its effects on human health, in a process governed by free radicals.

The focus of the review papers is on free radicals, ROS, and cancer therapy. As mentioned above, ROS modulate cellular signaling pathways and are therefore important to maintain redox homeostasis. A review by Kim et al. [ 10 ] provides an overview of cellular ROS production, both controlled and uncontrolled, as well as ROS elimination (keeping in mind the importance of this homeostasis). Further, redox changes in cancer are described, with emphasis on chemotherapy based on ROS production. The paradox of chemotherapy is discussed: the chemotherapy resistance can be acquired through either increased proliferation (leading to resistance) or by changing to a cancer stem-like cell phenotype, with a low proliferation rate. In hand with this review is the work of Mendes and Serpa [ 11 ], which discusses metabolic remodeling of lung cancer. These metabolic changes occur via several mechanisms, which include mutations, as well as responses to oxidative or alkylating treatments. These events lead to chemotherapy resistance that occur because of changes in drug transporters, as well as in antioxidants. Metabolic remodeling is therefore a challenge in cancer therapy, and can be used—if the changes are well monitored and defined—to adapt to clinical therapy, in order to avoid recurrence.

The review papers by Clavo et al. [ 12 ], and Prasad and Srivastava [ 13 ], discuss adjuvant cancer therapy by reduction of ROS. Natural compounds, such as Triphala and Ayurvedic medicine, have antioxidative properties, and prevent free radical formation and lipid peroxidation. In addition to antioxidative properties, the authors also discuss the chemopreventive and chemotherapeutic effects of Triphala, which are encouraged by the results of three clinical studies. Another strategy in fighting cancer, described by Clavo et al. [ 12 ], is the use of ozone as an adjuvant therapy to conventional chemotherapy. The authors present evidence of beneficial effects of ozone therapy on animal models and describe possible mechanisms by which these effect may occur.

Mechanisms, by which cellular processes are changed in cancer, spread on different molecules (such as enzymes, transcription factors, or ion channels). An example of an ion channel is the transient receptor potential melastatin 2 (TRPM2), a Ca 2+ channel that can be activated by H 2 O 2 [ 14 ]. A study presented by Hack et al. [ 14 ] showed parallel expression of NOX4 and TRPM2 in human granulosa cell tumor samples, suggesting that induction of oxidative stress could be beneficial for the therapy, as activation of this channel by H 2 O 2 increased Ca 2+ levels and apoptotic cell death.

Acquired resistance was a model in two papers and was achieved through growth of cells under conditions of chronic oxidative stress. Both models used breast cancer cell lines in their study. In a study by Glorieux and Calderon [ 15 ], NQO1 affected cancer redox homeostasis and sensitivity to drugs. Consequently, NQO1 polymorphism may be used as an important factor if quinone-based chemotherapeutic drugs are considered as cancer therapy. Interestingly, NQO1 is a target gene for NRF2, an antioxidative transcription factor. Using breast cancer cell lines stimulated for cancer-stem-like phenotypes under chronic oxidative stress, we showed an increase in NRF2, but also in some epithelial-mesenchymal transition markers, indicating that NRF2 can play a role in breast cancer resistance [ 16 ].

In addition to breast cancer, ROS and NRF2 were studied in regards to the androgen receptor and its splice-variant AR-V7 [ 17 ]. As therapy for prostate cancer, a triterpenoid antioxidant drug was tested for its ability to regulate androgen receptor expression. This drug proved to enhance efficacy of clinically approved anti-androgen, but also decreased ROS and increased NRF2, indicating possible mechanisms of action. There are numerous consequences of prostate cancer therapy due to ROS production, but effects on sperm are not fully investigated. Takeshima et al. [ 18 ] show evidence that cancer chemotherapy has similar effects on semen as idiopathic infertility, suggesting antioxidant therapy to reduce ROS.

As mentioned, many conventional cancer therapies are based on free radical/ROS production. Photodynamic therapy is also a cancer therapy that uses chemosensitizers to generate free radicals, which then act against the tumor. Such a photosensitizer, a tailored boron-dipyrromethene (BODIPY) derivative, was used on A375 and SKMEL28 cancer cell lines [ 19 ]. Authors show positive effects of this compound by inducing singlet oxygen and NO to cause cell death.

Finally, Rodríguez-García et al. [ 20 ] studied protein carbonylation in patients with myelodysplastic syndromes. These patients had increased protein carbonyls, but levels decreased after treatment with an iron chelator (deferasirox). Analysis of the p21 gene expression in bone marrow cells revealed correlation between high protein carbonyls and increased expression, and vice versa. The paper suggests that the fine-tuning of oxidative stress levels in bone marrow can determine the disease progression in these patients.

Conflicts of Interest

The authors declare no conflict of interest.