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Anticancer Antioxidants

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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: closed (30 June 2021) | Viewed by 67397

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Prof. Dr. Neven Zarkovic

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Laboratory for Oxidative Stress (LabOS), Rudjer Boskovic Institute, Bijenička 54, HR-10000 Zagreb, Croatia
Interests: oxidative stress; growth regulation; cancer; lipid peroxidation; 4-hydroxynonenal (HNE)
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Prof. Dr. Suzana Borović Šunjić

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Laboratory for Oxidative Stress, Rudjer Boskovic Institute, Zagreb, Croatia

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Current concepts of biomedicine consider oxidative stress to be one of the crucial pathophysiological processes behind major stress- and age-associated disorders, including cancer development. Consequently, antioxidants are frequently considered to be almost universal defense substances that could prevent or even cure malignant diseases. However, many anticancer treatments rely on the cytotoxic effects of ROS, even if affecting non-malignant cells, while differences in the antioxidant mechanisms between cancer cells and their counterpart non-malignant cells are not well understood.

Therefore, this Special Issue of Antioxidants will publish original research papers and reviews on complex aspects of the biomedical effects of antioxidants—enzymatic and non-enzymatic, whether natural, modified, or synthesized—that possess pronounced anticancer effects. Moreover, papers evaluating the differences in the antioxidant mechanisms between cancer and non-malignant cells and novel concepts of integrative biomedicine offering advanced options for anticancer treatment protocols based on bioactivities or pro- and anti-oxidants will be of particular interest.

Prof. Dr. Neven Zarkovic
Prof. Dr. Suzana Borović Šunjić
Guest Editors

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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 submissions that pass pre-check are 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 2900 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

anti-cancer treatments
cytotoxicity
antioxidants
integrative biomedicine
cancer growth regulation
oxidative stress
lipid peroxidation

Published Papers (13 papers)

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Editorial

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5 pages, 203 KiB

Open AccessEditorial

Editorial on Anticancer Antioxidants

by Suzana Borovic Sunjic and Neven Zarkovic

Antioxidants 2021, 10(11), 1782; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111782 - 08 Nov 2021

Cited by 1 | Viewed by 1510

Abstract

The current concepts of biomedicine consider oxidative stress to be one of crucial pathophysiological processes behind major stress- and age-associated diseases, including cancer [...] Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

Research

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13 pages, 316 KiB

Open AccessArticle

Associations of Human Colorectal Adenoma with Serum Biomarkers of Body Iron Stores, Inflammation and Antioxidant Protein Thiols

by Ben Schöttker, Xīn Gào, Eugène HJM Jansen and Hermann Brenner

Antioxidants 2021, 10(8), 1195; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10081195 - 27 Jul 2021

Cited by 3 | Viewed by 1813

Abstract

Red and processed meat consumption and obesity are established risk factors for colorectal adenoma (CRA). Adverse changes in biomarkers of body iron stores (total serum iron, ferritin, transferrin and transferrin saturation), inflammation (high-sensitivity C-reactive protein [hs-CRP]) and anti-oxidative capacity (total of thiol groups (-S-H) of proteins [SHP]) might reflect underlying mechanisms that could explain the association of red/processed meat consumption and obesity with CRA. Overall, 100 CRA cases (including 71 advanced cases) and 100 CRA-free controls were frequency-matched on age and sex and were selected from a colonoscopy screening cohort. Odds ratios (OR) and 95% confidence intervals (95%CI) for comparisons of top and bottom biomarker tertiles were derived from multivariable logistic regression models. Ferritin levels were significantly positively associated with red/processed meat consumption and hs-CRP levels with obesity. SHP levels were significantly inversely associated with obesity. Transferrin saturation was strongly positively associated with overall and advanced CRA (ORs [95%CIs]: 3.05 [1.30–7.19] and 2.71 [1.03–7.13], respectively). Due to the high correlation with transferrin saturation, results for total serum iron concentration were similar (but not statistically significant). Furthermore, SHP concentration was significantly inversely associated with advanced CRA (OR [95%CI]: 0.29 [0.10–0.84]) but not with overall CRA (OR [95%CI]: 0.65 [0.27–1.56]). Ferritin, transferrin, and hs-CRP levels were not associated with CRA. High transferrin saturation as a sign of iron overload and a low SHP concentration as a sign of redox imbalance in obese patients might reflect underlying mechanisms that could in part explain the associations of iron overload and obesity with CRA. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

27 pages, 14897 KiB

Open AccessArticle

In Vitro Anticancer Activity and Oxidative Stress Biomarkers Status Determined by Usnea barbata (L.) F.H. Wigg. Dry Extracts

by Violeta Popovici, Laura Bucur, Gabriela Vochita, Daniela Gherghel, Cosmin Teodor Mihai, Dan Rambu, Suzana Ioana Calcan, Teodor Costache, Iulia Elena Cucolea, Elena Matei, Florin Ciprian Badea, Aureliana Caraiane and Victoria Badea

Antioxidants 2021, 10(7), 1141; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071141 - 20 Jul 2021

Cited by 19 | Viewed by 5271

Abstract

Lichens represent an important resource for common traditional medicines due to their numerous metabolites that can exert diverse pharmacological activities including anticancer effects. To find new anticancer compounds with fewer side effects and low tumor resistance, a bioprospective study of Usnea barbata (L.) F.H. Wigg. (U. barbata), a lichen from the Călimani Mountains (Suceava county, Romania) was performed. The aim of this research was to investigate the anticancer potential, morphologic changes, wound healing property, clonogenesis, and oxidative stress biomarker status of four extracts of U. barbata in different solvents (methanol, ethanol, acetone, and ethyl acetate), and also of usnic acid (UA) as a positive control on the CAL-27 (ATCC^® CRL-2095™) oral squamous carcinoma (OSCC) cell line and V79 (ATCC^® CCL-93™) lung fibroblasts as normal cells. Using the MTT assay and according to IC₅₀ values, it was found that the most potent anticancer property was displayed by acetone and ethyl acetate extracts. All U. barbata extracts determined morphological modifications (losing adhesion capacity, membrane shrinkage, formation of abnormal cellular wrinkles, and vacuolization) with higher intensity in tumor cells than in normal ones. The most intense anti-migration effect was established in the acetone extract treatment. The clonogenic assay showed that some U. barbata extracts decreased the ability of cancer cells to form colonies compared to untreated cells, suggesting a potential anti-tumorigenic property of the tested extracts. Therefore, all the U. barbata extracts manifest anticancer activity of different intensity, based, at least partially, on an imbalance in antioxidant defense mechanisms, causing oxidative stress. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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16 pages, 5170 KiB

Open AccessArticle

Withaferin a Triggers Apoptosis and DNA Damage in Bladder Cancer J82 Cells through Oxidative Stress

by Tsu-Ming Chien, Kuang-Han Wu, Ya-Ting Chuang, Yun-Chiao Yeh, Hui-Ru Wang, Bi-Wen Yeh, Chia-Hung Yen, Tzu-Jung Yu, Wen-Jeng Wu and Hsueh-Wei Chang

Antioxidants 2021, 10(7), 1063; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071063 - 30 Jun 2021

Cited by 13 | Viewed by 2371

Abstract

Withaferin A (WFA), the Indian ginseng bioactive compound, exhibits an antiproliferation effect on several kinds of cancer, but it was rarely reported in bladder cancer cells. This study aims to assess the anticancer effect and mechanism of WFA in bladder cancer cells. WFA shows antiproliferation to bladder cancer J82 cells based on the finding of the MTS assay. WFA disturbs cell cycle progression associated with subG1 accumulation in J82 cells. Furthermore, WFA triggers apoptosis as determined by flow cytometry assays using annexin V/7-aminoactinomycin D and pancaspase detection. Western blotting also supports WFA-induced apoptosis by increasing cleavage of caspases 3, 8, and 9 and poly ADP-ribose polymerase. Mechanistically, WFA triggers oxidative stress-association changes, such as the generation of reactive oxygen species and mitochondrial superoxide and diminishment of the mitochondrial membrane potential, in J82 cells. In response to oxidative stresses, mRNA for antioxidant signaling, such as nuclear factor erythroid 2-like 2 (NFE2L2), catalase (CAT), superoxide dismutase 1 (SOD1), thioredoxin (TXN), glutathione-disulfide reductase (GSR), quinone dehydrogenase 1 (NQO1), and heme oxygenase 1 (HMOX1), are overexpressed in J82 cells. In addition, WFA causes DNA strand breaks and oxidative DNA damages. Moreover, the ROS scavenger N-acetylcysteine reverts all tested WFA-modulating effects. In conclusion, WFA possesses anti-bladder cancer effects by inducing antiproliferation, apoptosis, and DNA damage in an oxidative stress-dependent manner. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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14 pages, 4116 KiB

Open AccessArticle

Identification of a Stable, Non-Canonically Regulated Nrf2 Form in Lung Cancer Cells

by Sara Mikac, Michał Rychłowski, Alicja Dziadosz, Alicja Szabelska-Beresewicz, Robin Fahraeus, Theodore Hupp and Alicja Sznarkowska

Antioxidants 2021, 10(5), 786; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050786 - 15 May 2021

Cited by 5 | Viewed by 3796

Abstract

Nrf2 (nuclear factor erythroid 2 (NF-E2)-related factor 2) transcription factor is recognized for its pro-survival and cell protective role upon exposure to oxidative, chemical, or metabolic stresses. Nrf2 controls a number of cellular processes such as proliferation, differentiation, apoptosis, autophagy, lipid synthesis, and metabolism and glucose metabolism and is a target of activation in chronic diseases like diabetes, neurodegenerative, and inflammatory diseases. The dark side of Nrf2 is revealed when its regulation is imbalanced (e.g., via oncogene activation or mutations) and under such conditions constitutively active Nrf2 promotes cancerogenesis, metastasis, and radio- and chemoresistance. When there is no stress, Nrf2 is instantly degraded via Keap1-Cullin 3 (Cul3) pathway but despite this, cells exhibit a basal activation of Nrf2 target genes. It is yet not clear how Nrf2 maintains the expression of its targets under homeostatic conditions. Here, we found a stable 105 kDa Nrf2 form that is resistant to Keap1-Cul3-mediated degradation and translocates to the nucleus of lung cancer cells. RNA-Seq analysis indicate that it might originate from the exon 2 or exon 3-truncated transcripts. This stable 105 kDa Nrf2 form might help explain the constitutive activity of Nrf2 under normal cellular conditions. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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12 pages, 1583 KiB

Open AccessArticle

Astaxanthin Treatment Induces Maturation and Functional Change of Myeloid-Derived Suppressor Cells in Tumor-Bearing Mice

by Seong Mun Jeong and Yeon-Jeong Kim

Antioxidants 2020, 9(4), 350; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9040350 - 23 Apr 2020

Cited by 8 | Viewed by 2991

Abstract

Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells which accumulate in stress conditions such as infection and tumor. Astaxanthin (ATX) is a well-known antioxidant agent and has a little toxicity. It has been reported that ATX treatment induces antitumor effects via regulation of cell signaling pathways, including nuclear factor erythroid-derived 2-related factor 2 (Nrf2) signaling. In the present study, we hypothesized that treatment with ATX might induce maturation of MDSCs and modulate their immunosuppressive activity. Both in vivo and in vitro treatment with ATX resulted in up-regulation of surface markers such as CD80, MHC class II, and CD11c on both polymorphonuclear (PMN)-MDSCs and mononuclear (Mo)-MDSCs. Expression levels of functional mediators involved in immune suppression were significantly reduced, whereas mRNA levels of Nrf2 target genes were increased in ATX-treated MDSCs. In addition, ATX was found to have antioxidant activity reducing reactive oxygen species level in MDSCs. Finally, ATX-treated MDSCs were immunogenic enough to induce cytotoxic T lymphocyte response and contributed to the inhibition of tumor growth. This demonstrates the role of ATX as a regulator of the immunosuppressive tumor environment through induction of differentiation and functional conversion of MDSCs. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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Review

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13 pages, 678 KiB

Open AccessReview

Oxidative Stress and Cognitive Alterations Induced by Cancer Chemotherapy Drugs: A Scoping Review

by Omar Cauli

Antioxidants 2021, 10(7), 1116; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071116 - 13 Jul 2021

Cited by 22 | Viewed by 4276

Abstract

Cognitive impairment is one of the most deleterious effects of chemotherapy treatment in cancer patients, and this problem sometimes remains even after chemotherapy ends. Common classes of chemotherapy-based regimens such as anthracyclines, taxanes, and platinum derivatives can induce both oxidative stress in the blood and in the brain, and these effects can be reproduced in neuronal and glia cell cultures. In rodent models, both the acute and repeated administration of doxorubicin or adriamycin (anthracyclines) or cisplatin impairs cognitive functions, as shown by their diminished performance in different learning and memory behavioural tasks. Administration of compounds with strong antioxidant effects such as N-acetylcysteine, gamma-glutamyl cysteine ethyl ester, polydatin, caffeic acid phenethyl ester, and 2-mercaptoethane sulfonate sodium (MESNA) counteract both oxidative stress and cognitive alterations induced by chemotherapeutic drugs. These antioxidant molecules provide the scientific basis to design clinical trials in patients with the aim of reducing the oxidative stress and cognitive alterations, among other probable central nervous system changes, elicited by chemotherapy in cancer patients. In particular, N-acetylcysteine and MESNA are currently used in clinical settings and are therefore attracting scientific attention. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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21 pages, 2324 KiB

Open AccessReview

Redox Potential of Antioxidants in Cancer Progression and Prevention

by Sajan George and Heidi Abrahamse

Antioxidants 2020, 9(11), 1156; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9111156 - 20 Nov 2020

Cited by 79 | Viewed by 7361

Abstract

The benevolent and detrimental effects of antioxidants are much debated in clinical trials and cancer research. Several antioxidant enzymes and molecules are overexpressed in oxidative stress conditions that can damage cellular proteins, lipids, and DNA. Natural antioxidants remove excess free radical intermediates by reducing hydrogen donors or quenching singlet oxygen and delaying oxidative reactions in actively growing cancer cells. These reducing agents have the potential to hinder cancer progression only when administered at the right proportions along with chemo-/radiotherapies. Antioxidants and enzymes affect signal transduction and energy metabolism pathways for the maintenance of cellular redox status. A decline in antioxidant capacity arising from genetic mutations may increase the mitochondrial flux of free radicals resulting in misfiring of cellular signalling pathways. Often, a metabolic reprogramming arising from these mutations in metabolic enzymes leads to the overproduction of so called ’oncometabolites’ in a state of ‘pseudohypoxia’. This can inactivate several of the intracellular molecules involved in epigenetic and redox regulations, thereby increasing oxidative stress giving rise to growth advantages for cancerous cells. Undeniably, these are cell-type and Reactive Oxygen Species (ROS) specific, which is manifested as changes in the enzyme activation, differences in gene expression, cellular functions as well as cell death mechanisms. Photodynamic therapy (PDT) using light-activated photosensitizing molecules that can regulate cellular redox balance in accordance with the changes in endogenous ROS production is a solution for many of these challenges in cancer therapy. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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41 pages, 1756 KiB

Open AccessReview

The NRF2, Thioredoxin, and Glutathione System in Tumorigenesis and Anticancer Therapies

by Morana Jaganjac, Lidija Milkovic, Suzana Borovic Sunjic and Neven Zarkovic

Antioxidants 2020, 9(11), 1151; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9111151 - 19 Nov 2020

Cited by 86 | Viewed by 8744

Abstract

Cancer remains an elusive, highly complex disease and a global burden. Constant change by acquired mutations and metabolic reprogramming contribute to the high inter- and intratumor heterogeneity of malignant cells, their selective growth advantage, and their resistance to anticancer therapies. In the modern era of integrative biomedicine, realizing that a personalized approach could benefit therapy treatments and patients’ prognosis, we should focus on cancer-driving advantageous modifications. Namely, reactive oxygen species (ROS), known to act as regulators of cellular metabolism and growth, exhibit both negative and positive activities, as do antioxidants with potential anticancer effects. Such complexity of oxidative homeostasis is sometimes overseen in the case of studies evaluating the effects of potential anticancer antioxidants. While cancer cells often produce more ROS due to their increased growth-favoring demands, numerous conventional anticancer therapies exploit this feature to ensure selective cancer cell death triggered by excessive ROS levels, also causing serious side effects. The activation of the cellular NRF2 (nuclear factor erythroid 2 like 2) pathway and induction of cytoprotective genes accompanies an increase in ROS levels. A plethora of specific targets, including those involved in thioredoxin (TRX) and glutathione (GSH) systems, are activated by NRF2. In this paper, we briefly review preclinical research findings on the interrelated roles of the NRF2 pathway and TRX and GSH systems, with focus given to clinical findings and their relevance in carcinogenesis and anticancer treatments. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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44 pages, 1695 KiB

Open AccessReview

Regulation of Nrf2/ARE Pathway by Dietary Flavonoids: A Friend or Foe for Cancer Management?

by Tharindu L. Suraweera, H. P. Vasantha Rupasinghe, Graham Dellaire and Zhaolin Xu

Antioxidants 2020, 9(10), 973; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9100973 - 11 Oct 2020

Cited by 92 | Viewed by 9077

Abstract

The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway is an important cell signaling mechanism in maintaining redox homeostasis in humans. The role of dietary flavonoids in activating Nrf2/ARE in relation to cancer chemoprevention or cancer promotion is not well established. Here we summarize the dual effects of flavonoids in cancer chemoprevention and cancer promotion with respect to the regulation of the Nrf2/ARE pathway, while underlying the possible cellular mechanisms. Luteolin, apigenin, quercetin, myricetin, rutin, naringenin, epicatechin, and genistein activate the Nrf2/ARE pathway in both normal and cancer cells. The hormetic effect of flavonoids has been observed due to their antioxidant or prooxidant activity, depending on the concentrations. Reported in vitro and in vivo investigations suggest that the activation of the Nrf2/ARE pathway by either endogenous or exogenous stimuli under normal physiological conditions contributes to redox homeostasis, which may provide a mechanism for cancer chemoprevention. However, some flavonoids, such as luteolin, apigenin, myricetin, quercetin, naringenin, epicatechin, genistein, and daidzein, at low concentrations (1.5 to 20 µM) facilitate cancer cell growth and proliferation in vitro. Paradoxically, some flavonoids, including luteolin, apigenin, and chrysin, inhibit the Nrf2/ARE pathway in vitro. Therefore, even though flavonoids play a major role in cancer chemoprevention, due to their possible inducement of cancer cell growth, the effects of dietary flavonoids on cancer pathophysiology in patients or appropriate experimental animal models should be investigated systematically. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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22 pages, 882 KiB

Open AccessReview

Anticancer Properties of Carnosol: A Summary of In Vitro and In Vivo Evidence

by Eric J. O’Neill, Danja J. Den Hartogh, Karim Azizi and Evangelia Tsiani

Antioxidants 2020, 9(10), 961; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9100961 - 08 Oct 2020

Cited by 25 | Viewed by 3925

Abstract

Cancer is characterized by unrestricted cell proliferation, inhibition of apoptosis, enhanced invasion and migration, and deregulation of signalling cascades. These properties lead to uncontrolled growth, enhanced survival, and the formation of tumours. Carnosol, a naturally occurring phyto-polyphenol (diterpene) found in rosemary, has been studied for its extensive antioxidant, anti-inflammatory, and anticancer effects. In cancer cells, carnosol has been demonstrated to inhibit cell proliferation and survival, reduce migration and invasion, and significantly enhance apoptosis. These anticancer effects of carnosol are mediated by the inhibition of several signalling molecules including extracellular signal-regulated kinase (ERK), p38, c-Jun N-terminal kinase (JNK), Akt, mechanistic target of rapamycin (mTOR) and cyclooxygenase-2 (COX-2). Additionally, carnosol prevents the nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and promotes apoptosis, as indicated by increased levels of cleaved caspase-3, -8, -9, increased levels of the pro-apoptotic marker Bcl-2-associated X (BAX), and reduced levels of the anti-apoptotic marker B-cell lymphoma 2 (Bcl-2). The current review summarizes the existing in vitro and in vivo evidence examining the anticancer effects of carnosol across various tissues. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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20 pages, 7352 KiB

Open AccessReview

Dietary Polyphenols in Cancer Chemoprevention: Implications in Pancreatic Cancer

by Anita Thyagarajan, Andrew S. Forino, Raymond L. Konger and Ravi P. Sahu

Antioxidants 2020, 9(8), 651; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9080651 - 23 Jul 2020

Cited by 19 | Viewed by 3994

Abstract

Naturally occurring dietary agents present in a wide variety of plant products, are rich sources of phytochemicals possessing medicinal properties, and thus, have been used in folk medicine for ages to treat various ailments. The beneficial effects of such dietary components are frequently attributed to their anti-inflammatory and antioxidant properties, particularly in regards to their antineoplastic activities. As many tumor types exhibit greater oxidative stress levels that are implicated in favoring autonomous cell growth activation, most chemotherapeutic agents can also enhance tumoral oxidative stress levels in part via generating reactive oxygen species (ROS). While ROS-mediated imbalance of the cellular redox potential can provide novel drug targets, as a consequence, this ROS-mediated excessive damage to cellular functions, including oncogenic mutagenesis, has also been implicated in inducing chemoresistance. This remains one of the major challenges in the treatment and management of human malignancies. Antioxidant-enriched natural compounds offer one of the promising approaches in mitigating some of the underlying mechanisms involved in tumorigenesis and metastasis, and therefore, have been extensively explored in cancer chemoprevention. Among various groups of dietary phytochemicals, polyphenols have been extensively explored for their underlying chemopreventive mechanisms in other cancer models. Thus, the current review highlights the significance and mechanisms of some of the highly studied polyphenolic compounds, with greater emphasis on pancreatic cancer chemoprevention. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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15 pages, 1878 KiB

Open AccessReview

An Overview of the Antioxidant Effects of Ascorbic Acid and Alpha Lipoic Acid (in Liposomal Forms) as Adjuvant in Cancer Treatment

by Mohamed Attia, Ebtessam Ahmed Essa, Randa Mohammed Zaki and Amal Ali Elkordy

Antioxidants 2020, 9(5), 359; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9050359 - 25 Apr 2020

Cited by 53 | Viewed by 10622

Abstract

Antioxidants are known to minimize oxidative stress by interacting with free radicals produced as a result of cell aerobic reactions. Oxidative stress has long been linked to many diseases, especially tumours. Therefore, antioxidants play a crucial role in the prevention or management of free radical-related diseases. However, most of these antioxidants have anticancer effects only if taken in large doses. Others show inadequate bioavailability due to their instability in the blood or having a hydrophilic nature that limits their permeation through the cell membrane. Therefore, entrapping antioxidants in liposomes may overcome these drawbacks as liposomes have the capability to accommodate both hydrophilic and hydrophobic compounds with a considerable stability. Additionally, liposomes have the capability to accumulate at the cancer tissue passively, due to their small sizes, with enhanced drug delivery. Additionally, liposomes can be engineered with targeting moieties to increase the delivery of chemotherapeutic agents to specific tumour cells with decreased accumulation in healthy tissues. Therefore, combined use of liposomes and antioxidants, with or without chemotherapeutic agents, is an attractive strategy to combat varies tumours. This mini review focuses on the liposomal delivery of selected antioxidants, namely ascorbic acid (AA) and alpha-lipoic acid (ALA). The contribution of these nanocarriers in enhancing the antioxidant effect of AA and ALA and consequently their anticancer potentials will be demonstrated. Full article

(This article belongs to the Special Issue Anticancer Antioxidants)

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