Administration of antioxidants in cancer: debate of the decade

Khurana, Rajneet Kaur; Jain, Ashay; Jain, Atul; Sharma, Teenu; Singh, Bhupinder; Kesharwani, Prashant

doi:10.1016/j.drudis.2018.01.021

Cited by 72 publications

(40 citation statements)

References 53 publications

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“…Under normal physiological conditions, cells maintain a balance between oxidant species and antioxidants, referred to as redox homeostasis. At low concentrations, RONS act to regulate proliferation, cell death, and other metabolic processes [ 59 ]. An increase in oxidative stress has been associated with several types of cell death, including oxeiptosis, a recently described cell death pathway exhibiting the morphological features of apoptosis that is independent of caspase activation [ 60 ].…”

Section: Resultsmentioning

confidence: 99%

Emodin, Physcion, and Crude Extract of Rhamnus sphaerosperma var. pubescens Induce Mixed Cell Death, Increase in Oxidative Stress, DNA Damage, and Inhibition of AKT in Cervical and Oral Squamous Carcinoma Cell Lines

Moreira

Sorbo

Souza

et al. 2018

Oxidative Medicine and Cellular Longevity

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There have been few studies on the pharmacological properties of Rhamnus sphaerosperma var. pubescens, a native Brazilian species popularly known as “fruto-de-pombo.” The aim of this study was to investigate the scavenging capacity of emodin, physcion, and the ethanolic crude extract of Rhamnus sphaerosperma var. pubescens against reactive oxygen and nitrogen species, as well as their role and plausible mechanisms in prompting cell death and changes in AKT phosphorylation after cervical (SiHa and C33A) and oral (HSC-3) squamous cell carcinoma treatments. Emodin was shown to be the best scavenger of NO• and O2•−, while all samples were equally effective in HOCl/OCl− capture. Emodin, physcion, and the ethanolic extract all exhibited cytotoxic effects on SiHa, C33A, HSC-3, and HaCaT (immortalized human keratinocytes, nontumorigenic cell line), involving mixed cell death (apoptosis and necrosis) independent of the caspase activation pathway. Emodin, physcion, and the ethanolic extract increased intracellular oxidative stress and DNA damage. Emodin decreased the activation of AKT in all tumor cells, physcion in HSC-3 and HaCaT cells, and the ethanolic extract in C33A and HaCaT cells, respectively. The induction of cancer cell death by emodin, physcion, and the ethanolic crude extract of Rhamnus sphaerosperma var. pubescens was related to an increase in intracellular oxidative stress and DNA damage and a decrease in AKT activation. These molecules are therefore emerging as interesting candidates for further study as novel options to treat cervical and oral carcinomas.

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Section: Resultsmentioning

confidence: 99%

Emodin, Physcion, and Crude Extract of Rhamnus sphaerosperma var. pubescens Induce Mixed Cell Death, Increase in Oxidative Stress, DNA Damage, and Inhibition of AKT in Cervical and Oral Squamous Carcinoma Cell Lines

Moreira

Sorbo

Souza

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Numerous drugs used for cancer therapy, including doxorubicin, vinblastine, paclitaxel, and camptothecin, have been obtained from natural sources [ 20 ]. The use of chemo-herbal combination therapy has been found to increase the anticancer effects of chemotherapeutic agents and to ameliorate drug resistance and chemotherapy-related adverse effects [ 21 , 22 ]. Natural secondary metabolites have shown pleiotropic effects and target various cancer hallmarks, including inflammation, cancer cell proliferation, migration, invasion, angiogenesis, and metastasis [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

Targeting Multiple Signaling Pathways in Cancer: The Rutin Therapeutic Approach

Nouri

Fakhri

Nouri

et al. 2020

Cancers

139

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Multiple dysregulated signaling pathways are implicated in the pathogenesis of cancer. The conventional therapies used in cancer prevention/treatment suffer from low efficacy, considerable toxicity, and high cost. Hence, the discovery and development of novel multi-targeted agents to attenuate the dysregulated signaling in cancer is of great importance. In recent decades, phytochemicals from dietary and medicinal plants have been successfully introduced as alternative anticancer agents due to their ability to modulate numerous oncogenic and oncosuppressive signaling pathways. Rutin (also known as rutoside, quercetin-3-O-rutinoside and sophorin) is an active plant-derived flavonoid that is widely distributed in various vegetables, fruits, and medicinal plants, including asparagus, buckwheat, apricots, apples, cherries, grapes, grapefruit, plums, oranges, and tea. Rutin has been shown to target various inflammatory, apoptotic, autophagic, and angiogenic signaling mediators, including nuclear factor-κB, tumor necrosis factor-α, interleukins, light chain 3/Beclin, B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein, caspases, and vascular endothelial growth factor. A comprehensive and critical analysis of the anticancer potential of rutin and associated molecular targets amongst various cancer types has not been performed previously. Accordingly, the purpose of this review is to present an up-to-date and critical evaluation of multiple cellular and molecular mechanisms through which the anticancer effects of rutin are known to be exerted. The current challenges and limitations as well as future directions of research are also discussed.

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“…ROS can attack polyunsaturated fatty acids of lipid membranes and induce lipid peroxidation (LPO). An excessive increase in the amount of ROS and LPO induced by different prooxidants leads to oxidative stress and apoptosis leading to overcleaning of the cellular antioxidant defense system [5][6]. Antioxidants have been widely used as dietary supplements and have been investigated for their effectiveness in prevention of many diseases including various types of cancer.…”

Section: Introductionmentioning

confidence: 99%

Apoptotic Effects of Beta-Carotene, Alpha-Tocopherol and Ascorbic Acid on Pc-3 Prostate Cancer Cells

Ayna¹

2020

Hacettepe Journal of Biology and Chemistry

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P rostat kanseri (PC), özellikle 50 yaşın üzerindeki erkeklerde kansere bağlı ölümlerin ikinci büyük nedeni olan ve en yaygın olarak teşhis edilen kanser tiplerinden biridir. Bilimsel çalışmalar oksidatif stres ve Reaktif oksijen türlerinin (ROS) prostat kanseri üzerindeki rolünü göstermektedir. ROS, kanserojen moleküller, enfeksiyon, toksi bileşikler gibi homeostaza ve genetik mutasyona neden olabilecek bileşikler tarafından üretilir. Antioksidanlar, ROS'un olumsuz etkilerini in vitro olarak azaltabilir. C vitamini (Askorbik asit, Asc), A vitamini (beta karotenoidler ve retinoidler, β-Crt) ve E vitamini (alfa tokoferol, α-Toc) oksidasyonun önlenmesinde ve vücuttaki serbest radikallerin konsantrasyonunun azaltılmasında önemli rol oynar. Bu çalışmanın amacı, α-Toc, β-Crt ve Asc'nin PC-3 prostat kanseri hücreleri üzerindeki in vitro antikanser etkisini belirlemektir. Bu amaç, hücre çoğalması, ROS ve Lipid Peroksidasyon deneyi, kaspaz-3 ve propidium iyodür boyama deneyleri ile gerçekleştirildi. Bulgular, bu ajanların, prostat kanseri hücrelerinde hücre canlılığını azaltarak ve ROS ve LPO üretimini artırarak proksidan olarak davrandığını göstermektedir. Bu oksidanlar kaspaz-3 (programlı hücre ölümünde rol alan önemli bir enzim) boyamasıyla desteklendiği üzere apoptozu kaspaz-3 enziminin ekspresyonunu artırarak indüklemiştir.

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Administration of antioxidants in cancer: debate of the decade

Cited by 72 publications

References 53 publications

Emodin, Physcion, and Crude Extract of Rhamnus sphaerosperma var. pubescens Induce Mixed Cell Death, Increase in Oxidative Stress, DNA Damage, and Inhibition of AKT in Cervical and Oral Squamous Carcinoma Cell Lines

Emodin, Physcion, and Crude Extract of Rhamnus sphaerosperma var. pubescens Induce Mixed Cell Death, Increase in Oxidative Stress, DNA Damage, and Inhibition of AKT in Cervical and Oral Squamous Carcinoma Cell Lines

Targeting Multiple Signaling Pathways in Cancer: The Rutin Therapeutic Approach

Apoptotic Effects of Beta-Carotene, Alpha-Tocopherol and Ascorbic Acid on Pc-3 Prostate Cancer Cells

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