scholarly journals Pro-oxidant Actions of Carotenoids in Triggering Apoptosis of Cancer Cells: A Review of Emerging Evidence

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 532 ◽  
Author(s):  
Juhyun Shin ◽  
Min-Ho Song ◽  
Jae-Wook Oh ◽  
Young-Soo Keum ◽  
Ramesh Kumar Saini
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Research Gaps ◽  
Cytotoxic Effects ◽  
Normal Cells ◽  
Anti Cancer ◽  
Antioxidant Function ◽  
High Level ◽  
Β Carotene

Carotenoids are well known for their potent antioxidant function in the cellular system. However, in cancer cells with an innately high level of intracellular reactive oxygen species (ROS), carotenoids may act as potent pro-oxidant molecules and trigger ROS-mediated apoptosis. In recent years, the pro-oxidant function of several common dietary carotenoids, including astaxanthin, β-carotene, fucoxanthin, and lycopene, has been investigated for their effective killing effects on various cancer cell lines. Besides, when carotenoids are delivered with ROS-inducing cytotoxic drugs (e.g., anthracyclines), they can minimize the adverse effects of these drugs on normal cells by acting as antioxidants without interfering with their cytotoxic effects on cancer cells as pro-oxidants. These dynamic actions of carotenoids can optimize oxidative stress in normal cells while enhancing oxidative stress in cancer cells. This review discusses possible mechanisms of carotenoid-triggered ROS production in cancer cells, the activation of pro-apoptotic signaling by ROS, and apoptotic cell death. Moreover, synergistic actions of carotenoids with ROS-inducing anti-cancer drugs are discussed, and research gaps are suggested.

Natural-Derived Molecules as a Potential Adjuvant in Chemotherapy: Normal Cell Protectors and Cancer Cell Sensitizers

2021 ◽  
Vol 21 ◽  
Author(s):  
Rajib Hossain ◽  
Muhammad Torequl Islam ◽  
Mohammad S. Mubarak ◽  
Divya Jain ◽  
Rasel Khan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Cancer Cells ◽  
Chemotherapeutic Agents ◽  
Polyphenolic Compounds ◽  
Anticancer Effect ◽  
Anticancer Activities ◽  
Normal Cells ◽  
Anti Cancer ◽  
Global Threat

Background: Cancer is a global threat to humans and a leading cause of death worldwide. Cancer treatment includes, among other things, the use of chemotherapeutic agents, compounds that are vital for treating and preventing cancer. However, chemotherapeutic agents produce oxidative stress along with other side effects that would affect the human body. Objective: To reduce the oxidative stress of chemotherapeutic agents in cancer and normal cells by naturally derived compounds with anti-cancer properties, and protect normal cells from the oxidation process. Therefore, the need to develop more potent chemotherapeutics with fewer side effects has become increasingly important. Method: Recent literature dealing with the antioxidant and anticancer activities of the naturally naturally-derived compounds: morin, myricetin, malvidin, naringin, eriodictyol, isovitexin, daidzein, naringenin, chrysin, and fisetin has been surveyed and examined in this review. For this, data were gathered from different search engines, including Google Scholar, ScienceDirect, PubMed, Scopus, Web of Science, Scopus, and Scifinder, among others. Additionally, several patient offices such as WIPO, CIPO, and USPTO were consulted to obtain published articles related to these compounds. Result: Numerous plants contain flavonoids and polyphenolic compounds such as morin, myricetin, malvidin, naringin, eriodictyol, isovitexin, daidzein, naringenin, chrysin, and fisetin, which exhibit ‎antioxidant, anti-inflammatory, and anti-carcinogenic actions via several mechanisms. These compounds show sensitizers of cancer cells and protectors of healthy cells. Moreover, these compounds can reduce oxidative stress, which is accelerated by chemotherapeutics and exhibit a potent anticancer effect on cancer cells. Conclusions: Based on these findings, more research is recommended to explore and evaluate such flavonoids and polyphenolic compounds.

scholarly journals C-Glycosylated cinnamoylfuran derivatives as novel anti-cancer agents

RSC Advances ◽  
2017 ◽  
Vol 7 (46) ◽  
pp. 28853-28864 ◽  
Author(s):  
Ananya Dutta ◽  
Debashis Dhara ◽  
Pravat Kumar Parida ◽  
Anshupriya Si ◽  
Ravichandran Yesuvadian ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cytotoxic Effects ◽  
Normal Cells ◽  
Anti Cancer ◽  
Mcf 7

Synthesis of C-glycosylated cinnamoylfuran derivatives and their cytotoxic effects on cancer cells (MCF-7 and HeLa) and normal cells is presented.

scholarly journals Increased Oxidative Stress Induced by Rubus Bioactive Compounds Induce Apoptotic Cell Death in Human Breast Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Blassan P. George ◽  
Heidi Abrahamse
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cell Death ◽  
Cytochrome C ◽  
Cancer Cells ◽  
Bioactive Compounds ◽  
Breast Cancer Cells ◽  
Apoptotic Cell ◽  
Ros Production ◽  
Caspase 9

Bioactive compounds from plants represent good candidate drugs for the prevention and treatment of various forms of cancer. Berries are rich sources of bioactive compounds, and there has been an increasing interest in the study of therapeutic action of wild berries. Oxidants are generated continuously in biological system as a result of physiological process. When there is an imbalance between oxidants and antioxidants, it leads to a condition called oxidative stress. Natural compounds as inducers of oxidative stress are able to modulate the physiological functions of cancer cells leading to cell death or survival. The aim of this study was to evaluate the induction of apoptosis by isolated bioactive compounds (1-(2-hydroxyphenyl)-4-methylpentan-1-one (C1) and 2-[(3-methylbutoxy) carbonyl] benzoic acid (C2)) from Rubus fairholmianus against MCF-7 breast cancer cells. The exposure of C1 and C2 reduced viability (IC50 of C1: 4.69; C2: 8.36 μg/mL) and proliferation. Cytochrome c release from mitochondria and changes in mitochondrial membrane potential of treated cells supported the intrinsic apoptotic cell death. Reactive oxygen species (ROS) production after treatment with C1 and C2 was found to be higher and induced nuclear damage. Expression of apoptotic proteins after the treatments was significantly upregulated as indicated using immunofluorescence (caspase 9, p53, and Bax), western blotting (p53, cleaved PARP, cytochrome c, and Bax), and ELISA (caspase 9) analysis. Overall, C1 was more cytotoxic, increased the ROS production in dichlorodihydrofluorescein diacetate assay, and induced apoptosis in breast cancer cells. These results illustrate that berry bioactive compounds have strong chemopreventive potential. In this article, we provide information on prooxidant and anticancer activities of Rubus bioactive compounds. Natural products have always demonstrated a significant contribution to the development of several cancer chemotherapeutic drugs. Most of these compounds are known to affect the redox state of the cell; and studies on these compounds have focused on their antioxidant property instead of prooxidant properties.

scholarly journals Increased levels of superoxide and H2O2 mediate the differential susceptibility of cancer cells versus normal cells to glucose deprivation

2009 ◽  
Vol 418 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Nùkhet Aykin-Burns ◽  
Iman M. Ahmad ◽  
Yueming Zhu ◽  
Larry W. Oberley ◽  
Douglas R. Spitz
Keyword(s):  
Oxidative Stress ◽  
Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Human Cancer ◽  
Differential Susceptibility ◽  
Glucose Deprivation ◽  
Human Colon ◽  
Normal Cells ◽  
Ht29 Cells ◽  
And Oxidative Stress

Cancer cells, relative to normal cells, demonstrate increased sensitivity to glucose-deprivation-induced cytotoxicity. To determine whether oxidative stress mediated by O2•− and hydroperoxides contributed to the differential susceptibility of human epithelial cancer cells to glucose deprivation, the oxidation of DHE (dihydroethidine; for O2•−) and CDCFH2 [5- (and 6-)carboxy-2′,7′-dichlorodihydrofluorescein diacetate; for hydroperoxides] was measured in human colon and breast cancer cells (HT29, HCT116, SW480 and MB231) and compared with that in normal human cells [FHC cells, 33Co cells and HMECs (human mammary epithelial cells)]. Cancer cells showed significant increases in DHE (2–20-fold) and CDCFH2 (1.8–10-fold) oxidation, relative to normal cells, that were more pronounced in the presence of the mitochondrial electron-transport-chain blocker, antimycin A. Furthermore, HCT116 and MB231 cells were more susceptible to glucose-deprivation-induced cytotoxicity and oxidative stress, relative to 33Co cells and HMECs. HT29 cells were also more susceptible to 2DG (2-deoxyglucose)-induced cytotoxicity, relative to FHC cells. Overexpression of manganese SOD (superoxide dismutase) and mitochondrially targeted catalase significantly protected HCT116 and MB231 cells from glucose-deprivation-induced cytotoxicity and oxidative stress and also protected HT29 cells from 2DG-induced cytotoxicity. These results show that cancer cells (relative to normal cells) demonstrate increased steady-state levels of ROS (reactive oxygen species; i.e. O2•− and H2O2) that contribute to differential susceptibility to glucose-deprivation-induced cytotoxicity and oxidative stress. These studies support the hypotheses that cancer cells increase glucose metabolism to compensate for excess metabolic production of ROS and that inhibition of glucose and hydroperoxide metabolism may provide a biochemical target for selectively enhancing cytotoxicity and oxidative stress in human cancer cells.

Hydroxytyrosol induces apoptosis in human colon cancer cells through ROS generation

2014 ◽  
Vol 5 (8) ◽  
pp. 1909-1914 ◽  
Author(s):  
Lijuan Sun ◽  
Cheng Luo ◽  
Jiankang Liu
Keyword(s):  
Oxidative Stress ◽  
Colon Cancer ◽  
Cancer Cells ◽  
Human Colon ◽  
Ros Generation ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Normal Cells ◽  
Human Colon Cancer Cells

Cancer cells are usually under higher levels of oxidative stress compared to normal cells.

scholarly journals Oxidative Stress Plays an Important Role in Zoledronic Acid-Induced Autophagy

2014 ◽  
pp. S601-S612 ◽  
Author(s):  
V. K. M. KHANDELWAL ◽  
L. M. MITROFAN ◽  
J. M. T. HYTTINEN ◽  
K. R. CHAUDHARI ◽  
R. BUCCIONE ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zoledronic Acid ◽  
Cancer Cells ◽  
Mevalonate Pathway ◽  
Continuous Treatment ◽  
Autophagy Induction ◽  
Anti Cancer ◽  
Dose Dependent ◽  
And Oxidative Stress ◽  
Mcf 7

Several pre-clinical and clinical studies have demonstrated zoledronic acid (Zol), which regulates the mevalonate pathway, has efficient anti-cancer effects. Zol can also induce autophagy. The aim of this study is to add new understanding to the mechanism of autophagy induction by Zol. LC3B-II, the marker for autophagy was increased by Zol treatment in breast cancer cells. Autophagosomes induced by Zol were visualized and quantified in both transient (pDendra2-hLC3) and stable MCF-7-GFP-LC3 cell lines. Acidic vesicular organelles were quantified using acridine orange. Zol induced a dose and time dependent autophagy. Treatment of Zol increased oxidative stress in MCF-7 cells, which was reversed by GGOH or anti-oxidants. On the other hand, treatment with GGOH or anti-oxidants resulted in decreased levels of LC3B-II. Further, the induced autophagy was irreversible, as the washout of Zol after 2 h or 24 h resulted in similar levels of autophagy, as induced by continuous treatment after 72 h. Thus, it can be summarized that Zol can induce a dose dependent but irreversible autophagy, by its effect on the mevalonate pathway and oxidative stress. This study adds to the understanding of the mechanism of action of Zol, and that it can induce autophagy at clinically relevant shorter exposure times in cancer cells.

scholarly journals A Triple Co-Delivery Liposomal Carrier That Enhances Apoptosis via an Intrinsic Pathway in Melanoma Cells

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1982 ◽  
Author(s):  
Nina Filipczak ◽  
Anna Jaromin ◽  
Adriana Piwoni ◽  
Mohamed Mahmud ◽  
Can Sarisozen ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Melanoma Cells ◽  
Mitochondrial Pathway ◽  
Cytotoxic Action ◽  
Cancer Therapies ◽  
Normal Cells ◽  
Freeze And Thaw ◽  
Anti Cancer ◽  
Remote Loading ◽  
Activity Mechanism

The effectiveness of existing anti-cancer therapies is based mainly on the stimulation of apoptosis of cancer cells. Most of the existing therapies are somewhat toxic to normal cells. Therefore, the quest for nontoxic, cancer-specific therapies remains. We have demonstrated the ability of liposomes containing anacardic acid, mitoxantrone and ammonium ascorbate to induce the mitochondrial pathway of apoptosis via reactive oxygen species (ROS) production by the killing of cancer cells in monolayer culture and shown its specificity towards melanoma cells. Liposomes were prepared by a lipid hydration, freeze-and-thaw (FAT) procedure and extrusion through polycarbonate filters, a remote loading method was used for dug encapsulation. Following characterization, hemolytic activity, cytotoxicity and apoptosis inducing effects of loaded nanoparticles were investigated. To identify the anticancer activity mechanism of these liposomes, ROS level and caspase 9 activity were measured by fluorescence and by chemiluminescence respectively. We have demonstrated that the developed liposomal formulations produced a high ROS level, enhanced apoptosis and cell death in melanoma cells, but not in normal cells. The proposed mechanism of the cytotoxic action of these liposomes involved specific generation of free radicals by the iron ions mechanism.

scholarly journals Antioxidant Defenses: A Context-Specific Vulnerability of Cancer Cells

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1208 ◽  
Author(s):  
Jordan A. Cockfield ◽  
Zachary T. Schafer
Keyword(s):  
Dna Damage ◽  
Antioxidant Activity ◽  
Cancer Cells ◽  
Antioxidant Defenses ◽  
Oxygen Species ◽  
Normal Cells ◽  
Anti Cancer ◽  
Selective Elimination ◽  
Specific Vulnerability ◽  
Context Specific

Reactive oxygen species (ROS) are well known for their capacity to cause DNA damage, augment mutagenesis, and thereby promote oncogenic transformation. Similarly, agents that reduce ROS levels (antioxidants) are frequently thought to have anti-cancer properties given their propensity to minimize DNA damage and mutagenesis. However, numerous clinical studies focused on antioxidants suggest that this is a facile premise and that antioxidant capacity can be important for cancer cells in a similar fashion to normal cells. As a consequence of this realization, numerous laboratories have been motivated to investigate the biological underpinnings explaining how and when antioxidant activity can potentially be beneficial to cancer cells. Relatedly, it has become clear that the reliance of cancer cells on antioxidant activity in certain contexts represents a potential vulnerability that could be exploited for therapeutic gain. Here, we review some of the recent, exciting findings documenting how cancer cells utilized antioxidant activity and under what circumstances this activity could represent an opportunity for selective elimination of cancer cells.

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