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Article: Hydrogen Peroxide Mediates Artemisinin-Derived C-16 Carba-Dimer-Induced Toxicity of Human Cancer Cells.

Kalen, Amanda L / Wagner, Brett A / Sarsour, Ehab H / Kumar, Maneesh G / Reedy, Jessica L / Buettner, Garry R / Barua, Nabin C / Goswami, Prabhat C

Antioxidants (Basel, Switzerland)

2020 Volume 9, Issue 2

Abstract: This study used a nitroaliphatic chemistry approach to synthesize a novel artemisinin-derived carba-dimer (AG-1) and determined its anti-proliferative effects in human normal and cancer cells. AG-1 treatments selectively inhibit proliferation of cancer ... ...

Abstract	This study used a nitroaliphatic chemistry approach to synthesize a novel artemisinin-derived carba-dimer (AG-1) and determined its anti-proliferative effects in human normal and cancer cells. AG-1 treatments selectively inhibit proliferation of cancer cells compared to normal human fibroblasts. Compared to artemisinin, AG-1 is more toxic to human breast, prostate, head-neck, pancreas and skin cancer cells; 50% inhibition (IC
Language	English
Publishing date	2020-01-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox9020108
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Article ; Online: N-alkyl triphenylvinylpyridinium conjugated dihydroartemisinin perturbs mitochondrial functions resulting in enhanced cancer versus normal cell toxicity.

Varmazyad, Mahboubeh / Modi, Mira M / Kalen, Amanda L / Sarsour, Ehab H / Wagner, Brett / Du, Juan / Schultz, Michael K / Buettner, Garry R / Pigge, F Christopher / Goswami, Prabhat C

Free radical biology & medicine

2021 Volume 165, Page(s) 421–434

Abstract: Dihydroartemisinin (DHA) is an FDA-approved antimalarial drug that has been repurposed for cancer therapy because of its preferential antiproliferative effects on cancer versus normal cells. Mitochondria represent an attractive target for cancer therapy ... ...

Abstract	Dihydroartemisinin (DHA) is an FDA-approved antimalarial drug that has been repurposed for cancer therapy because of its preferential antiproliferative effects on cancer versus normal cells. Mitochondria represent an attractive target for cancer therapy based on their regulatory role in proliferation and cell death. This study investigates whether DHA conjugated to innately fluorescent N-alkyl triphenylvinylpyridinium (TPVP) perturbs mitochondrial functions resulting in a differential toxicity of cancer versus normal cells. TPVP-DHA treatments resulted in a dose-dependent toxicity of human melanoma and pancreatic cancer cells, whereas normal human fibroblasts were resistant to this treatment. TPVP-DHA treatments resulted in a G
MeSH term(s)	Antimalarials/toxicity ; Apoptosis ; Artemisinins/pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Mitochondria ; Neoplasms
Chemical Substances	Antimalarials ; Artemisinins ; artenimol (6A9O50735X)
Language	English
Publishing date	2021-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2021.01.050
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Article ; Online: Methylseleninic Acid Induces Lipid Peroxidation and Radiation Sensitivity in Head and Neck Cancer Cells.

Lafin, John T / Sarsour, Ehab H / Kalen, Amanda L / Wagner, Brett A / Buettner, Garry R / Goswami, Prabhat C

International journal of molecular sciences

2019 Volume 20, Issue 1

Abstract: Combination radiation and chemotherapy are commonly used to treat locoregionally advanced head and neck squamous cell carcinoma (HNSCC). Aggressive dosing of these therapies is significantly hampered by side effects due to normal tissue toxicity. ... ...

Abstract	Combination radiation and chemotherapy are commonly used to treat locoregionally advanced head and neck squamous cell carcinoma (HNSCC). Aggressive dosing of these therapies is significantly hampered by side effects due to normal tissue toxicity. Selenium represents an adjuvant that selectively sensitizes cancer cells to these treatments modalities, potentially by inducing lipid peroxidation (LPO). This study investigated whether one such selenium compound, methylseleninic acid (MSA), induces LPO and radiation sensitivity in HNSCC cells. Results from 4,4-difluoro-4-bora-3a,4a-diaza-
MeSH term(s)	Acetylcysteine/pharmacology ; Apoptosis/drug effects ; Apoptosis/radiation effects ; Cell Line, Tumor ; Gamma Rays ; Glutathione/metabolism ; Head and Neck Neoplasms/metabolism ; Head and Neck Neoplasms/pathology ; Humans ; Lipid Peroxidation/drug effects ; Lipid Peroxidation/radiation effects ; Organoselenium Compounds/pharmacology ; Oxygen Consumption/drug effects ; Radiation Tolerance/drug effects ; Radiation Tolerance/radiation effects ; Time Factors
Chemical Substances	Organoselenium Compounds ; methylselenic acid (9900C6V162) ; Glutathione (GAN16C9B8O) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2019-01-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20010225
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Article ; Online: Manganese superoxide dismutase regulates a redox cycle within the cell cycle.

Sarsour, Ehab H / Kalen, Amanda L / Goswami, Prabhat C

Antioxidants & redox signaling

2013 Volume 20, Issue 10, Page(s) 1618–1627

Abstract: Significance: Manganese superoxide dismutase (MnSOD) is a nuclear-encoded and mitochondria-matrix-localized oxidation-reduction (redox) enzyme that regulates cellular redox homeostasis. Cellular redox processes are known to regulate proliferative and ... ...

Abstract	Significance: Manganese superoxide dismutase (MnSOD) is a nuclear-encoded and mitochondria-matrix-localized oxidation-reduction (redox) enzyme that regulates cellular redox homeostasis. Cellular redox processes are known to regulate proliferative and quiescent growth states. Therefore, MnSOD and mitochondria-generated reactive oxygen species (ROS) are believed to be critical regulators of quiescent cells' entry into the cell cycle and exit from the proliferative cycle back to the quiescent state. Recent advances/critical issues: Recent evidence suggests that the intracellular redox environment fluctuates during the cell cycle, shifting toward a more oxidized status during mitosis. MnSOD activity is higher in G0/G1 cells compared with S, G2 and M phases. After cell division, MnSOD activity increases in the G1 phase of the daughter generation. The periodic fluctuation in MnSOD activity during the cell cycle inversely correlates with cellular superoxide levels as well as glucose and oxygen consumption. Based on an inverse correlation between MnSOD activity and glucose consumption during the cell cycle, it is proposed that MnSOD is a central molecular player for the "Warburg effect." Future directions: In general, loss of MnSOD activity results in aberrant proliferation. A better understanding of the MnSOD and mitochondrial ROS-dependent cell cycle processes may lead to novel approaches to overcome aberrant proliferation. Since ROS have both deleterious (pathological) and beneficial (physiological) effects, it is proposed that "eustress" should be used when discussing ROS processes that regulate normal physiological functions, while "oxidative stress" should be used to discuss the deleterious effects of ROS.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Energy Metabolism ; Humans ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/physiology
Chemical Substances	Antioxidants ; Cell Cycle Proteins ; Reactive Oxygen Species ; Superoxide Dismutase (EC 1.15.1.1) ; superoxide dismutase 2 (EC 1.15.1.1)
Language	English
Publishing date	2013-05-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2013.5303
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Article ; Online: Methylseleninic Acid Induces Lipid Peroxidation and Radiation Sensitivity in Head and Neck Cancer Cells

John T. Lafin / Ehab H. Sarsour / Amanda L. Kalen / Brett A. Wagner / Garry R. Buettner / Prabhat C. Goswami

International Journal of Molecular Sciences, Vol 20, Iss 1, p

2019 Volume 225

Abstract	Combination radiation and chemotherapy are commonly used to treat locoregionally advanced head and neck squamous cell carcinoma (HNSCC). Aggressive dosing of these therapies is significantly hampered by side effects due to normal tissue toxicity. Selenium represents an adjuvant that selectively sensitizes cancer cells to these treatments modalities, potentially by inducing lipid peroxidation (LPO). This study investigated whether one such selenium compound, methylseleninic acid (MSA), induces LPO and radiation sensitivity in HNSCC cells. Results from 4,4-difluoro-4-bora-3a,4a-diaza-S-indacene (BODIPY) C11 oxidation and ferric thiocyanate assays revealed that MSA induced LPO in cells rapidly and persistently. Propidium iodide (PI) exclusion assay found that MSA was more toxic to cancer cells than other related selenium compounds; this toxicity was abrogated by treatment with α-tocopherol, an LPO inhibitor. MSA exhibited no toxicity to normal fibroblasts at similar doses. MSA also sensitized HNSCC cells to radiation as determined by clonogenic assay. Intracellular glutathione in cancer cells was depleted following MSA treatment, and supplementation of the intracellular glutathione pool with N-acetylcysteine sensitized cells to MSA. The addition of MSA to a cell-free solution of glutathione resulted in an increase in oxygen consumption, which was abrogated by catalase, suggesting the formation of H2O2. Results from this study identify MSA as an inducer of LPO, and reveal its capability to sensitize HNSCC to radiation. MSA may represent a potent adjuvant to radiation therapy in HNSCC.
Keywords	head and neck cancer ; selenium ; methylseleninic acid ; radiation ; lipid peroxidation ; glutathione ; tocopherol ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2019-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Arachidonate 12-lipoxygenase and 12-hydroxyeicosatetraenoic acid contribute to stromal aging-induced progression of pancreatic cancer.

Sarsour, Ehab H / Son, Jyung Mean / Kalen, Amanda L / Xiao, Wusheng / Du, Juan / Alexander, Matthew S / O'Leary, Brianne R / Cullen, Joseph J / Goswami, Prabhat C

The Journal of biological chemistry

2020 Volume 295, Issue 20, Page(s) 6946–6957

Abstract: The incidence of pancreatic cancer increases with age, suggesting that chronological aging is a significant risk factor for this disease. Fibroblasts are the major nonmalignant cell type in the stroma of human pancreatic ductal adenocarcinoma (PDAC). In ... ...

Abstract	The incidence of pancreatic cancer increases with age, suggesting that chronological aging is a significant risk factor for this disease. Fibroblasts are the major nonmalignant cell type in the stroma of human pancreatic ductal adenocarcinoma (PDAC). In this study, we investigated whether the chronological aging of normal human fibroblasts (NHFs), a previously underappreciated area in pancreatic cancer research, influences the progression and therapeutic outcomes of PDAC. Results from experiments with murine xenografts and 2D and 3D co-cultures of NHFs and PDAC cells revealed that older NHFs stimulate proliferation of and confer resistance to radiation therapy of PDAC. MS-based metabolite analysis indicated that older NHFs have significantly increased arachidonic acid 12-lipoxygenase (ALOX12) expression and elevated levels of its mitogenic metabolite, 12-(
MeSH term(s)	Animals ; Arachidonate 12-Lipoxygenase/genetics ; Arachidonate 12-Lipoxygenase/metabolism ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Cell Line, Tumor ; Cellular Senescence ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Humans ; Hydroxyeicosatetraenoic Acids/metabolism ; Mice ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Stromal Cells/metabolism ; Stromal Cells/pathology
Chemical Substances	Hydroxyeicosatetraenoic Acids ; Neoplasm Proteins ; Arachidonate 12-Lipoxygenase (EC 1.13.11.31) ; ALOX12 protein, human (EC 1.13.11.31.)
Language	English
Publishing date	2020-04-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA120.012798
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Article: Hydrogen Peroxide Mediates Artemisinin-Derived C-16 Carba-Dimer-Induced Toxicity of Human Cancer Cells

Kalen, Amanda L / Wagner, Brett A / Sarsour, Ehab H / Kumar, Maneesh G / Reedy, Jessica L / Buettner, Garry R / Barua, Nabin C / Goswami, Prabhat C

Antioxidants. 2020 Jan. 26, v. 9, no. 2

2020

Abstract: ... at 72 h post-treatment, as measured by micronuclei frequency and γH2AX protein levels. Results ...

Abstract	This study used a nitroaliphatic chemistry approach to synthesize a novel artemisinin-derived carba-dimer (AG-1) and determined its anti-proliferative effects in human normal and cancer cells. AG-1 treatments selectively inhibit proliferation of cancer cells compared to normal human fibroblasts. Compared to artemisinin, AG-1 is more toxic to human breast, prostate, head–neck, pancreas and skin cancer cells; 50% inhibition (IC₅₀) 123 µM in AG-1 vs. 290 µM in artemisinin-treated breast cancer cells. AG-1 treatment decreased (~5 folds) cyclin D1 protein expression that correlated with an increase in the percentage of cells in the G₁-phase, suggesting a G₁ delay. AG-1-induced toxicity was independent of the DNA damage at 72 h post-treatment, as measured by micronuclei frequency and γH2AX protein levels. Results from electron paramagnetic resonance spectroscopy showed Fe-catalyzed formation of AG-1 carbon-centered radicals in a cell-free system. Flow cytometry analysis of H₂DCF-DA oxidation showed a significant increase in the steady-state levels of reactive oxygen species (ROS) in AG-1-treated cells. Pre-treatment with N-acetyl-l-cysteine and antioxidant enzymes (superoxide dismutase and catalase) significantly suppressed AG-1-induced toxicity, suggesting that superoxide and hydrogen peroxide contribute to AG-1-induced toxicity in human cancer cells. AG-1 represents a novel class of anti-cancer drug that is more potent than its parent compound, artemisinin.
Keywords	D1 protein ; DNA damage ; acetylcysteine ; antineoplastic agents ; antioxidant enzymes ; artemisinin ; breast neoplasms ; catalase ; catalytic activity ; cell free system ; cell proliferation ; cyclins ; electron paramagnetic resonance spectroscopy ; fibroblasts ; flow cytometry ; free radicals ; head and neck neoplasms ; human cell lines ; human diseases ; humans ; hydrogen peroxide ; inhibitory concentration 50 ; interphase ; iron ; neoplasm cells ; oxidation ; pancreatic neoplasms ; prostatic neoplasms ; protein content ; protein synthesis ; skin neoplasms ; superoxide dismutase ; toxicity
Language	English
Dates of publication	2020-0126
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox9020108
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Hydrogen Peroxide Mediates Artemisinin-Derived C-16 Carba-Dimer-Induced Toxicity of Human Cancer Cells

Amanda L. Kalen / Brett A. Wagner / Ehab H. Sarsour / Maneesh G. Kumar / Jessica L. Reedy / Garry R. Buettner / Nabin C. Barua / Prabhat C. Goswami

Antioxidants, Vol 9, Iss 2, p

2020 Volume 108

Abstract: ... at 72 h post-treatment, as measured by micronuclei frequency and γH2AX protein levels. Results ... in a cell-free system. Flow cytometry analysis of H 2 DCF-DA oxidation showed a significant increase in the steady-state ...

Abstract	This study used a nitroaliphatic chemistry approach to synthesize a novel artemisinin-derived carba-dimer (AG-1) and determined its anti-proliferative effects in human normal and cancer cells. AG-1 treatments selectively inhibit proliferation of cancer cells compared to normal human fibroblasts. Compared to artemisinin, AG-1 is more toxic to human breast, prostate, head−neck, pancreas and skin cancer cells; 50% inhibition (IC 50 ) 123 µM in AG-1 vs. 290 µM in artemisinin-treated breast cancer cells. AG-1 treatment decreased (~5 folds) cyclin D1 protein expression that correlated with an increase in the percentage of cells in the G 1 -phase, suggesting a G 1 delay. AG-1-induced toxicity was independent of the DNA damage at 72 h post-treatment, as measured by micronuclei frequency and γH2AX protein levels. Results from electron paramagnetic resonance spectroscopy showed Fe-catalyzed formation of AG-1 carbon-centered radicals in a cell-free system. Flow cytometry analysis of H 2 DCF-DA oxidation showed a significant increase in the steady-state levels of reactive oxygen species (ROS) in AG-1-treated cells. Pre-treatment with N -acetyl- l -cysteine and antioxidant enzymes (superoxide dismutase and catalase) significantly suppressed AG-1-induced toxicity, suggesting that superoxide and hydrogen peroxide contribute to AG-1-induced toxicity in human cancer cells. AG-1 represents a novel class of anti-cancer drug that is more potent than its parent compound, artemisinin.
Keywords	artemisinin ; carba-dimer ; aliphatic nitro chemistry ; oxidative stress ; cyclin d1 ; Therapeutics. Pharmacology ; RM1-950
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: MnSOD and Cyclin B1 Coordinate a Mito-Checkpoint during Cell Cycle Response to Oxidative Stress.

Kalen, Amanda L / Ahmad, Iman M / Abdalla, Maher Y / O'Malley, Yunxia Q / Goswami, Prabhat C / Sarsour, Ehab H

Antioxidants (Basel, Switzerland)

2017 Volume 6, Issue 4

Abstract: Communication between the nucleus and mitochondrion could coordinate many cellular processes. While the mechanisms regulating this communication are not completely understood, we hypothesize that cell cycle checkpoint proteins coordinate the cross-talk ... ...

Abstract	Communication between the nucleus and mitochondrion could coordinate many cellular processes. While the mechanisms regulating this communication are not completely understood, we hypothesize that cell cycle checkpoint proteins coordinate the cross-talk between nuclear and mitochondrial functions following oxidative stress. Human normal skin fibroblasts, representative of the G₂-phase, were irradiated with 6 Gy of ionizing radiation and assayed for cyclin B1 translocation, mitochondrial function, reactive oxygen species (ROS) levels, and cytotoxicity. In un-irradiated controls, cyclin B1 was found primarily in the nucleus of G₂-cells. However, following irradiation, cyclin B1 was excluded from the nucleus and translocated to the cytoplasm and mitochondria. These observations were confirmed further by performing transmission electron microscopy and cell fractionation assays. Cyclin B1 was absent in mitochondria isolated from un-irradiated G₂-cells and present in irradiated G₂-cells. Radiation-induced translocation of cyclin B1 from the nucleus to the mitochondrion preceded changes in the activities of mitochondrial proteins, that included decreases in the activities of aconitase and the mitochondrial antioxidant enzyme, manganese superoxide dismutase (MnSOD), and increases in complex II activity. Changes in the activities of mito-proteins were followed by an increase in dihydroethidium (DHE) oxidation (indicative of increased superoxide levels) and loss of the mitochondrial membrane potential, events that preceded the restart of the stalled cell cycle and subsequently the loss in cell viability. Comparable results were also observed in un-irradiated control cells overexpressing mitochondria-targeted cyclin B1. These results indicate that MnSOD and cyclin B1 coordinate a cross-talk between nuclear and mitochondrial functions, to regulate a mito-checkpoint during the cell cycle response to oxidative stress.
Language	English
Publishing date	2017-11-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox6040092
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Article ; Online: N-acetyl-L-cysteine increases MnSOD activity and enhances the recruitment of quiescent human fibroblasts to the proliferation cycle during wound healing.

Mao, Gaowei / Goswami, Monali / Kalen, Amanda L / Goswami, Prabhat C / Sarsour, Ehab H

Molecular biology reports

2015 Volume 43, Issue 1, Page(s) 31–39

Abstract: The rebuilding of the connective tissue during wound healing requires the recruitment of fibroblasts to the wound area as well as reentry of quiescent fibroblasts to the proliferative cycle. Whether this process can be modulated by a small molecular ... ...

Abstract	The rebuilding of the connective tissue during wound healing requires the recruitment of fibroblasts to the wound area as well as reentry of quiescent fibroblasts to the proliferative cycle. Whether this process can be modulated by a small molecular weight thiol antioxidant N-acetyl-L-cysteine (NAC) was tested in normal human skin fibroblasts (NHFs) using a uni-directional wound healing assay. NAC treated cells demonstrated a decreased migration rate but increased number of proliferating cells recruited into the wound area post wounding. Fifteen day quiescent control and NAC treated NHFs were re-plated at a lower density and cell numbers counted at different days post-plating. Interestingly, NAC treated cells exhibited increased cellular proliferation indicated by both decreased cell population doubling time and increased S phase cells. NAC treated cells demonstrated decreased steady state levels of reactive oxygen species as well as increased protein and activity levels of manganese superoxide dismutase (MnSOD). NAC treatment failed to induce proliferation in quiescent cells lacking MnSOD expression. These results demonstrate that NAC enhanced the recruitment of quiescent NHFs into proliferation cycle during wound healing. Our results also suggest that the wound healing properties of NAC might be due to its ability to induce and enhance MnSOD expression and activity. Altogether, these findings suggest NAC might be potentially developed as a dietary intervention to improve tissue injury in animals and humans.
MeSH term(s)	Acetylcysteine/pharmacology ; Animals ; Antioxidants/pharmacology ; Cell Cycle/drug effects ; Cell Proliferation/drug effects ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; Mice ; Mice, Knockout ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/metabolism ; Wound Healing/drug effects
Chemical Substances	Antioxidants ; Reactive Oxygen Species ; Superoxide Dismutase (EC 1.15.1.1) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	2015-12-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-015-3935-1
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