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Article: Exploring the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity: a literature review.

Cameron, Keyuna S / Buchner, Virginia / Tchounwou, Paul B

2011 Volume 26, Issue 2, Page(s) 81–92

Abstract: Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical ... ...

Abstract	Nickel, a naturally occurring element that exists in various mineral forms, is mainly found in soil and sediment, and its mobilization is influenced by the physicochemical properties of the soil. Industrial sources of nickel include metallurgical processes such as electroplating, alloy production, stainless steel, and nickel-cadmium batteries. Nickel industries, oil- and coal-burning power plants, and trash incinerators have been implicated in its release into the environment. In humans, nickel toxicity is influenced by the route of exposure, dose, and solubility of the nickel compound. Lung inhalation is the major route of exposure for nickel-induced toxicity. Nickel can also be ingested or absorbed through the skin. The primary target organs are the kidneys and lungs. Other organs such as the liver, spleen, heart, and testes can also be affected to a lesser extent. Although the most common health effect is an allergic reaction, research has also demonstrated that nickel is carcinogenic to humans. The focus of the present review is on recent research concerning the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity. We first present a background on the occurrence of nickel in the environment, human exposure, and human health effects.
MeSH term(s)	Animals ; Carcinogens, Environmental/metabolism ; Carcinogens, Environmental/pharmacokinetics ; Carcinogens, Environmental/toxicity ; Chromosome Aberrations ; DNA Damage/drug effects ; Environmental Exposure ; Epigenesis, Genetic ; Gene Expression Regulation ; Humans ; Nickel/metabolism ; Nickel/pharmacokinetics ; Nickel/toxicity
Chemical Substances	Carcinogens, Environmental ; Nickel (7OV03QG267)
Language	English
Publishing date	2011-08-28
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	184450-7
ISSN	2191-0308 ; 0048-7554 ; 0048-7562
ISSN (online)	2191-0308
ISSN	0048-7554 ; 0048-7562
DOI	10.1515/reveh.2011.012
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Sensitivity and mechanisms of taxol-resistant prostate adenocarcinoma cells to Vernonia amygdalina extract.

Cameron, Keyuna S / Howard, Carolyn B / Izevbigie, Ernest B / Hill, Brandon J / Tchounwou, Paul B

Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie

2012 Volume 65, Issue 6, Page(s) 759–765

Abstract: Prostate cancer (PC) patients once Paclitaxel (TAX) treatment responsive later develop hormone refractory PC, thus becoming TAX-insensitive. This underscores the urgent need to develop novel anti-PC therapies. Vernonia amygdalina (VA) could be one such ... ...

Abstract	Prostate cancer (PC) patients once Paclitaxel (TAX) treatment responsive later develop hormone refractory PC, thus becoming TAX-insensitive. This underscores the urgent need to develop novel anti-PC therapies. Vernonia amygdalina (VA) could be one such candidate agent. We have shown that androgen-independent PC-3 cells are sensitive to VA treatment in vitro. VA extract (0.01, 0.1 and 1 mg/ml) inhibited DNA synthesis by 12%, 45% (p<0.05), and 73% (p<0.01) respectively. In contrast, TAX (0.01, 0.1, and 1 μM) failed to significantly affect cell growth, suggesting TAX resistance. We tested molecular mechanisms which may lend to the observed PC-3 cell VA sensitivity/TAX resistance. Though both VA and TAX stimulated MAPK activity, VA's induction was more intense, but transient, compared to TAX's sustained action. NF-κB activation was inhibited on average by 50% by either 1 mg/ml VA or 1 μM TAX. VA extract caused 35% and 45% increases in c-Myc activity at 10 and 60 min intervals respectively, with the highest stimulation attained 1h after treatment. In contrast, similar levels were attained by TAX rapidly (within 5 min) and were sustained compared to the slow/multi-phasic action of VA. VA extract treatments had no effect on AKT gene expression, while TAX treatments yielded a four-fold (P<0.01) increase; and P-glycoprotein (P-gp) activity was inhibited by VA and stimulated by TAX, compared to control (basal ATPase activity). This study shows that TAX-resistant PC-3 cells are sensitive to VA, perhaps explained by differential regulatory patterns of MAPK, c-Myc, AKT, and Pgp activities/expressions.
MeSH term(s)	Adenocarcinoma/drug therapy ; Adenocarcinoma/enzymology ; Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Antineoplastic Agents, Phytogenic/pharmacology ; Cell Culture Techniques ; Cell Line, Tumor ; Cell Proliferation/drug effects ; DNA, Neoplasm/biosynthesis ; Drug Resistance, Neoplasm/drug effects ; Humans ; Male ; Paclitaxel/pharmacology ; Plant Extracts/pharmacology ; Plant Leaves/chemistry ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/enzymology ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Vernonia/chemistry
Chemical Substances	Antineoplastic Agents, Phytogenic ; DNA, Neoplasm ; Plant Extracts ; Paclitaxel (P88XT4IS4D)
Language	English
Publishing date	2012-12-11
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1107321-4
ISSN	1618-1433 ; 0940-2993
ISSN (online)	1618-1433
ISSN	0940-2993
DOI	10.1016/j.etp.2012.11.002
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Sensitivity and mechanisms of taxol-resistant prostate adenocarcinoma cells to Vernonia amygdalina extract

Cameron, Keyuna S / Howard, Carolyn B / Izevbigie, Ernest B / Hill, Brandon J / Tchounwou, Paul B

Experimental and toxicologic pathology. 2013 Sept., v. 65, no. 6

2013

Abstract	Prostate cancer (PC) patients once Paclitaxel (TAX) treatment responsive later develop hormone refractory PC, thus becoming TAX-insensitive. This underscores the urgent need to develop novel anti-PC therapies. Vernonia amygdalina (VA) could be one such candidate agent. We have shown that androgen-independent PC-3 cells are sensitive to VA treatment in vitro. VA extract (0.01, 0.1 and 1mg/ml) inhibited DNA synthesis by 12%, 45% (p<0.05), and 73% (p<0.01) respectively. In contrast, TAX (0.01, 0.1, and 1μM) failed to significantly affect cell growth, suggesting TAX resistance. We tested molecular mechanisms which may lend to the observed PC-3 cell VA sensitivity/TAX resistance. Though both VA and TAX stimulated MAPK activity, VA's induction was more intense, but transient, compared to TAX's sustained action. NF-κB activation was inhibited on average by 50% by either 1mg/ml VA or 1μM TAX. VA extract caused 35% and 45% increases in c-Myc activity at 10 and 60min intervals respectively, with the highest stimulation attained 1h after treatment. In contrast, similar levels were attained by TAX rapidly (within 5min) and were sustained compared to the slow/multi-phasic action of VA. VA extract treatments had no effect on AKT gene expression, while TAX treatments yielded a four-fold (P<0.01) increase; and P-glycoprotein (P-gp) activity was inhibited by VA and stimulated by TAX, compared to control (basal ATPase activity). This study shows that TAX-resistant PC-3 cells are sensitive to VA, perhaps explained by differential regulatory patterns of MAPK, c-Myc, AKT, and Pgp activities/expressions.
Keywords	DNA ; Vernonia amygdalina ; adenocarcinoma ; adenosinetriphosphatase ; cell growth ; gene expression ; mitogen-activated protein kinase ; paclitaxel ; patients ; prostatic neoplasms ; transcription factor NF-kappa B
Language	English
Dates of publication	2013-09
Size	p. 759-765.
Publishing place	Elsevier GmbH
Document type	Article
ZDB-ID	1107321-4
ISSN	1618-1433 ; 0940-2993
ISSN (online)	1618-1433
ISSN	0940-2993
DOI	10.1016/j.etp.2012.11.002
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Dipyridamole analogs as pharmacological inhibitors of equilibrative nucleoside transporters. Identification of novel potent and selective inhibitors of the adenosine transporter function of human equilibrative nucleoside transporter 4 (hENT4).

Wang, Chunmei / Lin, Wenwei / Playa, Hilaire / Sun, Shan / Cameron, Keyuna / Buolamwini, John K

Biochemical pharmacology

2013 Volume 86, Issue 11, Page(s) 1531–1540

Abstract: To identify needed human equilibrative nucleoside transporter 4 (hENT4) inhibitors, we cloned and stably expressed the recombinant protein in PK15NTD (nucleoside transporter deficient) cells, and, investigated its interaction with a series of ... ...

Abstract	To identify needed human equilibrative nucleoside transporter 4 (hENT4) inhibitors, we cloned and stably expressed the recombinant protein in PK15NTD (nucleoside transporter deficient) cells, and, investigated its interaction with a series of dipyridamole analogs synthesized in our laboratory. Compounds were tested in this newly established hENT4 expressing system as well in previous stably expressed hENT1 and hENT2 expressing systems. Of the dipyridamole analogs evaluated, about one fourth of the compounds inhibited hENT4 with higher potencies than dipyridamole. The most potent of them, Compound 30 displayed an IC₅₀ of 74.4 nM, making it about 38 times more potent than dipyridamole (IC₅₀=2.8 μM), and selectivities of about 80-fold and 20-fold relative to ENT1 and ENT2, respectively. Structure-activity relationship showed nitrogen-containing monocyclic rings and noncyclic substituents at the 4- and 8-positions of the pyrimido[5,4-d]pyrimidine were important for the inhibitory activity against hENT4. The most potent and selective hENT4 inhibitors tended to have a 2,6-di(N-monohydroxyethyl) substitution on the pyrimidopyrimidine ring system. The inhibitors of hENT4 identified in this study are the most selective and potent inhibitors of hENT4 adenosine transporter function to date, and should serve as useful pharmacological/biochemical tools and/or potential leads for ENT4-based therapeutics. Also, the new hENT4-expressing PK15 cell line established will serve as a useful screening tool for the discovery and design of hENT4 ligands.
MeSH term(s)	Animals ; Blotting, Western ; Cell Culture Techniques ; Cell Line ; Cell Survival/drug effects ; Dipyridamole/analogs & derivatives ; Dipyridamole/chemistry ; Dipyridamole/pharmacology ; Drug Design ; Equilibrative Nucleoside Transport Proteins/antagonists & inhibitors ; Equilibrative Nucleoside Transport Proteins/genetics ; Humans ; Ligands ; Molecular Structure ; Nucleoside Transport Proteins/antagonists & inhibitors ; Nucleoside Transport Proteins/genetics ; Structure-Activity Relationship ; Swine ; Transfection
Chemical Substances	Equilibrative Nucleoside Transport Proteins ; Ligands ; Nucleoside Transport Proteins ; SLC29A4 protein, human ; adenosine transporter ; Dipyridamole (64ALC7F90C)
Language	English
Publishing date	2013-09-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2013.08.063
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Sensitivity and mechanisms of taxol-resistant prostate adenocarcinoma cells to Vernonia amygdalina extract

Cameron, Keyuna S. / Howard, Carolyn B. / Izevbigie, Ernest B. / Hill, Brandon J. / Tchounwou, Paul B.

Experimental and toxicologic pathology

Volume v. 65,, Issue no. 6

Abstract	Prostate cancer (PC) patients once Paclitaxel (TAX) treatment responsive later develop hormone refractory PC, thus becoming TAX-insensitive. This underscores the urgent need to develop novel anti-PC therapies. Vernonia amygdalina (VA) could be one such candidate agent. We have shown that androgen-independent PC-3 cells are sensitive to VA treatment in vitro. VA extract (0.01, 0.1 and 1mg/ml) inhibited DNA synthesis by 12%, 45% (p<0.05), and 73% (p<0.01) respectively. In contrast, TAX (0.01, 0.1, and 1μM) failed to significantly affect cell growth, suggesting TAX resistance. We tested molecular mechanisms which may lend to the observed PC-3 cell VA sensitivity/TAX resistance. Though both VA and TAX stimulated MAPK activity, VA's induction was more intense, but transient, compared to TAX's sustained action. NF-κB activation was inhibited on average by 50% by either 1mg/ml VA or 1μM TAX. VA extract caused 35% and 45% increases in c-Myc activity at 10 and 60min intervals respectively, with the highest stimulation attained 1h after treatment. In contrast, similar levels were attained by TAX rapidly (within 5min) and were sustained compared to the slow/multi-phasic action of VA. VA extract treatments had no effect on AKT gene expression, while TAX treatments yielded a four-fold (P<0.01) increase; and P-glycoprotein (P-gp) activity was inhibited by VA and stimulated by TAX, compared to control (basal ATPase activity). This study shows that TAX-resistant PC-3 cells are sensitive to VA, perhaps explained by differential regulatory patterns of MAPK, c-Myc, AKT, and Pgp activities/expressions.
Keywords	patients ; paclitaxel ; transcription factor NF-kappa B ; adenocarcinoma ; DNA ; Vernonia amygdalina ; gene expression ; mitogen-activated protein kinase ; adenosinetriphosphatase ; cell growth ; prostatic neoplasms
Language	English
Document type	Article
ISSN	0940-2993
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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Article: Dipyridamole analogs as pharmacological inhibitors of equilibrative nucleoside transporters. Identification of novel potent and selective inhibitors of the adenosine transporter function of human equilibrative nucleoside transporter 4 (hENT4)

Wang, Chunmei / Lin, Wenwei / Playa, Hilaire / Sun, Shan / Cameron, Keyuna / Buolamwini, John K.

Biochemical Pharmacology

Volume v. 86,, Issue no. 1

Abstract	To identify needed human equilibrative nucleoside transporter 4 (hENT4) inhibitors, we cloned and stably expressed the recombinant protein in PK15NTD (nucleoside transporter deficient) cells, and, investigated its interaction with a series of dipyridamole analogs synthesized in our laboratory. Compounds were tested in this newly established hENT4 expressing system as well in previous stably expressed hENT1 and hENT2 expressing systems. Of the dipyridamole analogs evaluated, about one fourth of the compounds inhibited hENT4 with higher potencies than dipyridamole. The most potent of them, Compound 30 displayed an IC₅₀ of 74.4nM, making it about 38 times more potent than dipyridamole (IC₅₀=2.8μM), and selectivities of about 80-fold and 20-fold relative to ENT1 and ENT2, respectively. Structure–activity relationship showed nitrogen-containing monocyclic rings and noncyclic substituents at the 4- and 8-positions of the pyrimido[5,4-d]pyrimidine were important for the inhibitory activity against hENT4. The most potent and selective hENT4 inhibitors tended to have a 2,6-di(N-monohydroxyethyl) substitution on the pyrimidopyrimidine ring system. The inhibitors of hENT4 identified in this study are the most selective and potent inhibitors of hENT4 adenosine transporter function to date, and should serve as useful pharmacological/biochemical tools and/or potential leads for ENT4-based therapeutics. Also, the new hENT4-expressing PK15 cell line established will serve as a useful screening tool for the discovery and design of hENT4 ligands.
Keywords	therapeutics ; dipyridamole ; adenosine ; structure-activity relationships ; screening ; transporters ; humans ; pharmacology
Language	English
Document type	Article
ISSN	0006-2952
Database	AGRIS - International Information System for the Agricultural Sciences and Technology

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Article: Exploring the molecular mechanisms of nickel-induced genotoxicity and carcinogenicity: a literature review.

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Article ; Online: Sensitivity and mechanisms of taxol-resistant prostate adenocarcinoma cells to Vernonia amygdalina extract.

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Article: Sensitivity and mechanisms of taxol-resistant prostate adenocarcinoma cells to Vernonia amygdalina extract

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Article ; Online: Dipyridamole analogs as pharmacological inhibitors of equilibrative nucleoside transporters. Identification of novel potent and selective inhibitors of the adenosine transporter function of human equilibrative nucleoside transporter 4 (hENT4).

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Article: Sensitivity and mechanisms of taxol-resistant prostate adenocarcinoma cells to Vernonia amygdalina extract

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Article: Dipyridamole analogs as pharmacological inhibitors of equilibrative nucleoside transporters. Identification of novel potent and selective inhibitors of the adenosine transporter function of human equilibrative nucleoside transporter 4 (hENT4)

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