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Article: In response to: Beecroft P., Santner S., Lacy M.L., Kunzman L. & Dorsey F. (2006) New graduate nurses' perceptions of mentoring: six-year programme evaluation. Journal of Advanced Nursing55(6), 736-747.

Parker, Karen E

2007 Volume 58, Issue 2, Page(s) 201

MeSH term(s)	Humans ; Inservice Training ; Mentors ; Nurses ; Nursing Education Research ; Program Evaluation
Language	English
Publishing date	2007-04
Publishing country	England
Document type	Comment ; Letter
ZDB-ID	197634-5
ISSN	1365-2648 ; 0309-2402
ISSN (online)	1365-2648
ISSN	0309-2402
DOI	10.1111/j.1365-2648.2007.04210.x
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Zs.B 1851: Show issues

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Article ; Online: Retraction. RE: A chimeric vitronectin: IGF-1 protein supports feeder-cell-free and serum-free culture of human embryonic stem cells, by Manton KJ, S Richards, D Van Lonkhuyzen, L Cormack, D Leavesley, and Z Upton. Stem Cells Dev 19:1298-1305.

Parker, Graham C

Stem cells and development

2012 Volume 22, Issue 4, Page(s) 687

Language	English
Publishing date	2012-05-07
Publishing country	United States
Document type	Retraction of Publication
ZDB-ID	2142214-X
ISSN	1557-8534 ; 1547-3287
ISSN (online)	1557-8534
ISSN	1547-3287
DOI	10.1089/scd.2012.0706
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Zs.A 3616: Show issues

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Article: Melanin content and downregulation of glutathione S-transferase contribute to the action of L-buthionine-S-sulfoximine on human melanoma.

Fruehauf, J P / Zonis, S / al-Bassam, M / Kyshtoobayeva, A / Dasgupta, C / Milovanovic, T / Parker, R J / Buzaid, A C

Chemico-biological interactions

1998 Volume 111-112, Page(s) 277–305

Abstract: L-buthionine-S,R-sulfoximine (L-S,R-BSO) was enriched for the active L-buthionine-S-sulfoximine (L ... fresh human tumor samples. Increased activity was observed for the enriched preparation of L-S-BSO ... in direct proportion to its increased L-S-diastereomeric percentage. Significant antitumor activity ...

Abstract	L-buthionine-S,R-sulfoximine (L-S,R-BSO) was enriched for the active L-buthionine-S-sulfoximine (L-S-BSO) diastereomer. Comparative analysis was performed to determine if this enriched form possessed an increased capacity to deplete glutathione (GSH), and to inhibit the proliferation of tumor cell lines and fresh human tumor samples. Increased activity was observed for the enriched preparation of L-S-BSO in direct proportion to its increased L-S-diastereomeric percentage. Significant antitumor activity towards melanoma, breast and ovarian carcinoma specimens was noted, with the greatest activity directed against malignant melanoma. The activity of BSO on melanoma specimens was found to be correlated with their melanin content, suggesting that free radicals generated during melanin synthesis may become cytotoxic after GSH-dependent scavenging has been eliminated by BSO treatment. The antimelanoma activity of melphalan and BCNU were found to be significantly enhanced in combination with L-S-BSO. With respect to the mechanism of L-S-BSO synergy with alkylators, L-S-BSO treatment of M14 and ZAZ human melanoma cell lines resulted in decreased GSH levels and glutathione S-transferase (GST) activity. Western and Northern blot analyses indicated that GST-mu was the predominant isozyme downregulated after L-S-BSO treatment. Both M14 and ZAZ cell lines selected for resistance to L-S-BSO also showed decreased levels of GST-mu expression. However, in drug free media GST enzyme activity returned to pre-treatment levels without altering the BSO-resistance status of the cell lines. We conclude that L-S-BSO may be an active agent in the treatment of melanoma, and that it may enhance alkylator activity on melanoma through depletion of GSH and down-regulation of GST expression. Purified L-S-BSO should be explored clinically as an active agent for the treatment of melanoma.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Buthionine Sulfoximine/administration & dosage ; Buthionine Sulfoximine/pharmacology ; Carmustine/administration & dosage ; Down-Regulation ; Drug Resistance ; Enzyme Inhibitors/administration & dosage ; Enzyme Inhibitors/pharmacology ; Female ; Glutamate-Cysteine Ligase/antagonists & inhibitors ; Glutathione Transferase/genetics ; Glutathione Transferase/metabolism ; Humans ; Melanins/metabolism ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/metabolism ; Melphalan/administration & dosage ; Ovarian Neoplasms/drug therapy ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; Tumor Cells, Cultured
Chemical Substances	Enzyme Inhibitors ; Melanins ; Buthionine Sulfoximine (5072-26-4) ; Glutathione Transferase (EC 2.5.1.18) ; Glutamate-Cysteine Ligase (EC 6.3.2.2) ; Melphalan (Q41OR9510P) ; Carmustine (U68WG3173Y)
Language	English
Publishing date	1998-04-24
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/s0009-2797(97)00167-1
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Zs.A 686: Show issues

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Article: Selective and synergistic activity of L-S,R-buthionine sulfoximine on malignant melanoma is accompanied by decreased expression of glutathione-S-transferase.

Fruehauf, J P / Zonis, S / al-Bassam, M / Kyshtoobayeva, A / Dasgupta, C / Milovanovic, T / Parker, R J / Buzaid, A C

Pigment cell research

1997 Volume 10, Issue 4, Page(s) 236–249

Abstract: L-buthionine-S,R-sulfoximine (BSO) selectivley inhibits glutathione (GSH) synthesis. Malignant ... melanoma may be uniquely dependent on GSH and its linked enzymes, glutathione S-transferase (GST) and GSH ...

Abstract	L-buthionine-S,R-sulfoximine (BSO) selectivley inhibits glutathione (GSH) synthesis. Malignant melanoma may be uniquely dependent on GSH and its linked enzymes, glutathione S-transferase (GST) and GSH-peroxidase, for metabolism of reactive orthoquinones and peroxides produced during melanin synthesis. We compared the in vitro effects of BSO on melanoma cell lines and fresh melanoma specimens (n = 118) with breast and ovarian cell lines and solid tumors (n = 244). IC50 values (microM) for BSO on melanoma, breast and ovarian tumor specimens were 1.9, 8.6, and 29, respectively. The IC90 for melanoma was 25.5 microM, a level 20-fold lower than steady state levels achieved clinically. The sensitivity of individual specimens of melanoma correlated with their melanin content (r = 0.63). BSO synergistically enhanced BCNU activity against melanoma cell lines and human tumors. We followed GSH levels, GST enzyme activity, GST isoenzyme profiles and mRNA levels after BSO. BSO (50 microM) treatment for 48 hr resulted in a 95% decrease in ZAZ and M14 melanoma cell line GSH levels, and a 60% decrease in GST enzyme activity. GST-mu protein and mRNA levels were significantly reduced in both cell lines. GST-pi expression was unaffected. These data suggest that BSO action on melanoma may be related to GSH depletion, diminishing the capacity to scavenge toxic metabolites produced during melanin synthesis. We report here for the first time that BSO enhancement of alkylator action may be related in part to down regulation of GST. BSO may be a clinically useful adjunct in the treatment of malignant melanoma.
MeSH term(s)	Antimetabolites, Antineoplastic/pharmacology ; Antineoplastic Agents, Alkylating/pharmacology ; Breast Neoplasms/drug therapy ; Buthionine Sulfoximine/pharmacology ; Carmustine/pharmacology ; Drug Synergism ; Female ; Glutathione/metabolism ; Glutathione Transferase/antagonists & inhibitors ; Glutathione Transferase/biosynthesis ; Glutathione Transferase/genetics ; Humans ; Melanins/metabolism ; Melanoma/drug therapy ; Ovarian Neoplasms/drug therapy ; Tumor Cells, Cultured
Chemical Substances	Antimetabolites, Antineoplastic ; Antineoplastic Agents, Alkylating ; Melanins ; Buthionine Sulfoximine (5072-26-4) ; Glutathione Transferase (EC 2.5.1.18) ; Glutathione (GAN16C9B8O) ; Carmustine (U68WG3173Y)
Language	English
Publishing date	1997-08
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	645056-8
ISSN	1600-0749 ; 0893-5785
ISSN (online)	1600-0749
ISSN	0893-5785
DOI	10.1111/j.1600-0749.1997.tb00490.x
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Zs.A 2444: Show issues

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Article: Dose-dependent induction or depression of cysteine conjugate beta-lyase in rat kidney by N-acetyl-S-(1,2,3,4,4-pentachloro-1,3-butadienyl)-L-cysteine.

MacFarlane, M / Schofield, M / Parker, N / Roelandt, L / David, M / Lock, E A / King, L J / Goldfarb, P S / Gibson, G G

Toxicology

1993 Volume 77, Issue 1-2, Page(s) 133–144

Abstract: The influence of N-acetyl-S-(1,2,3,4,4-pentachloro-1,3-butadienyl)-L-cysteine (NAc-PCBD ...

Abstract	The influence of N-acetyl-S-(1,2,3,4,4-pentachloro-1,3-butadienyl)-L-cysteine (NAc-PCBD) on cysteine conjugate beta-lyase in female rat kidney has been examined. After a single, non-nephrotoxic dose of NAc-PCBD (3 mg/kg), cytosolic beta-lyase enzyme activity was increased 1.5 to 3-fold commensurate with a corresponding increase in enzyme protein levels as assessed by both Western blot and ELISA analyses. Using a cDNA probe for beta-lyase, this induction was found to be accompanied by an increase in the cognate mRNA. In contrast, a higher, nephrotoxic dose of NAc-PCBD (10 mg/kg) decreased all the above parameters. These effects appeared to be specific to the cytosolic form of the enzyme as no changes in kidney mitochondrial beta-lyase or enzyme protein levels were observed. Repeated dosing with the lower dose level (3 mg/kg) resulted in either no change, or in some instances, a reduction in the above parameters, suggesting an accumulation of the xenobiotic and a masking of the induction phenomenon. The molecular mechanisms underlying these observations are discussed in terms of the nephrotoxicity of halogenated xenobiotics.
MeSH term(s)	Acetylcysteine/administration & dosage ; Acetylcysteine/analogs & derivatives ; Acetylcysteine/toxicity ; Animals ; Blood Urea Nitrogen ; Blotting, Western ; Butadienes/administration & dosage ; Butadienes/toxicity ; Carbon-Sulfur Lyases ; Cytosol/enzymology ; Depression, Chemical ; Dose-Response Relationship, Drug ; Enzyme Induction/drug effects ; Enzyme-Linked Immunosorbent Assay ; Female ; Injections, Intraperitoneal ; Kidney/drug effects ; Kidney/enzymology ; Lyases/analysis ; Lyases/biosynthesis ; Mitochondria/enzymology ; RNA, Messenger/analysis ; Rats ; Transaminases/analysis
Chemical Substances	Butadienes ; RNA, Messenger ; N-acetyl-S-pentachloro-1,3-butadienylcysteine (89784-39-4) ; Transaminases (EC 2.6.1.-) ; glutamine-pyruvate aminotransferase (EC 2.6.1.15) ; Lyases (EC 4.-) ; Carbon-Sulfur Lyases (EC 4.4.-) ; S-alkylcysteine lyase (EC 4.4.1.6) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	1993-01-29
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/0300-483x(93)90144-h
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Zs.A 888: Show issues

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Article ; Online: Commentary on New Guidance for Human Papillomavirus-Related Cancer Screening Among Sexual and Gender Minority Populations.

Jackson, Sarah S / Parker, Karen L

Journal of lower genital tract disease

2023 Volume 27, Issue 4, Page(s) 322–323

MeSH term(s)	Humans ; Early Detection of Cancer ; Health Disparate Minority and Vulnerable Populations ; Human Papillomavirus Viruses ; Minority Groups ; Neoplasms ; Sexual Behavior ; Male ; Female
Language	English
Publishing date	2023-10-10
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2041332-4
ISSN	1526-0976 ; 1089-2591
ISSN (online)	1526-0976
ISSN	1089-2591
DOI	10.1097/LGT.0000000000000764
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Zs.A 5466: Show issues

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Article ; Online: Wastewater contaminants in a fractured bedrock aquifer and their potential use as enteric virus indicators.

Race, Amy S / Spoelstra, John / Parker, Beth L

Applied and environmental microbiology

2024 Volume 90, Issue 2, Page(s) e0121323

Abstract: Domestic wastewater is a source of persistent organic pollutants and pathogens to the aquatic environment, including groundwater aquifers. Wastewater contaminants include a variety of personal care products, pharmaceuticals, endocrine disrupters, ... ...

Abstract	Domestic wastewater is a source of persistent organic pollutants and pathogens to the aquatic environment, including groundwater aquifers. Wastewater contaminants include a variety of personal care products, pharmaceuticals, endocrine disrupters, bacteria, and viruses. Groundwater from 22 wells completed in a semi-confined to confined, fractured Silurian dolostone aquifer in southern Wellington County, Ontario, Canada, was analyzed for 14 organic wastewater contaminants (4 artificial sweeteners, 10 pharmaceuticals) as well as
MeSH term(s)	Humans ; Wastewater ; Escherichia coli ; Ibuprofen ; Triclosan ; Groundwater/microbiology ; Enterovirus ; Viruses ; Organic Chemicals ; Cosmetics ; Pharmaceutical Preparations ; Ontario ; Environmental Monitoring ; Water Pollutants, Chemical/analysis
Chemical Substances	Wastewater ; Ibuprofen (WK2XYI10QM) ; Triclosan (4NM5039Y5X) ; Organic Chemicals ; Cosmetics ; Pharmaceutical Preparations ; Water Pollutants, Chemical
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	223011-2
ISSN	1098-5336 ; 0099-2240
ISSN (online)	1098-5336
ISSN	0099-2240
DOI	10.1128/aem.01213-23
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Zs.B 201: Show issues

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Article: Renal activation of trichloroethene and S-(1,2-dichlorovinyl)-L-cysteine and cell proliferative responses in the kidneys of F344 rats and B6C3F1 mice.

Eyre, R J / Stevens, D K / Parker, J C / Bull, R J

Journal of toxicology and environmental health

1995 Volume 46, Issue 4, Page(s) 465–481

Abstract: Covalent binding of reactive intermediates formed by renal beta-lyase activation of S-(1,2 ... dichlorovinyl)-L-cysteine (DCVC) has been suggested to be responsible for the greater renal sensitivity of rats ... of TRI by the cysteine S-conjugate pathway was found to be greater in mice than rats and these findings ...

Abstract	Covalent binding of reactive intermediates formed by renal beta-lyase activation of S-(1,2-dichlorovinyl)-L-cysteine (DCVC) has been suggested to be responsible for the greater renal sensitivity of rats than mice to the carcinogenic effects of chronic treatment with trichloroethene (TRI). Previous work demonstrated that the activation of DCVC results in acid-labile adducts to protein that can be distinguished from adducts formed by other pathways of TRI metabolism. By analyzing acid-labile adduct formation, the relationship between DCVC formation and activation from TRI and increases in rates of cell division in the kidneys of male F344 rats and B6C3F1 mice could be investigated. The delivered dose of DCVC from an oral dose of 1000 mg/kg TRI was approximately six times greater in rats than mice. However, renal activation of DCVC in mice was approximately 12 times greater than in rats. Therefore, the overall activation of TRI was about two times greater in mice than rats. Induction of cell replication in liver and kidney following doses of 1, 5, or 25 mg/kg DCVC or 1000 mg/kg TRI was also measured through the use of miniosmotic pumps that delivered BrdU subcutaneously for 3 d. Acid-labile adduct formation from DCVC and TRI displayed a consistent relationship with increased cell replication in mice and between mice and rats. Both cell replication and acid-labile adduct formation in rats given 25 mg/kg DCVC were approximately equal to that observed in mice given 1 mg/kg. Increased cell replication was not observed in rats receiving 1 or 5 mg/kg DCVC or 1000 mg/kg TRI, nor were there histological signs of nephrotoxicity. Thus, net activation of TRI by the cysteine S-conjugate pathway was found to be greater in mice than rats and these findings appeared related to differences in cell proliferative responses of the kidneys of the two species. Based on these data, it would appear that other factors must contribute to the greater sensitivity of the rat to the induction of renal carcinogenesis by TRI.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Cell Division ; Cysteine/administration & dosage ; Cysteine/analogs & derivatives ; Cysteine/metabolism ; Dose-Response Relationship, Drug ; Kidney/cytology ; Kidney/metabolism ; Kidney Diseases/chemically induced ; Kidney Diseases/pathology ; Male ; Mice ; Rats ; Rats, Inbred F344 ; Species Specificity ; Trichloroethylene/administration & dosage ; Trichloroethylene/metabolism
Chemical Substances	Carrier Proteins ; Trichloroethylene (290YE8AR51) ; S-(1,2-dichlorovinyl)cysteine (627-72-5) ; Cysteine (K848JZ4886)
Language	English
Publishing date	1995-12
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	197268-6
ISSN	1087-2620 ; 0098-4108 ; 0040-9014
ISSN (online)	1087-2620
ISSN	0098-4108 ; 0040-9014
DOI	10.1080/15287399509532049
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Zs.A 1268: Show issues

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Article: Biotransformation of perchloroethene: dose-dependent excretion of trichloroacetic acid, dichloroacetic acid, and N-acetyl-S-(trichlorovinyl)-L-cysteine in rats and humans after inhalation.

Völkel, W / Friedewald, M / Lederer, E / Pähler, A / Parker, J / Dekant, W

Toxicology and applied pharmacology

1998 Volume 153, Issue 1, Page(s) 20–27

Abstract: ... to S-(trichlorovinyl)-L-cysteine (TCVC) and acetylated to N-acetyl-S-(trichlorovinyl)-L-cysteine (N-ac ... of S-(trichlorovinyl)glutathione (TCVG) from PER results in nephrotoxic metabolites. TCVG is cleaved ...

Abstract	Chronic exposure of rodents to perchloroethene (PER) increased the incidence of liver tumors in male mice and resulted in a small but significant increase in the incidence of renal tumors in male rats. The tumorigenicity of PER is mediated by metabolic activation reactions. PER is metabolized by cytochrome P450 and by conjugation with glutathione. Cytochrome P450 oxidation of PER results in trichloroacetyl chloride which reacts with water to trichloroacetic acid (TCA) which is excreted. The formation of S-(trichlorovinyl)glutathione (TCVG) from PER results in nephrotoxic metabolites. TCVG is cleaved to S-(trichlorovinyl)-L-cysteine (TCVC) and acetylated to N-acetyl-S-(trichlorovinyl)-L-cysteine (N-ac-TCVC), which is excreted with urine. TCVC is also cleaved in the kidney by cysteine conjugate beta-lyase to dichlorothioketene which may react with water to dichloroacetic acid (DCA) or with cellular macromolecules. The object of this study was to comparatively quantify the dose-dependent excretion of PER metabolites in urine of humans and rats after inhalation exposure. Three female and three male human volunteers and three female and three male rats were exposed to 10, 20, and 40 ppm PER for 6 h, and three female and three male rats to 400 ppm. A dose-dependent increase in the excretion of TCA and N-ac-TCVC after exposure to PER was found both in humans and in rats. A total of 20.4 +/- 7.77 mumol of TCA and 0.21 +/- 0.05 mumol of N-ac-TCVC were excreted in urine of human over 78 h after the start of exposure to 40 ppm PER; only traces of DCA were present. After identical exposure conditions, rats excreted 1.64 +/- 0.42 mumol of TCA, 0.006 +/- 0.002 mumol of N-ac-TCVC and 0.18 +/- 0.04 mumol of DCA. Excretion of N-ac-TCVC in male rats exposed to 400 ppm PER (103.7 nmol) was significantly higher, compared to female rats (31.5 nmol) exposed under identical conditions. N-ac-TCVC was rapidly eliminated with urine both in humans (t1/2 = 14.1 h) and in rats (t1/2 = 7.5 h). When comparing the urinary excretion of N-ac-TCVC, a potential marker for the formation of reactive intermediates in the kidney, humans received a significantly lower dose (3 nmol/kg at 40 ppm) compared to rats (23.0 nmol/kg) after identical exposure conditions. In addition, rats excreted large amounts of DCA which likely is a product of the beta-lyase-dependent metabolism of TCVC in the kidney. The obtained data suggest that glutathione conjugate formation and beta-lyase-dependent bioactivation of TCVC in PER metabolism is significantly higher in rats than in humans. Thus, using rat tumorigenicity data for human risk assessment of PER exposure may overestimate human tumor risks.
MeSH term(s)	Acetylcysteine/analogs & derivatives ; Acetylcysteine/urine ; Adult ; Aged ; Animals ; Biotransformation ; Carcinogens/pharmacokinetics ; Dichloroacetic Acid/urine ; Environmental Pollutants/pharmacokinetics ; Female ; Half-Life ; Humans ; Inhalation Exposure ; Male ; Middle Aged ; Rats ; Rats, Wistar ; Solvents/pharmacokinetics ; Tetrachloroethylene/pharmacokinetics ; Trichloroacetic Acid/urine
Chemical Substances	Carcinogens ; Environmental Pollutants ; Solvents ; S-trichlorovinyl-N-acetylcysteine (111348-61-9) ; Trichloroacetic Acid (5V2JDO056X) ; Dichloroacetic Acid (9LSH52S3LQ) ; Tetrachloroethylene (TJ904HH8SN) ; Acetylcysteine (WYQ7N0BPYC)
Language	English
Publishing date	1998-11
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1006/taap.1998.8548
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Article: BIOCHEMICAL STUDY OF THE TOXICITY OF S-DICHLOROVINYL-L-CYSTEINE.

PARKER, V H

Food and cosmetics toxicology

1965 Volume 3, Page(s) 75–84

MeSH term(s)	Cysteine ; Guinea Pigs ; Metabolism ; Poisoning ; Rats ; Research ; Toxicology
Chemical Substances	Cysteine (K848JZ4886)
Language	English
Publishing date	1965-07
Publishing country	England
Document type	Journal Article
ZDB-ID	80130-6
ISSN	0015-6264
ISSN	0015-6264
DOI	10.1016/s0015-6264(65)80011-6
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