@article {2628,
	title = {Glycosylated tetrahydrosalens as multifunctional molecules for Alzheimer{\textquoteright}s therapy},
	journal = {Dalton Transactions},
	number = {16},
	year = {2009},
	note = {ISI Document Delivery No.: 430GYTimes Cited: 8Cited Reference Count: 65Storr, Tim Scott, Lauren E. Bowen, Meryn L. Green, David E. Thompson, Katherine H. Schugar, Harvey J. Orvig, Chris},
	pages = {3034-3043},
	type = {Article},
	abstract = {The tetrahydrosalens N,N{\textquoteright}-bis(2-hydroxybenzyl)-ethane-1,2-diamine (H2L1), N, N{\textquoteright}-bis(2-hydroxybenzyl)-(-)-1,2-cyclohexane-(1R, 2R)-diamine (H2L2), N,N{\textquoteright}-bis(2-hydroxybenzyl)-N,N{\textquoteright}-dimethyl-ethane-1,2-diamine (H2L3), N,N{\textquoteright}-bis(2-hydroxybenzyl)-N,N{\textquoteright}-dibenzyl-ethane-1,2diamine (H2L4), and N,N{\textquoteright}-bis(2-(4-tert-butyl) hydroxybenzyl)-ethane-1,2-diamine (H2L5), as well as their prodrug glycosylated forms, GL(1-5), have been prepared and evaluated in vitro for their potential use as Alzheimer{\textquoteright}s disease (AD) therapeutics. Dysfunctional interactions of metal ions, especially those of Cu, Zn, and Fe, with the amyloid-beta (A beta) peptide are hypothesised to play an important role in the aetiology of AD, and disruption of these aberrant metal-peptide interactions via chelation therapy holds considerable promise as a therapeutic strategy. Tetrahydrosalens such as H2L1-5 have a significant affinity for metal ions, and thus should be able to compete with the A beta peptide for Cu, Zn, and Fe in the brain. This activity was assayed in vitro via a turbidity assay; H2L1 and H2L3 were found to attenuate A beta(1-40) aggregation after exposure to Cu2+ and Zn2+. In addition, H2L1-5 were determined to be potent antioxidants on the basis of an in vitro antioxidant assay. GL(1-5) were prepared as metal binding prodrugs; glycosylation is intended to prevent systemic metal binding, improve solubility, and enhance brain uptake. Enzymatic (beta-glucosidase) deprotection of the carbohydrate moieties was facile, with the exception of GL(4), demonstrating the general feasibility of this prodrug approach. Finally, a representative prodrug, GL(3), was determined to be non-toxic over a large concentration range in a cell viability assay.},
	keywords = {A-BETA, ACTIVITY, antioxidant, COMPLEXES, DISEASE, HYDROGEN-PEROXIDE, IN-VITRO, NEURODEGENERATIVE DISORDERS, OXIDATIVE STRESS, TRANSGENIC MICE, zinc},
	isbn = {1477-9226},
	url = {<Go to ISI>://000264978300018},
	author = {Storr, T. and Scott, L. E. and Bowen, M. L. and Green, D. E. and Thompson, K. H. and Schugar, H. J. and Orvig, Chris}
}
@article {2650,
	title = {Propofol protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via Akt activation and Bcl-2 up-regulation},
	journal = {Biochemical and Biophysical Research Communications},
	volume = {389},
	number = {1},
	year = {2009},
	note = {ISI Document Delivery No.: 555SMTimes Cited: 4Cited Reference Count: 26Wang, Baohua Shravah, Jayant Luo, Honglin Raedschelders, Koen Chen, David D. Y. Ansley, David M.},
	month = {Nov},
	pages = {105-111},
	type = {Article},
	abstract = {<p>Propofol is a widely used intravenous anesthetic agent with antioxidant properties secondary to its phenol based chemical structure. Treatment with propofol has been found to attenuate oxidative stress and prevent ischemia/reperfusion injury in rat heart. Here, we report that propofol protects cardiac H9c2 cells from hydrogen peroxide (H2O2)-induced injury by triggering the activation of Akt and a parallel up-regulation of Bcl-2. We show that pretreatment with propofol significantly protects against H2O2-induced injury. We further demonstrate that propofol activates the PI3K-Akt signaling pathway. The protective effect of propofol on H2O2-induced injury is reversed by PI3K inhibitor wortmannin, which effectively suppresses propofol-induced activation of Akt, up-regulation of Bcl-2, and protection from apoptosis. Collectively, our results reveal a new mechanism by which propofol inhibits H2O2-induced injury in cardiac H9c2 cells, supporting a potential application of propofol as a preemptive cardioprotectant in clinical settings such as coronary bypass surgery. (C) 2009 Elsevier Inc. All rights reserved.</p>},
	keywords = {15-F-2T-ISOPROSTANE FORMATION, Akt, antioxidant capacity, apoptosis, Bcl-2, CARDIOMYOCYTES, ENDOTHELIAL-CELLS, H9c2 cells, INJURY, KINASE-C, OXIDATIVE STRESS, Propofol, RAT-HEART, REDUCES APOPTOSIS, REPERFUSION, SENSITIVITY, SURVIVAL},
	isbn = {0006-291X},
	doi = {doi: 10.1016/j.bbrc.2009.08.097},
	url = {<Go to ISI>://000274534900020},
	author = {Wang, B. H. and Shravah, J. and Luo, H. L. and Raedschelders, K. and Chen, D. D. Y. and Ansley, D. M.}
}
@article {1010,
	title = {Complementary inhibition of synoviocyte, smooth muscle cell or mouse lymphoma cell proliferation by a vanadyl curcumin complex compared to curcumin alone},
	journal = {Journal of Inorganic Biochemistry},
	volume = {98},
	number = {12},
	year = {2004},
	note = {ISI Document Delivery No.: 876VBTimes Cited: 20Cited Reference Count: 62},
	month = {Dec},
	pages = {2063-2070},
	type = {Article},
	abstract = {A novel vanadyl curcumin complex (VO(cur)2) has been synthesized and and its physicochemical properties characterized. Biological characterization included in vitro testing for anti-rheumatic activity in synoviocytes, angiogenesis inhibition in smooth muscle cells and anti-cancer potential in mouse lymphoma cells; as well as in vivo testing for hypoglycemic activity by oral gavage in streptozotocin (STZ)-diabetic rats. VO(cur)2 was more effective as an anti-cancer agent, compared to uncomplexed curcumin or vanadyl ion alone, was more than twice as effective as curcumin alone as an anti-arthritic agent, and was more than four times as effective as curcumin alone in inhibiting smooth muscle cell proliferation. In both acute and chronic screening tests, VO(cur)2 was ineffective as an insulin mimetic agent; however, it also proved to be exceptionally non-toxic, with no evidence of negative symptornatology during a month-long treatment period, at doses up to and including 2.0 mmol kg(-1) day(-1). (C) 2004 Elsevier Inc. All rights reserved.},
	keywords = {antioxidant, apoptosis, arthritis lymphoma, BIS(MALTOLATO)OXOVANADIUM(IV), CELLS, COMPLEX, COORDINATION, curcurnin, DIABETIC-RATS, DIFERULOYL METHANE CURCUMIN, FREE-RADICALS, INDUCED LIPID-PEROXIDATION, INSULIN MIMICS, LEUKEMIA HL-60, METAL-IONS, OXIDATIVE STRESS, vanadyl ion},
	isbn = {0162-0134},
	url = {<Go to ISI>://000225525200010},
	author = {Thompson, K. H. and Bohmerle, K. and Polishchuk, E. and Martins, C. and Toleikis, P. and Tse, J. and Yuen, V. and McNeill, J. H. and Orvig, Chris}
}
@article {5209,
	title = {Coordination chemistry of vanadium in metallopharmaceutical candidate compounds},
	journal = {Coordination Chemistry Reviews},
	volume = {219},
	year = {2001},
	note = {ISI Document Delivery No.: 478JQTimes Cited: 138Cited Reference Count: 119},
	month = {Sep-Oct},
	pages = {1033-1053},
	type = {Review},
	abstract = {The discovery of vanadium{\textquoteright}s insulin-like behaviour in vitro, and later of the orally available glucose- and lipid-lowering capability of these same compounds in vivo, has stimulated renewed interest in vanadium coordination chemistry. Besides the anti-diabetic effects for which it is now so well known, vanadium also exhibits a number of other therapeutic effects including anti-tumour and anti-inflammatory activities. In this review, emphasis will be on the most recent developments in the coordination chemistry of vanadium(III), (IV) and (V), as related to development of these compounds for pharmaceutical use. How best to measure bioactivity and the pharmaceutical relevance of accompanying increased oxidative stress will also be considered. (C) 2001 Elsevier Science B.V. All rights reserved.},
	keywords = {bioactivity, BIOLOGICAL-ACTIVITY, CANCER, CRYSTAL-STRUCTURE, Diabetes mellitus, DIABETES-MELLITUS, ESEEM, INSULIN-LIKE ACTIVITIES, OXIDATIVE STRESS, OXOVANADIUM(IV) COMPLEXES, OXYGEN-BRIDGED DIMER, PEROXO HETEROLIGAND VANADATES(V), pharmaceutical agents, RAY, SPECTROSCOPIC PROPERTIES, structure-activity relationships, TYROSINE PHOSPHORYLATION, vanadium complexes},
	isbn = {0010-8545},
	url = {<Go to ISI>://000171343600035},
	author = {Thompson, K. H. and Orvig, Chris}
}
@article {4683,
	title = {Vanadium compounds as insulin mimics},
	journal = {Chemical Reviews},
	volume = {99},
	number = {9},
	year = {1999},
	note = {ISI Document Delivery No.: 235XUTimes Cited: 376Cited Reference Count: 124},
	month = {Sep},
	pages = {2561-2571},
	type = {Review},
	keywords = {AGENT BIS(MALTOLATO)OXOVANADIUM(IV) BMOV, BIOLOGICAL-SYSTEMS, COMPOUNDS, GLUCOSE-METABOLISM, IN-VIVO, MIMETIC AGENT, OXIDATIVE STRESS, PEROXOVANADIUM, PHOSPHOTYROSINE PHOSPHATASE INHIBITORS, STREPTOZOTOCIN-DIABETIC RATS, TYROSINE PHOSPHORYLATION},
	isbn = {0009-2665},
	url = {<Go to ISI>://000082569800015},
	author = {Thompson, K. H. and McNeill, J. H. and Orvig, Chris}
}
