1
40
4
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1517/13543784.2012.693479" target="_blank" rel="noreferrer noopener">http://doi.org/10.1517/13543784.2012.693479</a>
Pages
1123–1140
Issue
8
Volume
21
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Curcumin and neurodegenerative diseases: a perspective.
Publisher
An entity responsible for making the resource available
Expert opinion on investigational drugs
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-08
Subject
The topic of the resource
Humans; Animals; Oxidative Stress/drug effects; Neurodegenerative Diseases/*drug therapy/metabolism; Curcumin/adverse effects/pharmacokinetics/*pharmacology/*therapeutic use; Neuroprotective Agents/adverse effects/pharmacokinetics/*pharmacology/*therapeutic use; Drug Evaluation; Preclinical
Creator
An entity primarily responsible for making the resource
Darvesh Altaf S; Carroll Richard T; Bishayee Anupam; Novotny Nicholas A; Geldenhuys Werner J; Van der Schyf Cornelis J
Description
An account of the resource
INTRODUCTION: Curcumin, a dietary polyphenol found in the curry spice turmeric, possesses potent antioxidant and anti-inflammatory properties and an ability to modulate multiple targets implicated in the pathogenesis of chronic illness. Curcumin has shown therapeutic potential for neurodegenerative diseases including Alzheimer's disease (AD) and Parkinson's disease (PD). AREAS COVERED: This article highlights the background and epidemiological evidence of curcumin's health benefits and its pharmacodynamic and pharmacokinetic profile. Curcumin's ability to counteract oxidative stress and inflammation and its capacity to modulate several molecular targets is reviewed. We highlight the neuroprotective properties of curcumin including pre-clinical evidence for its pharmacological effects in experimental models of AD and PD. The bioavailability and safety of curcumin, the development of semi-synthetic curcuminoids as well as novel formulations of curcumin are addressed. EXPERT OPINION: Curcumin possesses therapeutic potential in the amelioration of a host of neurodegenerative ailments as evidenced by its antioxidant, anti-inflammatory and anti-protein aggregation effects. However, issues such as limited bioavailability and a paucity of clinical studies examining its therapeutic effectiveness in illnesses such as AD and PD currently limit its therapeutic outreach. Considerable effort will be required to adapt curcumin as a neuroprotective agent to be used in the treatment of AD, PD and other neurodegenerative diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1517/13543784.2012.693479" target="_blank" rel="noreferrer noopener">10.1517/13543784.2012.693479</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Animals
Bishayee Anupam
Carroll Richard T
Curcumin/adverse effects/pharmacokinetics/*pharmacology/*therapeutic use
Darvesh Altaf S
Department of Pharmaceutical Sciences
Drug Evaluation
Expert opinion on investigational drugs
Geldenhuys Werner J
Humans
NEOMED College of Pharmacy
Neurodegenerative Diseases/*drug therapy/metabolism
Neuroprotective Agents/adverse effects/pharmacokinetics/*pharmacology/*therapeutic use
Novotny Nicholas A
Oxidative Stress/drug effects
Preclinical
Van der Schyf Cornelis J
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.ntt.2012.03.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ntt.2012.03.003</a>
Pages
338–343
Issue
3
Volume
34
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Markers associated with testosterone enhancement of methamphetamine-induced striatal dopaminergic neurotoxicity.
Publisher
An entity responsible for making the resource available
Neurotoxicology and teratology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-06
Subject
The topic of the resource
Animals; Biomarkers/metabolism; Blotting; Body Temperature/drug effects; Body Weight/drug effects; Corpus Striatum/*drug effects/metabolism; Dopamine Plasma Membrane Transport Proteins/metabolism; Dopamine/*metabolism; Drug Synergism; HSP70 Heat-Shock Proteins/metabolism; Inbred Strains; Male; Methamphetamine/*toxicity; Mice; Neurotoxicity Syndromes/*etiology/metabolism; Oxidative Stress/drug effects; Testosterone Propionate/*pharmacology; Vesicular Monoamine Transport Proteins/metabolism; Western
Creator
An entity primarily responsible for making the resource
Buletko A Blake; Dluzen Dean E; McDermott Janet L; Darvesh Altaf S; Geldenhuys Werner J
Description
An account of the resource
Intact male CD-1 mice received an injection of testosterone propionate (TP–5 ug), progesterone (P–5 mg), the oil vehicle or remained untreated (control). At 24 hours after hormonal treatments the mice received an injection of methamphetamine (MA–40 mg/kg) and rectal temperatures were measured. At 5 days post-MA, assays were performed to assess effects of these treatments. Maximal increases in body temperatures, that were significantly greater than oil-treated controls, were obtained in TP-treated mice. At 5 days post-MA, maximal weight reductions were obtained with TP-treated mice, while P-treated mice showed no significant decrease between the pre- versus post-MA determinations. Striatal dopamine concentrations showed maximal reductions and heat-shock protein-70 maximal increases in the TP group, with both differing significantly as compared with all other groups. Protein levels of dopamine transporters were significantly decreased in P-treated mice, while vesicular monoamine transporter-2 was significantly decreased in TP-treated mice. Taken together, these results suggest that testosterone exacerbates the deleterious effects of MA within male mice as indicated by a number of markers related to neurotoxicity. The changes in markers as associated with this enhanced neurotoxicity suggest that TP may increase thermal/energy responses and/or oxidative stress to produce this effect.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.ntt.2012.03.003" target="_blank" rel="noreferrer noopener">10.1016/j.ntt.2012.03.003</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Animals
Biomarkers/metabolism
Blotting
Body Temperature/drug effects
Body Weight/drug effects
Buletko A Blake
Corpus Striatum/*drug effects/metabolism
Darvesh Altaf S
Department of Pharmaceutical Sciences
Dluzen Dean E
Dopamine Plasma Membrane Transport Proteins/metabolism
Dopamine/*metabolism
Drug Synergism
Geldenhuys Werner J
HSP70 Heat-Shock Proteins/metabolism
Inbred Strains
Male
McDermott Janet L
Methamphetamine/*toxicity
Mice
NEOMED College of Pharmacy
Neurotoxicity Syndromes/*etiology/metabolism
Neurotoxicology and teratology
Oxidative Stress/drug effects
Testosterone Propionate/*pharmacology
Vesicular Monoamine Transport Proteins/metabolism
Western
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2011.05.034" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2011.05.034</a>
Pages
876–883
Issue
4
Volume
51
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Vitamin B12 protects against superoxide-induced cell injury in human aortic endothelial cells.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
Aorta/pathology; Apoptosis/drug effects; Atherosclerosis/*drug therapy/metabolism/pathology/physiopathology; Cell Line; Cell Survival/drug effects; Cytoprotection; Endothelium; Free Radical Scavengers/*pharmacology; Humans; Mitochondria/drug effects/metabolism/pathology; Oxidative Stress/drug effects; Reperfusion Injury/*drug therapy/metabolism/pathology/physiopathology; Superoxides/metabolism; Vascular/*drug effects/metabolism/pathology; Vitamin B 12/*pharmacology; Vitamin B Complex/*pharmacology
Creator
An entity primarily responsible for making the resource
Moreira Edward S; Brasch Nicola E; Yun June
Description
An account of the resource
Superoxide (O(2)(*-)) is implicated in inflammatory states including arteriosclerosis and ischemia-reperfusion injury. Cobalamin (Cbl) supplementation is beneficial for treating many inflammatory diseases and also provides protection in oxidative-stress-associated pathologies. Reduced Cbl reacts with O(2)(*-) at rates approaching that of superoxide dismutase (SOD), suggesting a plausible mechanism for its anti-inflammatory properties. Elevated homocysteine (Hcy) is an independent risk factor for cardiovascular disease and endothelial dysfunction. Hcy increases O(2)(*-) levels in human aortic endothelial cells (HAEC). Here, we explore the protective effects of Cbl in HAEC exposed to various O(2)(*-) sources, including increased Hcy levels. Hcy increased O(2)(*-) levels (1.6-fold) in HAEC, concomitant with a 20% reduction in cell viability and a 1.5-fold increase in apoptotic death. Pretreatment of HAEC with physiologically relevant concentrations of cyanocobalamin (CNCbl) (10-50nM) prevented Hcy-induced increases in O(2)(*-) and cell death. CNCbl inhibited both Hcy and rotenone-induced mitochondrial O(2)(*-) production. Similarly, HAEC challenged with paraquat showed a 1.5-fold increase in O(2)(*-) levels and a 30% decrease in cell viability, both of which were prevented with CNCbl pretreatment. CNCbl also attenuated elevated O(2)(*-) levels after exposure of cells to a Cu/Zn-SOD inhibitor. Our data suggest that Cbl acts as an efficient intracellular O(2)(*-) scavenger.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2011.05.034" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2011.05.034</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2011
Aorta/pathology
Apoptosis/drug effects
Atherosclerosis/*drug therapy/metabolism/pathology/physiopathology
Brasch Nicola E
Cell Line
Cell Survival/drug effects
Cytoprotection
Department of Integrative Medical Sciences
Endothelium
Free radical biology & medicine
Free Radical Scavengers/*pharmacology
Humans
Mitochondria/drug effects/metabolism/pathology
Moreira Edward S
NEOMED College of Medicine
Oxidative Stress/drug effects
Reperfusion Injury/*drug therapy/metabolism/pathology/physiopathology
Superoxides/metabolism
Vascular/*drug effects/metabolism/pathology
Vitamin B 12/*pharmacology
Vitamin B Complex/*pharmacology
Yun June
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.bcp.2014.03.012" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bcp.2014.03.012</a>
Pages
490–502
Issue
4
Volume
89
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
BCNU-induced gR2 defect mediates S-glutathionylation of Complex I and respiratory uncoupling in myocardium.
Publisher
An entity responsible for making the resource available
Biochemical pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-06
Subject
The topic of the resource
Alkylating/*adverse effects/pharmacology; Animals; Antineoplastic Agents; Cardiotoxins/adverse effects/pharmacology; Carmustine/*adverse effects/pharmacology; Cattle; Cell Line; Complex I; Electron Transport Complex I/chemistry/*metabolism; Fatty Acids; Glutathione reductase; Glutathione Reductase/*antagonists & inhibitors/metabolism; Glutathione/*metabolism; Heart Ventricles/drug effects/metabolism/physiopathology; Heart/*drug effects/metabolism; Ion Channels/metabolism; Left/*chemically induced/metabolism/physiopathology; Male; Mice; Mitochondria; Mitochondrial Proteins/metabolism; Nonesterified/metabolism; Oxidative stress; Oxidative Stress/drug effects; Post-Translational/drug effects; Protein Processing; Rats; S-Glutathionylation; Sprague-Dawley; Superoxide Dismutase/genetics/metabolism; Systolic dysfunction; Transgenic; Uncoupling Protein 3; Ventricular Dysfunction
Creator
An entity primarily responsible for making the resource
Kang Patrick T; Chen Chwen-Lih; Ren Pei; Guarini Giacinta; Chen Yeong-Renn
Description
An account of the resource
A deficiency of mitochondrial glutathione reductase (or GR2) is capable of adversely affecting the reduction of GSSG and increasing mitochondrial oxidative stress. BCNU [1,3-bis (2-chloroethyl)-1-nitrosourea] is an anticancer agent and known inhibitor of cytosolic GR ex vivo and in vivo. Here we tested the hypothesis that a BCNU-induced GR2 defect contributes to mitochondrial dysfunction and subsequent impairment of heart function. Intraperitoneal administration of BCNU (40 mg/kg) specifically inhibited GR2 activity by 79.8 +/- 2.7% in the mitochondria of rat heart. However, BCNU treatment modestly enhanced the activities of mitochondrial Complex I and other ETC components. The cardiac function of BCNU-treated rats was analyzed by echocardiography, revealing a systolic dysfunction associated with decreased ejection fraction, decreased cardiac output, and an increase in left ventricular internal dimension and left ventricular volume in systole. The respiratory control index of isolated mitochondria from the myocardium was moderately decreased after BCNU treatment, whereas NADH-linked uncoupling of oxygen consumption was significantly enhanced. Extracellular flux analysis to measure the fatty acid oxidation of myocytes indicated a 20% enhancement after BCNU treatment. When the mitochondria were immunoblotted with antibodies against GSH and UCP3, both protein
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bcp.2014.03.012" target="_blank" rel="noreferrer noopener">10.1016/j.bcp.2014.03.012</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Alkylating/*adverse effects/pharmacology
Animals
Antineoplastic Agents
Biochemical pharmacology
Cardiotoxins/adverse effects/pharmacology
Carmustine/*adverse effects/pharmacology
Cattle
Cell Line
Chen Chwen-Lih
Chen Yeong-Renn
Complex I
Department of Integrative Medical Sciences
Electron Transport Complex I/chemistry/*metabolism
Fatty Acids
Glutathione reductase
Glutathione Reductase/*antagonists & inhibitors/metabolism
Glutathione/*metabolism
Guarini Giacinta
Heart Ventricles/drug effects/metabolism/physiopathology
Heart/*drug effects/metabolism
Ion Channels/metabolism
Kang Patrick T
Left/*chemically induced/metabolism/physiopathology
Male
Mice
Mitochondria
Mitochondrial Proteins/metabolism
NEOMED College of Medicine
Nonesterified/metabolism
Oxidative Stress
Oxidative Stress/drug effects
Post-Translational/drug effects
Protein Processing
Rats
Ren Pei
S-Glutathionylation
Sprague-Dawley
Superoxide Dismutase/genetics/metabolism
Systolic dysfunction
Transgenic
Uncoupling Protein 3
Ventricular Dysfunction