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Article ; Online: AMPK: a cellular metabolic and redox sensor. A minireview.

Shirwany, Najeeb A / Zou, Ming-Hui

Frontiers in bioscience (Landmark edition)

2014 Volume 19, Issue 3, Page(s) 447–474

Abstract: AMPK is a serine/threonine kinase that is found in all eukaryotes and is ubiquitously expressed in all organ systems. Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and ... ...

Abstract	AMPK is a serine/threonine kinase that is found in all eukaryotes and is ubiquitously expressed in all organ systems. Once activated, AMPK stimulates hepatic fatty acid oxidation and ketogenesis, inhibits cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibits adipocyte lipolysis and lipogenesis, stimulates skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulates insulin secretion by the pancreas. Thus its importance in many critical cellular processes is well established. For cells it is critical that energy supply and demand are closely matched. AMPK is recognized as a critical integrator of this balance. It is known to be allosterically activated by an increased AMP:ATP ratio. Activation of the kinase switches on catabolic pathways while switching off anabolic ones. It also acts as a redox sensor in endothelial cells where oxidative stress can disturb NO signaling. Abnormal NO signaling leads to disturbed vasodilatory responses. By inhibiting the formation of reactive oxygen species in the endothelium, AMPK can optimize the redox balance in the vasculature. Here, we review the role of AMPK in the cell.
MeSH term(s)	Adenylate Kinase/metabolism ; Biosensing Techniques ; Cell Death ; Cell Division ; Enzyme Activation ; Mitochondria/enzymology ; Oxidation-Reduction ; Oxidative Stress ; Signal Transduction
Chemical Substances	Adenylate Kinase (EC 2.7.4.3)
Language	English
Publishing date	2014-01-01
Publishing country	Singapore
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/4218
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Article ; Online: Vascular inflammation is a missing link for diabetes-enhanced atherosclerotic cardiovascular diseases.

Shirwany, Najeeb A / Zou, Ming-Hui

Frontiers in bioscience (Landmark edition)

2012 Volume 17, Issue 3, Page(s) 1140–1164

Abstract: Diabetes is associated with major life-threatening complications such as a markedly increased risk of cardiovascular disease, even in the presence of rigid glycemic control. Indeed, nearly 75% of diabetic patients eventually die of cardiovascular disease ...

Abstract	Diabetes is associated with major life-threatening complications such as a markedly increased risk of cardiovascular disease, even in the presence of rigid glycemic control. Indeed, nearly 75% of diabetic patients eventually die of cardiovascular disease or cardiovascular complications. A striking feature of the diabetic cardiovascular phenotype is the appearance of accelerated atherosclerosis, which resembles atherosclerosis that may be encountered in the non-diabetic individual, except that it is more extensive, aggressive, and occurs at an earlier age. Atherosclerosis (or atherosclerotic vascular disease; ASVD), is a pathological syndrome affecting arterial vessels characterized by narrowing of the vascular lumen secondary to intravascular buildup of fatty material such as cholesterol, aggregated cellular debris, and inflammatory change in the vascular endothelium. Seemingly distinct, these two well-defined disorders are nevertheless, intimately and intricately linked. In fact, these two pathologies appear to be linked by common signaling pathways and shared regulatory systems that appear to go awry in an as yet poorly understood manner. In recent years, a body of evidence has been growing that suggests that inflammation peculiar to the vascular system, occurs in the diabetic patient. This review aims to present the empirical underpinning of the hypothesis that inflammatory change in the vasculature might be the integrated mechanism that connects a diabetic phenotype with its attendant vascular complications.
MeSH term(s)	Atherosclerosis/complications ; Cardiovascular Diseases/complications ; Diabetes Complications ; Humans ; Inflammation Mediators/metabolism ; Vasculitis/complications
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2012-01-01
Publishing country	Singapore
Document type	Journal Article
ZDB-ID	2704569-9
ISSN	2768-6698 ; 1093-9946
ISSN (online)	2768-6698
ISSN	1093-9946
DOI	10.2741/3978
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Article ; Online: Arterial stiffness: a brief review.

Shirwany, Najeeb A / Zou, Ming-hui

Acta pharmacologica Sinica

2010 Volume 31, Issue 10, Page(s) 1267–1276

Abstract: Physical stiffening of the large arteries is the central paradigm of vascular aging. Indeed, stiffening in the larger central arterial system, such as the aortic tree, significantly contributes to cardiovascular diseases in older individuals and is ... ...

Abstract	Physical stiffening of the large arteries is the central paradigm of vascular aging. Indeed, stiffening in the larger central arterial system, such as the aortic tree, significantly contributes to cardiovascular diseases in older individuals and is positively associated with systolic hypertension, coronary artery disease, stroke, heart failure and atrial fibrillation, which are the leading causes of mortality in the developed countries and also in the developing world as estimated in 2010 by World Health Organizations. Thus, better, less invasive and more accurate measures of arterial stiffness have been developed, which prove useful as diagnostic indices, pathophysiological markers and predictive indicators of disease. This article presents a review of the structural determinants of vascular stiffening, its pathophysiologic determinants and its implications for vascular research and medicine. A critical discussion of new techniques for assessing vascular stiffness is also presented.
MeSH term(s)	Aging/physiology ; Animals ; Arteries/metabolism ; Arteries/physiopathology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/physiopathology ; Diagnostic Techniques, Cardiovascular ; Diet ; Elasticity ; Endothelium, Vascular/physiopathology ; Glucose/physiology ; Humans ; Insulin/physiology ; Neurosecretory Systems/physiopathology ; Risk Factors ; Vascular Resistance
Chemical Substances	Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2010-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1360774-1
ISSN	1745-7254 ; 0253-9756 ; 1671-4083
ISSN (online)	1745-7254
ISSN	0253-9756 ; 1671-4083
DOI	10.1038/aps.2010.123
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Article ; Online: AMPK in cardiovascular health and disease.

Shirwany, Najeeb A / Zou, Ming-Hui

Acta pharmacologica Sinica

2010 Volume 31, Issue 9, Page(s) 1075–1084

Abstract: AbstractAdenosine Monophosphate-activated Protein Kinase (AMPK), a serine/threonine kinase and a member of the Snf1/AMPK protein kinase family, consists of three protein subunits that together make a functional enzyme. AMPK, which is expressed in a ... ...

Abstract	AbstractAdenosine Monophosphate-activated Protein Kinase (AMPK), a serine/threonine kinase and a member of the Snf1/AMPK protein kinase family, consists of three protein subunits that together make a functional enzyme. AMPK, which is expressed in a number of tissues, including the liver, brain, and skeletal muscle, is allosterically activated by a rise in the AMP: ATP ratio (ie in a low ATP or energy depleted state). The net effect of AMPK activation is to halt energy consuming (anabolic) pathways but to promote energy conserving (catabolic) cellular pathways. AMPK has therefore often been dubbed the "metabolic master switch". AMPK also plays a critical physiological role in the cardiovascular system. Increasing evidence suggest that AMPK might also function as a sensor by responding to oxidative stress. Mostly importantly, AMPK modulates endogenous antioxidant gene expression and/or suppress the production of oxidants. AMPK promotes cardiovascular homeostasis by ensuring an optimum redox balance on the heart and vascular tissues. Dysfunctional AMPK is thought to underlie several cardiovascular pathologies. Here we review this kinase from its structure and discovery to current knowledge of its adaptive and maladaptive role in the cardiovascular system.
MeSH term(s)	AMP-Activated Protein Kinases/chemistry ; AMP-Activated Protein Kinases/metabolism ; Animals ; Cardiovascular Diseases/enzymology ; Cardiovascular System/enzymology ; Humans
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2010-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1360774-1
ISSN	1745-7254 ; 0253-9756 ; 1671-4083
ISSN (online)	1745-7254
ISSN	0253-9756 ; 1671-4083
DOI	10.1038/aps.2010.139
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Article: Regulation of intracellular calcium in cortical neurons transgenic for human Abeta40 and Abeta42 following nutritive challenge.

Shirwany, Najeeb A / Xie, Jun / Guo, Qing

International journal of clinical and experimental medicine

2009 Volume 2, Issue 2, Page(s) 149–158

Abstract: The pathogenesis of Alzheimer's Disease (AD) is not fully understood. Amyloid plaques could be causally linked to neuronal loss in AD. Two proteolytic products of the Amyloid Precursor Protein (APP), Amyloid beta40 (Abeta40) and Amyloid beta42 (Abeta42), ...

Abstract	The pathogenesis of Alzheimer's Disease (AD) is not fully understood. Amyloid plaques could be causally linked to neuronal loss in AD. Two proteolytic products of the Amyloid Precursor Protein (APP), Amyloid beta40 (Abeta40) and Amyloid beta42 (Abeta42), are considered to be critical in the neurodegeneration seen in AD. However, in transgenic mice that overexpress human Abeta40 or Abeta42, it was shown that Abeta42 was much more amyloidogenic than Abeta40. In contrast to this observation, we have found that cultured cortical neurons from mice transgenic for human Abeta40 and for Abeta42 are both and statistically equally vulnerable to nutritive challenge induced by trophic factor withdrawal (TFW). Aberrant regulation of InsP(3)R (Inositol triphosphate receptor)-mediated calcium release has been implicated in neuronal cell death. It is however not clear whether this pathway plays a critical role in cortical neurons transgenic for different species of human Abeta. We now report that Abeta40 and Abeta42 equally exacerbated intracellular calcium response to TFW in cortical neurons following TFW. When bradykinin (BK), a potent stimulant of InsP(3)R-mediated calcium release from ER, was applied to these cells, wild-type (WT) neurons exhibited a steep rise in [Ca(2+)](i) but this was not observed in either Abeta transgenic type. Similarly, when 1 muM Xestopongin C (XeC), a specific blocker of InsP(3)R, was applied to these neurons, WT cells showed a significant attenuation of increase in [Ca(2+)](i) following TFW, while elevation in [Ca(2+)](i) induced by TFW remained largely unchanged in Abeta40 and Abeta42 cells. Finally, when we treated these cells with a Ca(2+) chelator (BAPTA; 10 muM), all three cell types had a marked attenuation of [Ca(2+)](i). These findings indicate that the exacerbated calcium dysregulation following TFW in Abeta transgenic neurons are likely to be mediated by calcium channels other than ER InsP3R receptors. Overall, our results also suggest that a highly amyloidogenic Abeta species, such as Abeta42, might not necessarily be significantly more neurotoxic than a less or non-amyloidogenic Abeta species, such as Abeta40.
Language	English
Publishing date	2009-06-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2418305-2
ISSN	1940-5901
ISSN	1940-5901
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Article ; Online: 2-Deoxy-D-glucose treatment of endothelial cells induces autophagy by reactive oxygen species-mediated activation of the AMP-activated protein kinase.

Wang, Qilong / Liang, Bin / Shirwany, Najeeb A / Zou, Ming-Hui

PloS one

2011 Volume 6, Issue 2, Page(s) e17234

Abstract: Autophagy is a cellular self-digestion process activated in response to stresses such as energy deprivation and oxidative stress. However, the mechanisms by which energy deprivation and oxidative stress trigger autophagy remain undefined. Here, we report ...

Abstract	Autophagy is a cellular self-digestion process activated in response to stresses such as energy deprivation and oxidative stress. However, the mechanisms by which energy deprivation and oxidative stress trigger autophagy remain undefined. Here, we report that activation of AMP-activated protein kinase (AMPK) by mitochondria-derived reactive oxygen species (ROS) is required for autophagy in cultured endothelial cells. AMPK activity, ROS levels, and the markers of autophagy were monitored in confluent bovine aortic endothelial cells (BAEC) treated with the glycolysis blocker 2-deoxy-D-glucose (2-DG). Treatment of BAEC with 2-DG (5 mM) for 24 hours or with low concentrations of H(2)O(2) (100 µM) induced autophagy, including increased conversion of microtubule-associated protein light chain 3 (LC3)-I to LC3-II, accumulation of GFP-tagged LC3 positive intracellular vacuoles, and increased fusion of autophagosomes with lysosomes. 2-DG-treatment also induced AMPK phosphorylation, which was blocked by either co-administration of two potent anti-oxidants (Tempol and N-Acetyl-L-cysteine) or overexpression of superoxide dismutase 1 or catalase in BAEC. Further, 2-DG-induced autophagy in BAEC was blocked by overexpressing catalase or siRNA-mediated knockdown of AMPK. Finally, pretreatment of BAEC with 2-DG increased endothelial cell viability after exposure to hypoxic stress. Thus, AMPK is required for ROS-triggered autophagy in endothelial cells, which increases endothelial cell survival in response to cell stress.
MeSH term(s)	AMP-Activated Protein Kinases/antagonists & inhibitors ; AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Animals ; Autophagy/drug effects ; Cattle ; Cell Survival/drug effects ; Cell Survival/genetics ; Cells, Cultured ; Deoxyglucose/pharmacology ; Drug Evaluation, Preclinical ; Endothelial Cells/drug effects ; Endothelial Cells/physiology ; Enzyme Activation/drug effects ; Enzyme Activation/genetics ; Gene Expression Regulation, Enzymologic/drug effects ; Humans ; RNA, Small Interfering/pharmacology ; Reactive Oxygen Species/metabolism ; Reactive Oxygen Species/pharmacology ; Up-Regulation/drug effects
Chemical Substances	RNA, Small Interfering ; Reactive Oxygen Species ; Deoxyglucose (9G2MP84A8W) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2011-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0017234
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Article ; Online: 2-Deoxy-D-glucose treatment of endothelial cells induces autophagy by reactive oxygen species-mediated activation of the AMP-activated protein kinase.

Qilong Wang / Bin Liang / Najeeb A Shirwany / Ming-Hui Zou

PLoS ONE, Vol 6, Iss 2, p e

2011 Volume 17234

Abstract	Autophagy is a cellular self-digestion process activated in response to stresses such as energy deprivation and oxidative stress. However, the mechanisms by which energy deprivation and oxidative stress trigger autophagy remain undefined. Here, we report that activation of AMP-activated protein kinase (AMPK) by mitochondria-derived reactive oxygen species (ROS) is required for autophagy in cultured endothelial cells. AMPK activity, ROS levels, and the markers of autophagy were monitored in confluent bovine aortic endothelial cells (BAEC) treated with the glycolysis blocker 2-deoxy-D-glucose (2-DG). Treatment of BAEC with 2-DG (5 mM) for 24 hours or with low concentrations of H(2)O(2) (100 µM) induced autophagy, including increased conversion of microtubule-associated protein light chain 3 (LC3)-I to LC3-II, accumulation of GFP-tagged LC3 positive intracellular vacuoles, and increased fusion of autophagosomes with lysosomes. 2-DG-treatment also induced AMPK phosphorylation, which was blocked by either co-administration of two potent anti-oxidants (Tempol and N-Acetyl-L-cysteine) or overexpression of superoxide dismutase 1 or catalase in BAEC. Further, 2-DG-induced autophagy in BAEC was blocked by overexpressing catalase or siRNA-mediated knockdown of AMPK. Finally, pretreatment of BAEC with 2-DG increased endothelial cell viability after exposure to hypoxic stress. Thus, AMPK is required for ROS-triggered autophagy in endothelial cells, which increases endothelial cell survival in response to cell stress.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2011-02-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A Veterans Affairs Primary Care Same-Day Open Access for New Patients Optimized Redesigned System (VA-HONORS): A Six-Year Analysis of 22,220 Patient Records.

Roman, Maher / Clark, Ralph / Shirwany, Najeeb / Ani, Chizobam / Beeson, W Lawrence

Joint Commission journal on quality and patient safety

2020 Volume 47, Issue 3, Page(s) 190–197

Abstract: Background: Delay in primary care access for new patients to US Department of Veterans Affairs (VA) health care services has been a persistent problem. This article presents the evaluation of a quality improvement (QI) intervention that provided new ... ...

Abstract	Background: Delay in primary care access for new patients to US Department of Veterans Affairs (VA) health care services has been a persistent problem. This article presents the evaluation of a quality improvement (QI) intervention that provided new patients with same-day primary care access. It involved redesign of an intake clinic (IC) through which new patients were initially seen and referred to primary care. The redesign included changes in clinic flow and reallocation of two full-time primary care providers (PCPs) from IC to their primary care teams. Methods: A pre-post retrospective study evaluating a QI intervention at a VA hospital examined 22,220 administrative patient records. Specifically, 9,909 new patients seen in the three years prior to implementation of VA-HONORS (preintervention group) were compared with 12,311 patients seen in the three years after implementation (postintervention group). Study outcomes were (1) number of days to first appointment with PCP, (2) proportion of patients receiving same-day primary care access, and (3) visit cycle time. Results: Preintervention, median first primary care appointment delay was 96 days, compared to 0 days postintervention (p < 0.001). Preintervention, 3.1% of new patients were able to obtain same-day primary care appointment, compared with 91.5% postintervention (p < 0.001). Median visit cycle time was 140 minutes preintervention vs. 148 minutes postintervention (p < 0.001). Conclusions: New patients' same-day access system redesign at one VA hospital dramatically eliminated first primary care appointment delay. The redesign was feasible and sustainable for a sizable population and serves as a model for similar settings with new patients' primary care access delay.
MeSH term(s)	Access to Information ; Humans ; Primary Health Care ; Retrospective Studies ; United States ; United States Department of Veterans Affairs ; Veterans
Language	English
Publishing date	2020-10-24
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1189890-2
ISSN	1938-131X ; 1549-425X ; 1553-7250 ; 1070-3241 ; 1549-3741
ISSN (online)	1938-131X ; 1549-425X
ISSN	1553-7250 ; 1070-3241 ; 1549-3741
DOI	10.1016/j.jcjq.2020.10.004
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Article: The amyloid beta ion channel hypothesis of Alzheimer's disease.

Shirwany, Najeeb A / Payette, Daniel / Xie, Jun / Guo, Qing

Neuropsychiatric disease and treatment

2009 Volume 3, Issue 5, Page(s) 597–612

Abstract: Alzheimer's disease (AD) is a leading cause of chronic dementia in the US. Its incidence is increasing with an attendant increase in associated health care costs. Since its first description in a patient by Dr. Alois Alzheimer over a century ago, a large ...

Abstract	Alzheimer's disease (AD) is a leading cause of chronic dementia in the US. Its incidence is increasing with an attendant increase in associated health care costs. Since its first description in a patient by Dr. Alois Alzheimer over a century ago, a large body of biomedical literature has established a detailed clinical and molecular profile of this disorder. Amyloid beta peptide (Abeta; a 39-42 amino acid molecule) is the major component of senile plaques, the lesions that are one of the pathologic hallmarks of AD (Wong et al 1985). Although many aspects of the biology of amyloid beta have been investigated, several fundamental questions about how this peptide causes AD neuropathology remain unanswered. The key question is: How is Abeta toxic to cerebral neurons? Because plaques are extra-neuronal deposits, it is difficult to imagine a structural basis for their toxicity. As an interesting contrast the other pathognomonic feature of AD, neurofibrillary tangles, are intra-axonal structural anomalies that are composed of the hyperphosphorylated microtubule associated (MAP) protein, tau. This review will assess the current thinking that relates to a recent hypothesis of Abeta toxicity. In 1992, Hardy and Higgins reported findings that suggested a new and intriguing possibility. These authors found that Abeta peptides disrupt Ca(2+) homeostasis in neurons and increase intracellular Ca(2+) [Ca(2+)](i). This was corroborated by Mattson and his colleagues who demonstrated that Abeta exposure to human cortical neurons raised [Ca2(+)](i) (Mattson, Cheng et al 1992); (Hardy and Higgins 1992). Finally, Nelson Arispe's group at the NIH specifically investigated the possibility that Abeta peptides might function like Ca(2+) ion channels (Arispe et al 1993). This and several subsequent studies have laid the foundation for a novel idea: "Abeta peptides are, in part, toxic to neurons because they form aberrant ion channels in neuronal membranes and thereby disrupt neuronal homeostasis". In this review we shall critically examine this theory in light of classic and contemporary literature.
Language	English
Publishing date	2009-03-20
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2186503-6
ISSN	1178-2021 ; 1176-6328
ISSN (online)	1178-2021
ISSN	1176-6328
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Article: Acrylonitrile potentiates noise-induced hearing loss in rat.

Fechter, Laurence D / Gearhart, Caroline / Shirwany, Najeeb A

Journal of the Association for Research in Otolaryngology : JARO

2004 Volume 5, Issue 1, Page(s) 90–98

Abstract: Acrylonitrile, one of the 50 most commonly produced industrial chemicals, has recently been identified as a promoter of noise-induced hearing loss (NIHL). This agent has the potential to produce oxidative stress through multiple pathways. We hypothesize ... ...

Abstract	Acrylonitrile, one of the 50 most commonly produced industrial chemicals, has recently been identified as a promoter of noise-induced hearing loss (NIHL). This agent has the potential to produce oxidative stress through multiple pathways. We hypothesize that acrylonitrile potentiates NIHL as a consequence of oxidative stress. The objectives of this study were to characterize acrylonitrile exposure conditions that promote permanent NIHL in rats and determine the ability of this nitrile to produce auditory dysfunction by itself. Additionally, we sought to determine whether a spin-trap agent that can form adducts with ROS would protect against the effects of acrylonitrile. Acrylonitrile administration produced significant elevation in NIHL detected as a loss in compound action potential sensitivity. The effect was particularly robust for high-frequency tones and particularly when acrylonitrile and noise were given on repeated occasions. Acrylonitrile by itself did not disrupt threshold sensitivity. Administration of the spin-trap agent phenyl- N- tert-butylnitrone (PBN), given to rats prior to acrylonitrile and noise, did block the elevation of NIHL by acrylonitrile. However, PBN at the dose and time interval given was ineffective in protecting auditory function in subjects exposed to noise alone. The results suggest that oxidative stress may play a role in the promotion of NIHL by acrylonitrile.
MeSH term(s)	Acrylonitrile/toxicity ; Animals ; Auditory Threshold/drug effects ; Carcinogens/toxicity ; Hearing Loss, Noise-Induced/metabolism ; Hearing Loss, Noise-Induced/physiopathology ; Male ; Noise/adverse effects ; Oxidative Stress/drug effects ; Rats ; Rats, Long-Evans
Chemical Substances	Carcinogens ; Acrylonitrile (MP1U0D42PE)
Language	English
Publishing date	2004-03
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2021417-0
ISSN	1438-7573 ; 1525-3961
ISSN (online)	1438-7573
ISSN	1525-3961
DOI	10.1007/s10162-003-4028-8
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