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Food constituents attenuate neurodeg...

Mazzio, Elizabeth Anne.

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Food constituents attenuate neurodegenerative processes in a Parkinson's disease model.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Food constituents attenuate neurodegenerative processes in a Parkinson's disease model./
Author:	Mazzio, Elizabeth Anne.
Description:	287 p.
Notes:	Major Professor: Natholyn Harris.
Contained By:	Dissertation Abstracts International60-08B.
Subject:	Biology, Neuroscience. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9942252
ISBN:	9780599437630

Food constituents attenuate neurodegenerative processes in a Parkinson's disease model.
Mazzio, Elizabeth Anne.

Food constituents attenuate neurodegenerative processes in a Parkinson's disease model. - 287 p.

Major Professor: Natholyn Harris.

Thesis (Ph.D.)--The Florida State University, 1999.

The etiology of neurodegeneration in Parkinson's disease is thought to involve oxidative stress, impaired mitochondrial activity, neuronal intracellular calcium (Ca+2i) overload, dopamine autoxidation, attenuation of reduced glutathione levels and immunological activity involving nitric oxide (NO) production in the substantia nigra pars compacta of the basal ganglia. The present study screened various dietary and pharmaceutical compounds for potential therapeutic value by acting on these systems. Compounds that suppressed NO production from lipopolysaccharide (LPS)/gamma-interferon (IFN-gamma) stimulated C6 astrocytoma cells with an IC50 less than 10-3 M include quercetin, (-)-epigallocatechin gallate, morin, curcumin, apigenin, sesamol, chlorogenic acid, fisetin, (+)-taxifolin, (+)-atechin, ellagic acid and caffeic acid. Compounds that reduced NO production with an IC50 less than 300 parts per million include milk thistle, silymarin, grapenol and green tea. Monoamine oxidase (MAO) in rat C6 astrocytoma cells was substantiated by dose dependent inhibition of enzyme activity by chlorgyline-HCl and L-deprenyl. Compounds that inhibit either C6 glial cell MAO enzyme activity or scavenge peroxide include chlorogenic acid, (+)-catechin, taxifolin, epigallo-catechin gallate (EGCG), fisetin, coenzyme Q0, curcumin, sesamol, morin, sesame oil, silymarin, green tea, rosemary leaf extract, ferulic acid, caffeic acid, rutin-hydrate, milk thistle (80% silymarin), grapenol, clove oil and shark cartilage. Plastic adhering PC12 cells (PA-PC12) underwent cell death with exposure to excitotoxins L-glutamate, quinolinic acid and NMDA (N-methyl-D-Aspartate). Excitotoxic cell death by NMDA and L-glutamate was blocked by NMDA antagonists kynurenic acid, 2-amino-5-phosphopentanoic acid (AP-5) and 7-chlorokynurenic acid. There was a concurrent rise in NO production and cNOS activity detected in the PA-PC12 cells in the presence of 15 mM L-glutamate and 1.5 MM CaCL2. Vulnerability to toxicity was corroborated by a significantly greater NMA receptor density Bmax = 8.06 pmol/mg protein in the PA-PC12 cell line, relative to Bmax = 0.163 pmol/mg protein in the original PC12 cell line. The effect of compounds tested against glutamate toxicity (15 mM) in PA-PC12 cells indicate protective effects by actinomycin D, coenzyme Q-0, coenzyme Q-10, L-deprenyl, N-acetyl-L-cysteine, nicotine and sesame oil. Compounds which attenuated cell toxicity from MPP+-HCl (5mM) were allopurinol, coenzyme Q-10, L-deprenyl, N-acetyl-L-cysteine, quinacrine and sesame oil.

ISBN: 9780599437630Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Food constituents attenuate neurodegenerative processes in a Parkinson's disease model.
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100 1 $a Mazzio, Elizabeth Anne. $3 1264949
245 1 0 $a Food constituents attenuate neurodegenerative processes in a Parkinson's disease model.
300 $a 287 p.
500 $a Major Professor: Natholyn Harris.
500 $a Source: Dissertation Abstracts International, Volume: 60-08, Section: B, page: 3860.
502 $a Thesis (Ph.D.)--The Florida State University, 1999.
520 $a The etiology of neurodegeneration in Parkinson's disease is thought to involve oxidative stress, impaired mitochondrial activity, neuronal intracellular calcium (Ca+2i) overload, dopamine autoxidation, attenuation of reduced glutathione levels and immunological activity involving nitric oxide (NO) production in the substantia nigra pars compacta of the basal ganglia. The present study screened various dietary and pharmaceutical compounds for potential therapeutic value by acting on these systems. Compounds that suppressed NO production from lipopolysaccharide (LPS)/gamma-interferon (IFN-gamma) stimulated C6 astrocytoma cells with an IC50 less than 10-3 M include quercetin, (-)-epigallocatechin gallate, morin, curcumin, apigenin, sesamol, chlorogenic acid, fisetin, (+)-taxifolin, (+)-atechin, ellagic acid and caffeic acid. Compounds that reduced NO production with an IC50 less than 300 parts per million include milk thistle, silymarin, grapenol and green tea. Monoamine oxidase (MAO) in rat C6 astrocytoma cells was substantiated by dose dependent inhibition of enzyme activity by chlorgyline-HCl and L-deprenyl. Compounds that inhibit either C6 glial cell MAO enzyme activity or scavenge peroxide include chlorogenic acid, (+)-catechin, taxifolin, epigallo-catechin gallate (EGCG), fisetin, coenzyme Q0, curcumin, sesamol, morin, sesame oil, silymarin, green tea, rosemary leaf extract, ferulic acid, caffeic acid, rutin-hydrate, milk thistle (80% silymarin), grapenol, clove oil and shark cartilage. Plastic adhering PC12 cells (PA-PC12) underwent cell death with exposure to excitotoxins L-glutamate, quinolinic acid and NMDA (N-methyl-D-Aspartate). Excitotoxic cell death by NMDA and L-glutamate was blocked by NMDA antagonists kynurenic acid, 2-amino-5-phosphopentanoic acid (AP-5) and 7-chlorokynurenic acid. There was a concurrent rise in NO production and cNOS activity detected in the PA-PC12 cells in the presence of 15 mM L-glutamate and 1.5 MM CaCL2. Vulnerability to toxicity was corroborated by a significantly greater NMA receptor density Bmax = 8.06 pmol/mg protein in the PA-PC12 cell line, relative to Bmax = 0.163 pmol/mg protein in the original PC12 cell line. The effect of compounds tested against glutamate toxicity (15 mM) in PA-PC12 cells indicate protective effects by actinomycin D, coenzyme Q-0, coenzyme Q-10, L-deprenyl, N-acetyl-L-cysteine, nicotine and sesame oil. Compounds which attenuated cell toxicity from MPP+-HCl (5mM) were allopurinol, coenzyme Q-10, L-deprenyl, N-acetyl-L-cysteine, quinacrine and sesame oil.
590 $a School code: 0071.
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Health Sciences, Nutrition. $3 1017801
690 $a 0317
690 $a 0570
710 2 $a The Florida State University. $3 1017727
773 0 $t Dissertation Abstracts International $g 60-08B.
790 $a 0071
790 1 0 $a Harris, Natholyn, $e advisor
791 $a Ph.D.
792 $a 1999
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9942252