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Hyperglycemia increases mitochondria...

University of Kansas., Pharmacology & Toxicology.

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Hyperglycemia increases mitochondrial protein expression in the absence of oxidative stress.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Hyperglycemia increases mitochondrial protein expression in the absence of oxidative stress./
Author:	Vasquez, Francisco E.
Description:	66 p.
Notes:	Adviser: Rick T. Dobrowsky.
Contained By:	Masters Abstracts International47-03.
Subject:	Health Sciences, Pharmacology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=1459922
ISBN:	9780549904182

Hyperglycemia increases mitochondrial protein expression in the absence of oxidative stress.
Vasquez, Francisco E.

Hyperglycemia increases mitochondrial protein expression in the absence of oxidative stress. - 66 p.

Adviser: Rick T. Dobrowsky.

Thesis (M.S.)--University of Kansas, 2008.

Long-term diabetes may cause diabetic peripheral neuropathy (DPN). Hyperglycemic-induced oxidative stress is widely accepted as the contributing factor in the development of diabetic complications. The mitochondrion has been singled out as the site of increased production of superoxide (O2-). Oxidative stress has been shown to be particularly deleterious to mitochondria because it is intimately associated with apoptosis. We utilized proteomics to study the effect chronic hyperglycemia may have on enriched Schwann Cell (SC) mitochondria. Through stable isotope labeling of amino acids in cell culture (SILAC) and mass spectrometry we were able to determine that chronic hyperglycemia induced an overexpression of proteins important in detoxification that occurred independently from oxidative stress. We conclude that the SCs under hyperglycemic stress react by increasing the levels of protective proteins to counter the influx of high glucose thus affording protection not only for itself but the crucial axon it enwraps.

ISBN: 9780549904182Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Hyperglycemia increases mitochondrial protein expression in the absence of oxidative stress.
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020 $a 9780549904182
035 $a (UMI)AAI1459922
035 $a AAI1459922
040 $a UMI $c UMI
100 1 $a Vasquez, Francisco E. $3 1023920
245 1 0 $a Hyperglycemia increases mitochondrial protein expression in the absence of oxidative stress.
300 $a 66 p.
500 $a Adviser: Rick T. Dobrowsky.
500 $a Source: Masters Abstracts International, Volume: 47-03, page: 1610.
502 $a Thesis (M.S.)--University of Kansas, 2008.
520 $a Long-term diabetes may cause diabetic peripheral neuropathy (DPN). Hyperglycemic-induced oxidative stress is widely accepted as the contributing factor in the development of diabetic complications. The mitochondrion has been singled out as the site of increased production of superoxide (O2-). Oxidative stress has been shown to be particularly deleterious to mitochondria because it is intimately associated with apoptosis. We utilized proteomics to study the effect chronic hyperglycemia may have on enriched Schwann Cell (SC) mitochondria. Through stable isotope labeling of amino acids in cell culture (SILAC) and mass spectrometry we were able to determine that chronic hyperglycemia induced an overexpression of proteins important in detoxification that occurred independently from oxidative stress. We conclude that the SCs under hyperglycemic stress react by increasing the levels of protective proteins to counter the influx of high glucose thus affording protection not only for itself but the crucial axon it enwraps.
590 $a School code: 0099.
650 4 $a Health Sciences, Pharmacology. $3 1017717
650 4 $a Health Sciences, Toxicology. $3 1017752
690 $a 0383
690 $a 0419
710 2 $a University of Kansas. $b Pharmacology & Toxicology. $3 1023919
773 0 $t Masters Abstracts International $g 47-03.
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790 1 0 $a Moskovitz, Jackob $e committee member
790 1 0 $a Staudinger, Jeff $e committee member
791 $a M.S.
792 $a 2008
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=1459922