東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Mitochondrial glutathione and calciu...

Lin, Lin.

FindBook

Google Book

Amazon

博客來

Mitochondrial glutathione and calcium regulation in cardiac myocytes: From oxidative stress to cardiomyopathy.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mitochondrial glutathione and calcium regulation in cardiac myocytes: From oxidative stress to cardiomyopathy./
作者:	Lin, Lin.
面頁冊數:	236 p.
附註:	Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1796.
Contained By:	Dissertation Abstracts International65-04B.
標題:	Health Sciences, Pharmacology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3130380

Mitochondrial glutathione and calcium regulation in cardiac myocytes: From oxidative stress to cardiomyopathy.
Lin, Lin.

Mitochondrial glutathione and calcium regulation in cardiac myocytes: From oxidative stress to cardiomyopathy. - 236 p.

Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1796.

Thesis (Ph.D.)--The University of Rochester, 2004.

Oxidative stress-induced cell death, caused by increased formation of reactive oxygen species and/or decreased antioxidant reserve, is implicated in the genesis of various cardiovascular abnormalities like heart failure. The most abundant cellular antioxidant, glutathione (GSH), has two major distinctively-regulated pools: cytosolic and mitochondrial GSH (cGSH and mGSH). We hypothesized that mGSH is more critical than cGSH in ameliorating oxidative stress-induced cell death. To test this hypothesis, we altered cGSH and mGSH levels in ventricular myocytes. H2O2 was used to induce oxidative stress in cultured neonatal rat ventricular myocytes. Prior to cell death, H2O 2 impaired mitochondrial respiration, depolarized the mitochondrial membrane potential (DeltaPsim), and translocated cytochrome c to the cytosol, suggesting the participation of mitochondria in this process. Interestingly, mGSH was decreased by H2O2 while no significant change in cGSH was observed. GSH monoethyl ester restored mGSH to control levels after H2O2. It also delayed the depolarization of DeltaPsim, abolished cytochrome c translocation and inhibited cell death. In contrast, N-acetylcysteine, which increased cGSH, had no effect on H2O2-induced damages. (R,S)-3-hydroxy-4-pentenoate (3HP) selectively diminished mGSH without significant changes in cGSH. Incubation of myocytes with 3HP prior to the H2O2 treatment accelerated the depolarization of DeltaPsim, released more cytochrome c and augmented cell death. Reducing cGSH level by L-buthionine-(S,R)-sulfoximine did not accentuate H2O2-induced cellular damages. In conclusion, an increase in mGSH protects while a decrease in mGSH potentiates cell death induced by H2O2. However, changes of cGSH show little effect on H2O2-induced cell death.Subjects--Topical Terms:

1017717
Health Sciences, Pharmacology.

Mitochondrial glutathione and calcium regulation in cardiac myocytes: From oxidative stress to cardiomyopathy.
LDR:03495nmm 2200277 4500 001 1861604
005 20041111122429.5
008 130614s2004 eng d
035 $a (UnM)AAI3130380
035 $a AAI3130380
040 $a UnM $c UnM
100 1 $a Lin, Lin. $3 907791
245 1 0 $a Mitochondrial glutathione and calcium regulation in cardiac myocytes: From oxidative stress to cardiomyopathy.
300 $a 236 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1796.
500 $a Supervisor: Shey-Shing Sheu.
502 $a Thesis (Ph.D.)--The University of Rochester, 2004.
520 $a Oxidative stress-induced cell death, caused by increased formation of reactive oxygen species and/or decreased antioxidant reserve, is implicated in the genesis of various cardiovascular abnormalities like heart failure. The most abundant cellular antioxidant, glutathione (GSH), has two major distinctively-regulated pools: cytosolic and mitochondrial GSH (cGSH and mGSH). We hypothesized that mGSH is more critical than cGSH in ameliorating oxidative stress-induced cell death. To test this hypothesis, we altered cGSH and mGSH levels in ventricular myocytes. H2O2 was used to induce oxidative stress in cultured neonatal rat ventricular myocytes. Prior to cell death, H2O 2 impaired mitochondrial respiration, depolarized the mitochondrial membrane potential (DeltaPsim), and translocated cytochrome c to the cytosol, suggesting the participation of mitochondria in this process. Interestingly, mGSH was decreased by H2O2 while no significant change in cGSH was observed. GSH monoethyl ester restored mGSH to control levels after H2O2. It also delayed the depolarization of DeltaPsim, abolished cytochrome c translocation and inhibited cell death. In contrast, N-acetylcysteine, which increased cGSH, had no effect on H2O2-induced damages. (R,S)-3-hydroxy-4-pentenoate (3HP) selectively diminished mGSH without significant changes in cGSH. Incubation of myocytes with 3HP prior to the H2O2 treatment accelerated the depolarization of DeltaPsim, released more cytochrome c and augmented cell death. Reducing cGSH level by L-buthionine-(S,R)-sulfoximine did not accentuate H2O2-induced cellular damages. In conclusion, an increase in mGSH protects while a decrease in mGSH potentiates cell death induced by H2O2. However, changes of cGSH show little effect on H2O2-induced cell death.
520 $a Dysregulation of mitochondrial Ca2+ uptake could result in disrupted excitation-contraction coupling and diminished energy production. Our laboratory has identified a mitochondrial ryanodine receptor (mRyR) responsible for rapid Ca2+ uptake. Ca2+ handling in heart mitochondria from hamsters with genetically inherited cardiomyopathy (CMP) was investigated. We observed the overexpression of mRyR in heart mitochondria from CMP hamsters by [3H]ryanodine binding and western blot. However, there was a significant decrease in mitochondrial Ca2+ uptake and the DeltaPsim of CMP hamster. Mitochondrial complex I and IV activities were also significantly reduced. Therefore, defects in the respiratory chain may lead to a lower DeltaPsim and ultimately an attenuated mitochondrial Ca2+ uptake.
590 $a School code: 0188.
650 4 $a Health Sciences, Pharmacology. $3 1017717
650 4 $a Biology, Cell. $3 1017686
690 $a 0419
690 $a 0379
710 2 0 $a The University of Rochester. $3 1249304
773 0 $t Dissertation Abstracts International $g 65-04B.
790 1 0 $a Sheu, Shey-Shing, $e advisor
790 $a 0188
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3130380