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Contribution of glucocorticoids and ...

Quadrilatero, Joe.

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Contribution of glucocorticoids and oxidative stress to intestinal lymphocyte apoptosis following strenuous endurance exercise in mice.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Contribution of glucocorticoids and oxidative stress to intestinal lymphocyte apoptosis following strenuous endurance exercise in mice./
Author:	Quadrilatero, Joe.
Description:	219 p.
Notes:	Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3096.
Contained By:	Dissertation Abstracts International66-06B.
Subject:	Health Sciences, Recreation. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR02942
ISBN:	0494029420

Contribution of glucocorticoids and oxidative stress to intestinal lymphocyte apoptosis following strenuous endurance exercise in mice.
Quadrilatero, Joe.

Contribution of glucocorticoids and oxidative stress to intestinal lymphocyte apoptosis following strenuous endurance exercise in mice. - 219 p.

Source: Dissertation Abstracts International, Volume: 66-06, Section: B, page: 3096.

Thesis (Ph.D.)--University of Waterloo (Canada), 2005.

Intestinal lymphocytes (IL) have an important role in the maintenance of intestinal and host defense against invading pathogens and cancer formation. Apoptosis (programmed cell death) is essential for the optimal function of the immune system since imbalance between excessive and inadequate apoptosis can lead to disease. Given the contribution of IL to gut mucosal immunity, the role of apoptosis in IL is important. It has been repeatedly demonstrated that intense exercise leads to a transient decline in lymphocyte numbers in several lymphoid compartments. This decline may contribute to the observed post-exercise immunosuppression seen in some athletes. Although it has been suggested that oxidative stress and glucocorticoids (GC) are involved in lymphocyte apoptosis with exercise, systematic testing of these mechanisms has not been conducted. Using a mouse model, the objectives of this thesis were to: (1) characterize several biochemical, cellular and molecular markers of apoptosis in IL following strenuous treadmill exercise, (2) determine the contribution of GC and oxidative stress to exercise-induced apoptosis and cell loss, and (3) determine whether provision of the antioxidant N-acetyl-L-cysteine (NAC) prevented exercise-induced apoptosis and loss of intestinal lymphocytes. Results from initial experiments showed that exercise led to a statistically significant reduction in total (p < 0.05) and CD3+ (p < 0.05) IL 24h after cessation of acute treadmill running. The IL loss was preceded by significant (p < 0.05) alterations in several hallmark features of apoptosis including phosphatidylserine externalization, mitochondrial membrane depolarization, decreased intracellular glutathione (GSH) levels and elevated pro-apoptotic caspase 3 and cytosolic cytochrome c as well as decreased anti-apoptotic Bcl-2 protein levels immediately following exercise. These exercise-associated changes in apoptosis were inhibited by the antioxidant NAC suggesting that oxidative stress plays a key role during exercise-induced apoptosis and cell loss. However, since GC can induce apoptosis via the generation of reactive oxygen species, the independent contribution of GC and oxidative stress (through increased aerobic metabolism) during exercise-induced lymphocyte apoptosis still remained unclear. Therefore, the direct contribution of GC during exercise-induced IL apoptosis and the contribution of oxidative stress, in the absence of GC, to exercise-induced IL apoptosis were examined. Mice were adrenalectomized (ADX) in order to remove endogenous GC and then given acute strenuous exercise. ADX in mice eliminated the exercise-induced elevation of GC but did not inhibit the hallmark features of IL apoptosis. (Abstract shortened by UMI.)

ISBN: 0494029420Subjects--Topical Terms:

1018003
Health Sciences, Recreation.

Contribution of glucocorticoids and oxidative stress to intestinal lymphocyte apoptosis following strenuous endurance exercise in mice.
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245 1 0 $a Contribution of glucocorticoids and oxidative stress to intestinal lymphocyte apoptosis following strenuous endurance exercise in mice.
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502 $a Thesis (Ph.D.)--University of Waterloo (Canada), 2005.
520 $a Intestinal lymphocytes (IL) have an important role in the maintenance of intestinal and host defense against invading pathogens and cancer formation. Apoptosis (programmed cell death) is essential for the optimal function of the immune system since imbalance between excessive and inadequate apoptosis can lead to disease. Given the contribution of IL to gut mucosal immunity, the role of apoptosis in IL is important. It has been repeatedly demonstrated that intense exercise leads to a transient decline in lymphocyte numbers in several lymphoid compartments. This decline may contribute to the observed post-exercise immunosuppression seen in some athletes. Although it has been suggested that oxidative stress and glucocorticoids (GC) are involved in lymphocyte apoptosis with exercise, systematic testing of these mechanisms has not been conducted. Using a mouse model, the objectives of this thesis were to: (1) characterize several biochemical, cellular and molecular markers of apoptosis in IL following strenuous treadmill exercise, (2) determine the contribution of GC and oxidative stress to exercise-induced apoptosis and cell loss, and (3) determine whether provision of the antioxidant N-acetyl-L-cysteine (NAC) prevented exercise-induced apoptosis and loss of intestinal lymphocytes. Results from initial experiments showed that exercise led to a statistically significant reduction in total (p < 0.05) and CD3+ (p < 0.05) IL 24h after cessation of acute treadmill running. The IL loss was preceded by significant (p < 0.05) alterations in several hallmark features of apoptosis including phosphatidylserine externalization, mitochondrial membrane depolarization, decreased intracellular glutathione (GSH) levels and elevated pro-apoptotic caspase 3 and cytosolic cytochrome c as well as decreased anti-apoptotic Bcl-2 protein levels immediately following exercise. These exercise-associated changes in apoptosis were inhibited by the antioxidant NAC suggesting that oxidative stress plays a key role during exercise-induced apoptosis and cell loss. However, since GC can induce apoptosis via the generation of reactive oxygen species, the independent contribution of GC and oxidative stress (through increased aerobic metabolism) during exercise-induced lymphocyte apoptosis still remained unclear. Therefore, the direct contribution of GC during exercise-induced IL apoptosis and the contribution of oxidative stress, in the absence of GC, to exercise-induced IL apoptosis were examined. Mice were adrenalectomized (ADX) in order to remove endogenous GC and then given acute strenuous exercise. ADX in mice eliminated the exercise-induced elevation of GC but did not inhibit the hallmark features of IL apoptosis. (Abstract shortened by UMI.)
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