scholarly journals Treatment by -acetylcysteine and melatonin increases cardiac baroreflex and improves antioxidant reserve

2004 ◽  
Vol 17 (10) ◽  
pp. 947-954 ◽  
Author(s):  
H GIROUARD ◽  
C DENAULT ◽  
C CHULAK ◽  
J DECHAMPLAIN
Keyword(s):  
Antioxidant Reserve

Anoxia-reoxygenation induced decrease of the antioxidant reserve in primary hepatocytes

1993 ◽  
Vol 15 (5) ◽  
pp. 535 ◽  
Author(s):  
V.E. Kagan ◽  
R. Goldman ◽  
D.A. Stoyanovsky ◽  
P. Caraceni ◽  
A.B. Borle
Keyword(s):  
Primary Hepatocytes ◽  
Antioxidant Reserve

Effect of triiodothyronine on reactive oxygen species generation by leukocytes, indices of oxidative damage, and antioxidant reserve

Metabolism ◽  
2000 ◽  
Vol 49 (6) ◽  
pp. 799-803 ◽  
Author(s):  
Cesar H. Magsino ◽  
Wael Hamouda ◽  
Husam Ghanim ◽  
Richard Browne ◽  
Ahmad Aljada ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Reserve

Dehydroepiandrosterone improves hepatic antioxidant reserve and stimulates Akt signaling in young and old rats

2011 ◽  
Vol 127 (3-5) ◽  
pp. 331-336 ◽  
Author(s):  
Maria Helena Vianna Metello Jacob ◽  
Daiane da Rocha Janner ◽  
Alex Sander da Rosa Araújo ◽  
Matheus Parmegiani Jahn ◽  
Luiz Carlos Rios Kucharski ◽  
...  
Keyword(s):  
Akt Signaling ◽  
Old Rats ◽  
Antioxidant Reserve

Ascorbic Acid Recycling Enhances the Antioxidant Reserve of Human Erythrocytes

Biochemistry ◽  
1995 ◽  
Vol 34 (39) ◽  
pp. 12721-12728 ◽  
Author(s):  
James M. May ◽  
Zhi-chao Qu ◽  
Richard R. Whitesell
Keyword(s):  
Ascorbic Acid ◽  
Human Erythrocytes ◽  
Antioxidant Reserve

Myocardial adaptation to ischemia by oxidative stress induced by endotoxin

1995 ◽  
Vol 269 (4) ◽  
pp. C907-C916 ◽  
Author(s):  
N. Maulik ◽  
M. Watanabe ◽  
D. Engelman ◽  
R. M. Engelman ◽  
V. E. Kagan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Antioxidant Defense ◽  
Ischemia Reperfusion ◽  
Antioxidant Defense System ◽  
Left Ventricular ◽  
Antioxidant Enzyme Activities ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Antioxidant Reserve

In this study, we examined the effects of oxidative stress adaptation on myocardial ischemic reperfusion injury. Oxidative stress was induced by injecting endotoxin (0.5 mg/kg) into the rat. After 24 h, rats were killed, hearts were isolated, and the effects of ischemia-reperfusion were studied using an isolated working heart preparation. The development of oxidative stress was examined by assessing malonaldehyde production in the heart. The antioxidant defense system was studied by estimating antioxidant enzyme activities and ascorbate- as well as thiol-dependent antioxidant reserve. The results of our study indicated that endotoxin induced oxidative stress within 1 h of treatment; the stress was reduced progressively and steadily up to 24 h. The antioxidant enzymes superoxide dismutase, catalase, glutathione (GSH) peroxidase, and GSH reductase were lowered up to 2 h and then increased. Both thiol- and ascorbate-dependent antioxidant reserve were enhanced, but the enhancement of the former was only transitory. After 24 h, endotoxin provided adequate protection to the heart from the ischemic-reperfusion injury, as evidenced by improved left ventricular function and aortic flow. Our results suggest that the induction of oxidative stress by endotoxin-induced adaptive modification of the antioxidant defense in the heart, thereby reducing ischemic-reperfusion injury.

Beneficial impact of term labor: Nonenzymatic antioxidant reserve in the human fetus

2003 ◽  
Vol 189 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Irina A. Buhimschi ◽  
Catalin S. Buhimschi ◽  
Marcos Pupkin ◽  
Carl P. Weiner
Keyword(s):  
Human Fetus ◽  
Beneficial Impact ◽  
Antioxidant Reserve ◽  
Term Labor

scholarly journals Comparison of antioxidant reserve capacity of children with acyanotic & cyanotic congenital heart disease

2020 ◽  
Vol 152 (6) ◽  
pp. 626
Author(s):  
HaleHatice Temel ◽  
Ulas Kumbasar ◽  
Esra Büber ◽  
Yasemin Aksoy ◽  
Sabanur Cavdar ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Congenital Heart ◽  
Cyanotic Congenital Heart Disease ◽  
Reserve Capacity ◽  
Antioxidant Reserve

Correlation between antioxidant changes during hypoxia and recovery on reoxygenation

1991 ◽  
Vol 261 (3) ◽  
pp. H632-H638 ◽  
Author(s):  
H. Dhaliwal ◽  
L. A. Kirshenbaum ◽  
A. K. Randhawa ◽  
P. K. Singal
Keyword(s):  
Contractile Function ◽  
Ultrastructural Changes ◽  
Resting Tension ◽  
Malondialdehyde Content ◽  
Function Recovery ◽  
Significant Depression ◽  
Endogenous Antioxidant ◽  
Improved Function ◽  
And Function ◽  
Antioxidant Reserve

Changes in myocardial antioxidants due to different durations of hypoxia at normal or lower temperatures were correlated with the recovery of structure and function on reoxygenation. Hearts perfused with substrate-free hypoxic buffer at 37 degrees C for 5 or 10 min and at 22 degrees C for 10 min showed a significant depression in the contractile function and rise in resting tension. Reoxygenation of these hearts at 37 degrees C for 20 min resulted in a recovery of these functions. On reoxygenation, hearts made hypoxic for 10 min at 37 degrees C showed poor recovery of the contractile function, increase in malondialdehyde content and a dramatic increase in the creatine phosphokinase activity in the coronary effluent. Addition of catalase to the perfusion medium markedly improved function recovery of these hearts. Hypoxia at 37 degrees C for 5 min or at 22 degrees C for 10 min with or without reoxygenation had no effect on superoxide dismutase (SOD) or glutathione peroxidase (GSHPx) activities. These antioxidants were depressed in hearts made hypoxic for 10 min at 37 degrees C with no further change on reoxygenation. Neither SOD nor GSHPx was detected in the coronary effluent during hypoxia or reoxygenation. Hypoxia at 37 or 22 degrees C for 10 min caused significant ultrastructural changes, and on reoxygenation 37 degrees C hypoxic hearts showed exacerbation, whereas the 22 degrees C hypoxic hearts showed recovery. These data support the hypothesis that reduced antioxidant reserve during hypoxia may contribute to the oxidative injury on reoxygenation, suggesting that maintenance of endogenous antioxidant levels during hypoxia may be important for recovery.

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