Interaction of singlet oxygen with 5′-nucleotidase in rat hearts

Xiaolin Zhai, Xiaobo Zhou, Muhammad Ashraf

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

This study was aimed to determine whether singlet oxygen (1O2) attenuates 5′-nucleotidase activity in the ischemic myocardium. Isolated rat hearts were exposed to either exogenous 1O2 produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5′-nucleotidase activity was inhibited by exogenous 1O2 (3.74 ± 0.38 μmol/min/g dry weight), when compared with normal control (7.52 ± 0.41 μmol/min/g dry weight; P < 0.05). The enzymatic activity was significantly preserved by histidine (25 mM) - a 1O2 scavenger (7.04 ± 0.61 μmol/min/g dry weight; P < 0.05 v rose bengal group). After ischemia, the activity of ecto-5′-nucleotidase was greatly reduced (2.51 ± 0.25 μmol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5′-nucleotidase activity (6.55 ± 0.52 μmol/min/g dry weight, P < 0.05 v ischemic control). Adenosine release was consistent with ecto-5′-nucleotidase activity. The time course studies of effects of 1O2 on coronary flow, cardiac function, and LDH release revealed that the damage by 1O2 to ecto-5′-nucleotidase activity and adenosine release primarily accounted for impaired coronary now cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous 1O2 or ischemia was in parallel with ecto-5′-nucleotidase deactivation by 1O2. It is concluded that 1O2 causes inactivation of ecto-5′-nucleotidase and attenuation of adenosine release which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.

Original languageEnglish (US)
Pages (from-to)2453-2464
Number of pages12
JournalJournal of molecular and cellular cardiology
Volume27
Issue number11
DOIs
StatePublished - Jan 1 1995

Fingerprint

Singlet Oxygen
5'-Nucleotidase
Weights and Measures
Adenosine
Rose Bengal
Ischemia
Histidine
Lipid Peroxidation
Reperfusion
Reactive Oxygen Species
Myocardium
Wounds and Injuries

Keywords

  • 5'-nucleotidase
  • Adenosine
  • Ischemia/reperfusion
  • O
  • Rose bengal

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Cite this

Interaction of singlet oxygen with 5′-nucleotidase in rat hearts. / Zhai, Xiaolin; Zhou, Xiaobo; Ashraf, Muhammad.

In: Journal of molecular and cellular cardiology, Vol. 27, No. 11, 01.01.1995, p. 2453-2464.

Research output: Contribution to journalArticle

@article{6c4ca8f2556148089688e90275aae47a,
title = "Interaction of singlet oxygen with 5′-nucleotidase in rat hearts",
abstract = "This study was aimed to determine whether singlet oxygen (1O2) attenuates 5′-nucleotidase activity in the ischemic myocardium. Isolated rat hearts were exposed to either exogenous 1O2 produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5′-nucleotidase activity was inhibited by exogenous 1O2 (3.74 ± 0.38 μmol/min/g dry weight), when compared with normal control (7.52 ± 0.41 μmol/min/g dry weight; P < 0.05). The enzymatic activity was significantly preserved by histidine (25 mM) - a 1O2 scavenger (7.04 ± 0.61 μmol/min/g dry weight; P < 0.05 v rose bengal group). After ischemia, the activity of ecto-5′-nucleotidase was greatly reduced (2.51 ± 0.25 μmol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5′-nucleotidase activity (6.55 ± 0.52 μmol/min/g dry weight, P < 0.05 v ischemic control). Adenosine release was consistent with ecto-5′-nucleotidase activity. The time course studies of effects of 1O2 on coronary flow, cardiac function, and LDH release revealed that the damage by 1O2 to ecto-5′-nucleotidase activity and adenosine release primarily accounted for impaired coronary now cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous 1O2 or ischemia was in parallel with ecto-5′-nucleotidase deactivation by 1O2. It is concluded that 1O2 causes inactivation of ecto-5′-nucleotidase and attenuation of adenosine release which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.",
keywords = "5'-nucleotidase, Adenosine, Ischemia/reperfusion, O, Rose bengal",
author = "Xiaolin Zhai and Xiaobo Zhou and Muhammad Ashraf",
year = "1995",
month = "1",
day = "1",
doi = "10.1006/jmcc.1995.0233",
language = "English (US)",
volume = "27",
pages = "2453--2464",
journal = "Journal of Molecular and Cellular Cardiology",
issn = "0022-2828",
publisher = "Academic Press Inc.",
number = "11",

}

TY - JOUR

T1 - Interaction of singlet oxygen with 5′-nucleotidase in rat hearts

AU - Zhai, Xiaolin

AU - Zhou, Xiaobo

AU - Ashraf, Muhammad

PY - 1995/1/1

Y1 - 1995/1/1

N2 - This study was aimed to determine whether singlet oxygen (1O2) attenuates 5′-nucleotidase activity in the ischemic myocardium. Isolated rat hearts were exposed to either exogenous 1O2 produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5′-nucleotidase activity was inhibited by exogenous 1O2 (3.74 ± 0.38 μmol/min/g dry weight), when compared with normal control (7.52 ± 0.41 μmol/min/g dry weight; P < 0.05). The enzymatic activity was significantly preserved by histidine (25 mM) - a 1O2 scavenger (7.04 ± 0.61 μmol/min/g dry weight; P < 0.05 v rose bengal group). After ischemia, the activity of ecto-5′-nucleotidase was greatly reduced (2.51 ± 0.25 μmol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5′-nucleotidase activity (6.55 ± 0.52 μmol/min/g dry weight, P < 0.05 v ischemic control). Adenosine release was consistent with ecto-5′-nucleotidase activity. The time course studies of effects of 1O2 on coronary flow, cardiac function, and LDH release revealed that the damage by 1O2 to ecto-5′-nucleotidase activity and adenosine release primarily accounted for impaired coronary now cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous 1O2 or ischemia was in parallel with ecto-5′-nucleotidase deactivation by 1O2. It is concluded that 1O2 causes inactivation of ecto-5′-nucleotidase and attenuation of adenosine release which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.

AB - This study was aimed to determine whether singlet oxygen (1O2) attenuates 5′-nucleotidase activity in the ischemic myocardium. Isolated rat hearts were exposed to either exogenous 1O2 produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5′-nucleotidase activity was inhibited by exogenous 1O2 (3.74 ± 0.38 μmol/min/g dry weight), when compared with normal control (7.52 ± 0.41 μmol/min/g dry weight; P < 0.05). The enzymatic activity was significantly preserved by histidine (25 mM) - a 1O2 scavenger (7.04 ± 0.61 μmol/min/g dry weight; P < 0.05 v rose bengal group). After ischemia, the activity of ecto-5′-nucleotidase was greatly reduced (2.51 ± 0.25 μmol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5′-nucleotidase activity (6.55 ± 0.52 μmol/min/g dry weight, P < 0.05 v ischemic control). Adenosine release was consistent with ecto-5′-nucleotidase activity. The time course studies of effects of 1O2 on coronary flow, cardiac function, and LDH release revealed that the damage by 1O2 to ecto-5′-nucleotidase activity and adenosine release primarily accounted for impaired coronary now cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous 1O2 or ischemia was in parallel with ecto-5′-nucleotidase deactivation by 1O2. It is concluded that 1O2 causes inactivation of ecto-5′-nucleotidase and attenuation of adenosine release which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.

KW - 5'-nucleotidase

KW - Adenosine

KW - Ischemia/reperfusion

KW - O

KW - Rose bengal

UR - http://www.scopus.com/inward/record.url?scp=0028848203&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028848203&partnerID=8YFLogxK

U2 - 10.1006/jmcc.1995.0233

DO - 10.1006/jmcc.1995.0233

M3 - Article

C2 - 8596196

AN - SCOPUS:0028848203

VL - 27

SP - 2453

EP - 2464

JO - Journal of Molecular and Cellular Cardiology

JF - Journal of Molecular and Cellular Cardiology

SN - 0022-2828

IS - 11

ER -