Immunotargeting of catalase to ACE or ICAM-1 protects perfused rat lungs against oxidative stress

Elena Nikolaevna Atochina-Vasserman, Irina V. Balyasnikova, Sergei M. Danilov, D. Neil Granger, Aron B. Fisher, Vladimir R. Muzykantov

Результат исследований: Материалы для журналаСтатья

87 Цитирования (Scopus)

Выдержка

The pulmonary endothelium is susceptible to oxidative insults. Catalase conjugated with monoclonal antibodies (MAbs) against endothelial surface antigens, angiotensin-converting enzyme (MAb 9B9) or intercellular adhesion molecule-1 (MAb 1A29), accumulates in the lungs after systemic injection in rats (V. Muzykantov, E. Atochina, H. Ischiropoulos, S. Danilov, and A. Fisher. Proc. Natl. Acad. Sci. USA 93: 5213-5218, 1996). The present study characterizes the augmentation of antioxidant defense by these antibody- catalase conjugates in isolated rat lungs perfused for 1 h with catalase conjugated with either MAb 9B9, MAb 1A29, or control mouse IgG. Approximately 20% of the injected dose of Ab-125I-catalase accumulated in the perfused rat lungs (vs. 125I-catalase). After elimination of nonbound material, the lungs were perfused further for 1 h with 5 mM hydrogen peroxide (H2O2). H2O2 induced an elevation in tracheal and pulmonary arterial pressures (126 ± 7 and 132 ± 5%, respectively, of the control level), lung wet-to-dry weight ratio (7.1 ± 0.4 vs. 6.0 ± 0.01 in the control lungs), and ACE release into the perfusate (436 ± 20 vs. 75 ± 7 mU in the control perfusates). Both MAb 9B9-catalase and MAb 1A29-catalase significantly attenuated the H2O2-induced elevation in 1) angiotensin-converting enzyme release to the perfusate (215 ± 14 and 217 ± 38 mU, respectively), 2) lung wet-to-dry ratio (6.25 ± 0.1 and 6.3 ± 0.3, respectively), 3) tracheal pressure (94 ± 4 and 101 ± 4%, respectively, of the control level), and 4) pulmonary arterial pressure (103 ± 3 and 104 ± 7%, respectively, of the control level). Nonconjugated catalase, nonconjugated antibodies, nonspecific IgG, and IgG-catalase conjugate had no protective effect, thus confirming the specificity of the effect of MAb-catalase. These results support a strategy of catalase immunotargeting for protection against pulmonary oxidative injury.

Язык оригиналаАнглийский
ЖурналAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Том275
Номер выпуска4 19-4
СостояниеОпубликовано - 1998
Опубликовано для внешнего пользованияДа

Отпечаток

Intercellular Adhesion Molecule-1
Catalase
Oxidative Stress
Lung
Immunoglobulin G
Peptidyl-Dipeptidase A
Pulmonary Edema
Arterial Pressure
Antibodies
Lung Injury
Surface Antigens
Hydrogen Peroxide
Endothelium
Antioxidants
Monoclonal Antibodies
Pressure
Weights and Measures
Injections

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)

Цитировать

Immunotargeting of catalase to ACE or ICAM-1 protects perfused rat lungs against oxidative stress. / Atochina-Vasserman, Elena Nikolaevna; Balyasnikova, Irina V.; Danilov, Sergei M.; Neil Granger, D.; Fisher, Aron B.; Muzykantov, Vladimir R.

В: American Journal of Physiology - Lung Cellular and Molecular Physiology, Том 275, № 4 19-4, 1998.

Результат исследований: Материалы для журналаСтатья

Atochina-Vasserman, Elena Nikolaevna ; Balyasnikova, Irina V. ; Danilov, Sergei M. ; Neil Granger, D. ; Fisher, Aron B. ; Muzykantov, Vladimir R. / Immunotargeting of catalase to ACE or ICAM-1 protects perfused rat lungs against oxidative stress. В: American Journal of Physiology - Lung Cellular and Molecular Physiology. 1998 ; Том 275, № 4 19-4.
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abstract = "The pulmonary endothelium is susceptible to oxidative insults. Catalase conjugated with monoclonal antibodies (MAbs) against endothelial surface antigens, angiotensin-converting enzyme (MAb 9B9) or intercellular adhesion molecule-1 (MAb 1A29), accumulates in the lungs after systemic injection in rats (V. Muzykantov, E. Atochina, H. Ischiropoulos, S. Danilov, and A. Fisher. Proc. Natl. Acad. Sci. USA 93: 5213-5218, 1996). The present study characterizes the augmentation of antioxidant defense by these antibody- catalase conjugates in isolated rat lungs perfused for 1 h with catalase conjugated with either MAb 9B9, MAb 1A29, or control mouse IgG. Approximately 20{\%} of the injected dose of Ab-125I-catalase accumulated in the perfused rat lungs (vs. 125I-catalase). After elimination of nonbound material, the lungs were perfused further for 1 h with 5 mM hydrogen peroxide (H2O2). H2O2 induced an elevation in tracheal and pulmonary arterial pressures (126 ± 7 and 132 ± 5{\%}, respectively, of the control level), lung wet-to-dry weight ratio (7.1 ± 0.4 vs. 6.0 ± 0.01 in the control lungs), and ACE release into the perfusate (436 ± 20 vs. 75 ± 7 mU in the control perfusates). Both MAb 9B9-catalase and MAb 1A29-catalase significantly attenuated the H2O2-induced elevation in 1) angiotensin-converting enzyme release to the perfusate (215 ± 14 and 217 ± 38 mU, respectively), 2) lung wet-to-dry ratio (6.25 ± 0.1 and 6.3 ± 0.3, respectively), 3) tracheal pressure (94 ± 4 and 101 ± 4{\%}, respectively, of the control level), and 4) pulmonary arterial pressure (103 ± 3 and 104 ± 7{\%}, respectively, of the control level). Nonconjugated catalase, nonconjugated antibodies, nonspecific IgG, and IgG-catalase conjugate had no protective effect, thus confirming the specificity of the effect of MAb-catalase. These results support a strategy of catalase immunotargeting for protection against pulmonary oxidative injury.",
keywords = "Angiotensin-converting enzyme, Endothelium, Hydrogen peroxide, Intercellular adhesion molecule-1",
author = "Atochina-Vasserman, {Elena Nikolaevna} and Balyasnikova, {Irina V.} and Danilov, {Sergei M.} and {Neil Granger}, D. and Fisher, {Aron B.} and Muzykantov, {Vladimir R.}",
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AU - Atochina-Vasserman, Elena Nikolaevna

AU - Balyasnikova, Irina V.

AU - Danilov, Sergei M.

AU - Neil Granger, D.

AU - Fisher, Aron B.

AU - Muzykantov, Vladimir R.

PY - 1998

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N2 - The pulmonary endothelium is susceptible to oxidative insults. Catalase conjugated with monoclonal antibodies (MAbs) against endothelial surface antigens, angiotensin-converting enzyme (MAb 9B9) or intercellular adhesion molecule-1 (MAb 1A29), accumulates in the lungs after systemic injection in rats (V. Muzykantov, E. Atochina, H. Ischiropoulos, S. Danilov, and A. Fisher. Proc. Natl. Acad. Sci. USA 93: 5213-5218, 1996). The present study characterizes the augmentation of antioxidant defense by these antibody- catalase conjugates in isolated rat lungs perfused for 1 h with catalase conjugated with either MAb 9B9, MAb 1A29, or control mouse IgG. Approximately 20% of the injected dose of Ab-125I-catalase accumulated in the perfused rat lungs (vs. 125I-catalase). After elimination of nonbound material, the lungs were perfused further for 1 h with 5 mM hydrogen peroxide (H2O2). H2O2 induced an elevation in tracheal and pulmonary arterial pressures (126 ± 7 and 132 ± 5%, respectively, of the control level), lung wet-to-dry weight ratio (7.1 ± 0.4 vs. 6.0 ± 0.01 in the control lungs), and ACE release into the perfusate (436 ± 20 vs. 75 ± 7 mU in the control perfusates). Both MAb 9B9-catalase and MAb 1A29-catalase significantly attenuated the H2O2-induced elevation in 1) angiotensin-converting enzyme release to the perfusate (215 ± 14 and 217 ± 38 mU, respectively), 2) lung wet-to-dry ratio (6.25 ± 0.1 and 6.3 ± 0.3, respectively), 3) tracheal pressure (94 ± 4 and 101 ± 4%, respectively, of the control level), and 4) pulmonary arterial pressure (103 ± 3 and 104 ± 7%, respectively, of the control level). Nonconjugated catalase, nonconjugated antibodies, nonspecific IgG, and IgG-catalase conjugate had no protective effect, thus confirming the specificity of the effect of MAb-catalase. These results support a strategy of catalase immunotargeting for protection against pulmonary oxidative injury.

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KW - Endothelium

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KW - Intercellular adhesion molecule-1

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