N-Allylsecoboldine as a novel antioxidant against peroxidative damage

Che Ming Teng, George Hsiao, Feng Nein Ko, Dong Tsamn Lin, Shoei Sheng Lee

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

N-Allylsecoboldine was evaluated for antioxidant properties by studying its ability to react with relevant reactive oxygen species, and its protective effect on human erythrocytes under oxidative stress. Using brain homogenates, we found that N-allylsecoboldine dose dependently inhibited lipid peroxidation (IC50 = 4.80 ± 0.16 μM) and markedly scavenged stable nitrogen-centered radicals. N-Allylsecoboldine was a very efficient scavenger for inhibiting peroxyl radical-mediated destruction of B-phycoerythrin, with a stoichiometry factor of 4.40 ± 0.59. It also trapped the hydroxyl radicals with a second-order rate constant of 6.92 ± 0.86 x 109 M-1 S-1. Additionally, human erythrocyte oxidative hemolysis induced by aqueous peroxyl radical or hydrogen peroxide was suppressed by N-allylsecoboldine. It not only attenuated the extent of lipid peroxidation but also decreased the formation of the high-molecular weight proteins and degradation of the band 6 protein in radical-treated erythrocytes. It also inhibited the shortening of Russell's viper venom-clotting time mediated by prelytic radical-treated erythrocytes. In the presence of exogenous oxidative stress, hemolysis and lipid peroxidation were significantly enhanced in β-thalassemic erythrocytes, as compared to the normal control. These elevated detrimental effects could be prevented by N-allylsecoboldine. It is concluded that N-allylsecoboldine may act as an effective antioxidant and protect cells against oxidative damage.

Original languageEnglish
Pages (from-to)129-139
Number of pages11
JournalEuropean Journal of Pharmacology
Volume303
Issue number1-2
DOIs
Publication statusPublished - May 6 1996
Externally publishedYes

Fingerprint

Antioxidants
Erythrocytes
Lipid Peroxidation
Hemolysis
Oxidative Stress
Phycoerythrin
Prothrombin Time
Hydroxyl Radical
Hydrogen Peroxide
Proteolysis
Inhibitory Concentration 50
N-allylsecoboldine
Reactive Oxygen Species
Nitrogen
Molecular Weight
Brain
Proteins
perhydroxyl radical

Keywords

  • β-Thalassemia
  • Antioxidant
  • Hydroxyl radical
  • Hypercoagulability
  • Lipid peroxidation
  • N-Allylsecoboldine
  • Oxidative hemolysis
  • Peroxyl radical

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

N-Allylsecoboldine as a novel antioxidant against peroxidative damage. / Teng, Che Ming; Hsiao, George; Ko, Feng Nein; Lin, Dong Tsamn; Lee, Shoei Sheng.

In: European Journal of Pharmacology, Vol. 303, No. 1-2, 06.05.1996, p. 129-139.

Research output: Contribution to journalArticle

Teng, Che Ming ; Hsiao, George ; Ko, Feng Nein ; Lin, Dong Tsamn ; Lee, Shoei Sheng. / N-Allylsecoboldine as a novel antioxidant against peroxidative damage. In: European Journal of Pharmacology. 1996 ; Vol. 303, No. 1-2. pp. 129-139.
@article{a5bcfbdd6c214660979c3f23d45d33c1,
title = "N-Allylsecoboldine as a novel antioxidant against peroxidative damage",
abstract = "N-Allylsecoboldine was evaluated for antioxidant properties by studying its ability to react with relevant reactive oxygen species, and its protective effect on human erythrocytes under oxidative stress. Using brain homogenates, we found that N-allylsecoboldine dose dependently inhibited lipid peroxidation (IC50 = 4.80 ± 0.16 μM) and markedly scavenged stable nitrogen-centered radicals. N-Allylsecoboldine was a very efficient scavenger for inhibiting peroxyl radical-mediated destruction of B-phycoerythrin, with a stoichiometry factor of 4.40 ± 0.59. It also trapped the hydroxyl radicals with a second-order rate constant of 6.92 ± 0.86 x 109 M-1 S-1. Additionally, human erythrocyte oxidative hemolysis induced by aqueous peroxyl radical or hydrogen peroxide was suppressed by N-allylsecoboldine. It not only attenuated the extent of lipid peroxidation but also decreased the formation of the high-molecular weight proteins and degradation of the band 6 protein in radical-treated erythrocytes. It also inhibited the shortening of Russell's viper venom-clotting time mediated by prelytic radical-treated erythrocytes. In the presence of exogenous oxidative stress, hemolysis and lipid peroxidation were significantly enhanced in β-thalassemic erythrocytes, as compared to the normal control. These elevated detrimental effects could be prevented by N-allylsecoboldine. It is concluded that N-allylsecoboldine may act as an effective antioxidant and protect cells against oxidative damage.",
keywords = "β-Thalassemia, Antioxidant, Hydroxyl radical, Hypercoagulability, Lipid peroxidation, N-Allylsecoboldine, Oxidative hemolysis, Peroxyl radical",
author = "Teng, {Che Ming} and George Hsiao and Ko, {Feng Nein} and Lin, {Dong Tsamn} and Lee, {Shoei Sheng}",
year = "1996",
month = "5",
day = "6",
doi = "10.1016/0014-2999(96)00102-1",
language = "English",
volume = "303",
pages = "129--139",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - N-Allylsecoboldine as a novel antioxidant against peroxidative damage

AU - Teng, Che Ming

AU - Hsiao, George

AU - Ko, Feng Nein

AU - Lin, Dong Tsamn

AU - Lee, Shoei Sheng

PY - 1996/5/6

Y1 - 1996/5/6

N2 - N-Allylsecoboldine was evaluated for antioxidant properties by studying its ability to react with relevant reactive oxygen species, and its protective effect on human erythrocytes under oxidative stress. Using brain homogenates, we found that N-allylsecoboldine dose dependently inhibited lipid peroxidation (IC50 = 4.80 ± 0.16 μM) and markedly scavenged stable nitrogen-centered radicals. N-Allylsecoboldine was a very efficient scavenger for inhibiting peroxyl radical-mediated destruction of B-phycoerythrin, with a stoichiometry factor of 4.40 ± 0.59. It also trapped the hydroxyl radicals with a second-order rate constant of 6.92 ± 0.86 x 109 M-1 S-1. Additionally, human erythrocyte oxidative hemolysis induced by aqueous peroxyl radical or hydrogen peroxide was suppressed by N-allylsecoboldine. It not only attenuated the extent of lipid peroxidation but also decreased the formation of the high-molecular weight proteins and degradation of the band 6 protein in radical-treated erythrocytes. It also inhibited the shortening of Russell's viper venom-clotting time mediated by prelytic radical-treated erythrocytes. In the presence of exogenous oxidative stress, hemolysis and lipid peroxidation were significantly enhanced in β-thalassemic erythrocytes, as compared to the normal control. These elevated detrimental effects could be prevented by N-allylsecoboldine. It is concluded that N-allylsecoboldine may act as an effective antioxidant and protect cells against oxidative damage.

AB - N-Allylsecoboldine was evaluated for antioxidant properties by studying its ability to react with relevant reactive oxygen species, and its protective effect on human erythrocytes under oxidative stress. Using brain homogenates, we found that N-allylsecoboldine dose dependently inhibited lipid peroxidation (IC50 = 4.80 ± 0.16 μM) and markedly scavenged stable nitrogen-centered radicals. N-Allylsecoboldine was a very efficient scavenger for inhibiting peroxyl radical-mediated destruction of B-phycoerythrin, with a stoichiometry factor of 4.40 ± 0.59. It also trapped the hydroxyl radicals with a second-order rate constant of 6.92 ± 0.86 x 109 M-1 S-1. Additionally, human erythrocyte oxidative hemolysis induced by aqueous peroxyl radical or hydrogen peroxide was suppressed by N-allylsecoboldine. It not only attenuated the extent of lipid peroxidation but also decreased the formation of the high-molecular weight proteins and degradation of the band 6 protein in radical-treated erythrocytes. It also inhibited the shortening of Russell's viper venom-clotting time mediated by prelytic radical-treated erythrocytes. In the presence of exogenous oxidative stress, hemolysis and lipid peroxidation were significantly enhanced in β-thalassemic erythrocytes, as compared to the normal control. These elevated detrimental effects could be prevented by N-allylsecoboldine. It is concluded that N-allylsecoboldine may act as an effective antioxidant and protect cells against oxidative damage.

KW - β-Thalassemia

KW - Antioxidant

KW - Hydroxyl radical

KW - Hypercoagulability

KW - Lipid peroxidation

KW - N-Allylsecoboldine

KW - Oxidative hemolysis

KW - Peroxyl radical

UR - http://www.scopus.com/inward/record.url?scp=0030015303&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030015303&partnerID=8YFLogxK

U2 - 10.1016/0014-2999(96)00102-1

DO - 10.1016/0014-2999(96)00102-1

M3 - Article

C2 - 8804921

AN - SCOPUS:0030015303

VL - 303

SP - 129

EP - 139

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1-2

ER -