Inhibitory effect of eugenol on non-enzymatic lipid peroxidation in rat liver mitochondria

Nagababu Enika, N. Lakshmaiah

Research output: Contribution to journalArticle

Abstract

The anti-peroxidative activity of eugenol on Fe2+-ascorbate- and Fe2+-H2O2-induced lipid peroxidation was studied using rat liver mitochondria. Eugenol inhibited thiobarbituric acid reactive substance (TBARS) formation induced by both the systems in addition to oxygen uptake and mitochondrial swelling induced by Fe2+-ascorbate. Time course studies on TBARS formation indicated the ability of eugenol to inhibit initiation and propagation reactions. There was no measurable chemical modification of eugenol during the course of mitochondrial peroxidation by both the systems. Mitochondrial peroxidation by Fe2+-H2O2 was inhibited by hydroxyl radical (OH) scavengers like mannitol, benzoate, formate and dimethyl sulfoxide apart from eugenol. The OH scavenging ability of eugenol was evident from its inhibitory effect on OH-mediated deoxyribose degradation. The second-order rate constant for the reaction of OH with eugenol was about 4.8 × 1010 M-1sec-1. Eugenol reduced Fe3+ ions and Fe3+ chelated to citrate or ADP but it did not exhibit pro-oxidant activity in OH-mediated deoxyribose degradation. Incubation of mitochondria with eugenol resulted in the uptake of small but significant quantities of eugenol which inhibited subsequent lipid peroxidation by acting as a chain breaking antioxidant.

Original languageEnglish (US)
Pages (from-to)2393-2400
Number of pages8
JournalBiochemical Pharmacology
Volume43
Issue number11
DOIs
StatePublished - Jun 9 1992
Externally publishedYes

Fingerprint

Eugenol
Mitochondria
Liver Mitochondrion
Liver
Lipid Peroxidation
Rats
Lipids
Deoxyribose
formic acid
Thiobarbituric Acid Reactive Substances
Mitochondrial Swelling
Degradation
Time and motion study
Benzoates
Scavenging
Chemical modification
Mannitol
Dimethyl Sulfoxide
Citric Acid
Hydroxyl Radical

ASJC Scopus subject areas

  • Pharmacology

Cite this

Inhibitory effect of eugenol on non-enzymatic lipid peroxidation in rat liver mitochondria. / Enika, Nagababu; Lakshmaiah, N.

In: Biochemical Pharmacology, Vol. 43, No. 11, 09.06.1992, p. 2393-2400.

Research output: Contribution to journalArticle

Enika, Nagababu ; Lakshmaiah, N. / Inhibitory effect of eugenol on non-enzymatic lipid peroxidation in rat liver mitochondria. In: Biochemical Pharmacology. 1992 ; Vol. 43, No. 11. pp. 2393-2400.
@article{1f172e1a1f0e4c7b9604a6f789bc5211,
title = "Inhibitory effect of eugenol on non-enzymatic lipid peroxidation in rat liver mitochondria",
abstract = "The anti-peroxidative activity of eugenol on Fe2+-ascorbate- and Fe2+-H2O2-induced lipid peroxidation was studied using rat liver mitochondria. Eugenol inhibited thiobarbituric acid reactive substance (TBARS) formation induced by both the systems in addition to oxygen uptake and mitochondrial swelling induced by Fe2+-ascorbate. Time course studies on TBARS formation indicated the ability of eugenol to inhibit initiation and propagation reactions. There was no measurable chemical modification of eugenol during the course of mitochondrial peroxidation by both the systems. Mitochondrial peroxidation by Fe2+-H2O2 was inhibited by hydroxyl radical (OH) scavengers like mannitol, benzoate, formate and dimethyl sulfoxide apart from eugenol. The OH scavenging ability of eugenol was evident from its inhibitory effect on OH-mediated deoxyribose degradation. The second-order rate constant for the reaction of OH with eugenol was about 4.8 × 1010 M-1sec-1. Eugenol reduced Fe3+ ions and Fe3+ chelated to citrate or ADP but it did not exhibit pro-oxidant activity in OH-mediated deoxyribose degradation. Incubation of mitochondria with eugenol resulted in the uptake of small but significant quantities of eugenol which inhibited subsequent lipid peroxidation by acting as a chain breaking antioxidant.",
author = "Nagababu Enika and N. Lakshmaiah",
year = "1992",
month = "6",
day = "9",
doi = "10.1016/0006-2952(92)90318-D",
language = "English (US)",
volume = "43",
pages = "2393--2400",
journal = "Biochemical Pharmacology",
issn = "0006-2952",
publisher = "Elsevier Inc.",
number = "11",

}

TY - JOUR

T1 - Inhibitory effect of eugenol on non-enzymatic lipid peroxidation in rat liver mitochondria

AU - Enika, Nagababu

AU - Lakshmaiah, N.

PY - 1992/6/9

Y1 - 1992/6/9

N2 - The anti-peroxidative activity of eugenol on Fe2+-ascorbate- and Fe2+-H2O2-induced lipid peroxidation was studied using rat liver mitochondria. Eugenol inhibited thiobarbituric acid reactive substance (TBARS) formation induced by both the systems in addition to oxygen uptake and mitochondrial swelling induced by Fe2+-ascorbate. Time course studies on TBARS formation indicated the ability of eugenol to inhibit initiation and propagation reactions. There was no measurable chemical modification of eugenol during the course of mitochondrial peroxidation by both the systems. Mitochondrial peroxidation by Fe2+-H2O2 was inhibited by hydroxyl radical (OH) scavengers like mannitol, benzoate, formate and dimethyl sulfoxide apart from eugenol. The OH scavenging ability of eugenol was evident from its inhibitory effect on OH-mediated deoxyribose degradation. The second-order rate constant for the reaction of OH with eugenol was about 4.8 × 1010 M-1sec-1. Eugenol reduced Fe3+ ions and Fe3+ chelated to citrate or ADP but it did not exhibit pro-oxidant activity in OH-mediated deoxyribose degradation. Incubation of mitochondria with eugenol resulted in the uptake of small but significant quantities of eugenol which inhibited subsequent lipid peroxidation by acting as a chain breaking antioxidant.

AB - The anti-peroxidative activity of eugenol on Fe2+-ascorbate- and Fe2+-H2O2-induced lipid peroxidation was studied using rat liver mitochondria. Eugenol inhibited thiobarbituric acid reactive substance (TBARS) formation induced by both the systems in addition to oxygen uptake and mitochondrial swelling induced by Fe2+-ascorbate. Time course studies on TBARS formation indicated the ability of eugenol to inhibit initiation and propagation reactions. There was no measurable chemical modification of eugenol during the course of mitochondrial peroxidation by both the systems. Mitochondrial peroxidation by Fe2+-H2O2 was inhibited by hydroxyl radical (OH) scavengers like mannitol, benzoate, formate and dimethyl sulfoxide apart from eugenol. The OH scavenging ability of eugenol was evident from its inhibitory effect on OH-mediated deoxyribose degradation. The second-order rate constant for the reaction of OH with eugenol was about 4.8 × 1010 M-1sec-1. Eugenol reduced Fe3+ ions and Fe3+ chelated to citrate or ADP but it did not exhibit pro-oxidant activity in OH-mediated deoxyribose degradation. Incubation of mitochondria with eugenol resulted in the uptake of small but significant quantities of eugenol which inhibited subsequent lipid peroxidation by acting as a chain breaking antioxidant.

UR - http://www.scopus.com/inward/record.url?scp=0026643731&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026643731&partnerID=8YFLogxK

U2 - 10.1016/0006-2952(92)90318-D

DO - 10.1016/0006-2952(92)90318-D

M3 - Article

C2 - 1319160

AN - SCOPUS:0026643731

VL - 43

SP - 2393

EP - 2400

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

IS - 11

ER -