Abstract:
:The anti-peroxidative activity of eugenol on Fe(2+)-ascorbate- and Fe(2+)-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 Fe(2+)-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 Fe(2+)-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 x 10(10) M-1 sec-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.
journal_name
Biochem Pharmacoljournal_title
Biochemical pharmacologyauthors
Nagababu E,Lakshmaiah Ndoi
10.1016/0006-2952(92)90318-dsubject
Has Abstractpub_date
1992-06-09 00:00:00pages
2393-400issue
11eissn
0006-2952issn
1873-2968pii
0006-2952(92)90318-Djournal_volume
43pub_type
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journal_title:Biochemical pharmacology
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