Cyperus rotundus (Family Cyperaceae) is used both as a functional food and as a drug In this study, the antioxidative potential of a hydroalcoholic extract of C rotundus (CRE) was evaluated by various antioxidant assays, including antioxidant capacity by the phosphomolybdenum method, total antioxidant activity in linoleic acid emulsion systems, 1,1-diphenyl-2-picrylhydrazyl (DPPH), superoxide, hydroxyl radicals, and nitric oxide (NO) scavenging We further evaluated the reducing potential of the extract as well as Fe(2+)/ascorbate-induced lipid peroxidation in rat liver homogenate These various antioxidant activities were compared to standard antioxidants such as butylated hydroxytoluene, tocopherol, L-ascorbic acid, and catechin Total phenolic and flavonoid content of CRE was also determined by a colorimetric method The extract exhibited high reduction capability and powerful free radical scavenging, especially against DPPH and superoxide anions as well as a moderate effect on NO CRE also showed inhibited lipid peroxidation in rat liver homogenate induced by Fe(2+)/ascorbate and prevented deoxyribose degradation in both non-site-specific and site-specific assays showing the hydroxyl radical scavenging and metal chelating activity of the hydroalcoholic extract Moreover, the peroxidation inhibiting activity of CRE was demonstrated in the linoleic acid emulsion system These results clearly established the antioxidative potency of C rotundus, which may account for some of the medical claims attributed to this plant

In vitro antioxidant and free radical scavenging activity of Cyperus rotundus.

1. Hydroxyl radicals (OH) are thought to be generated at sites of inflammation and to contribute to tissue damage. All anti-inflammatory drugs tested were able to scavenge ˙ OH generated in free solution at almost diffusion-controlled rates (rate constants about 1010 M−1 s−1).2. Much ˙ OH generation in vivo occurs at specific sites, where bound metal ions (such as Fe2+) react with H2O2 to produce ˙ OH that immediately attacks the site. Only ˙ OH scavengers that have sufficient metal-binding ability to withdraw metal ions from this site can protect against site-specific damage.3. All anti-inflammatory drugs tested were able to protect against site-specific damage by ˙ OH in a simple model system in vitro. Penicillamine, diclofenac sodium, piroxicam, azathioprine, primaquine, chloroquine and hydroxychloroquine were especially effective.4. The ability of an anti-inflammatory drug to protect against ˙ OH formation in vivo depends not only on its rate constant for reaction with ˙ OH, but also on its metal-bind...

The iron-binding and hydroxyl radical scavenging action of anti-inflammatory drugs

It is known that the visual loss in severe uveitis is due primarily to retinal tissue damage. In order to test the hypothesis that this damage may result from oxygen free radical-induced peroxidation of retinal membrane lipids, the generation of oxygen metabolites at the site of intraocular inflammation was investigated in an animal model of uveitis induced by retinal S-antigen. The effect of these metabolites on the initiation of retinal damage was characterized by histochemical, biochemical, morphologic, and morphometric methods. Light and electron microscopic studies at the early stage of the inflammation disclosed disorganization, degeneration, and necrosis of the photoreceptors and other retinal cells. Novel histochemical procedures demonstrated formation of superoxide and hydrogen peroxide at the site of uveoretinitis. Chemiluminescence measurements on uveoretinal tissue from these experimental animals revealed generation of superoxide anion and hydroxyl radicals. During the early phase of the uveoretinitis, concomitant with generation of the oxygen metabolites, there was peroxidation of retinal membrane lipids. The peroxidation products consisted of CD, MDA, hydroperoxides, and others. Associated with these changes was a selective depletion of the PUFA 22:6, decrease of which in the retinal composition has been shown to affect visual function. The morphologic and biochemical investigations clearly indicate that oxygen free radicals are generated at the site of uveoretinitis and that the retinal damage is mediated by peroxidation of lipids that are present in the retinal cell membranes. It would thus seem logical that such intraocular inflammation and the resultant retinal damage could be suppressed by antioxidant enzymes and oxygen free radical scavengers. These studies provide for the first time clear indication for developing new therapeutic agents that possess oxygen free radical scavenging properties, for treatment of human uveitis.

Role of oxygen free radicals in retinal damage associated with experimental uveitis.

The hydroxyl radical (.OH) -scavenging activity of d-2–[4–(3-methyl-2-thienyl)phenyl]propionic acid (M-5011), a novel nonsteroidal anti-inflammatory drug (NSAID), and that of several other NSAIDs were investigated by the hyaluronic acid (HA) degradation method and the electron spin resonance (ESR) spin-trapping technique. The superoxide anion (O2) -scavenging activity of M-5011 was also measured by the ESR technique. (1) M-5011 and the other NSAIDs examined inhibited the degradation of HA induced by the Fenton reaction system in a dose-dependent manner.(2) M-5011 and the other NSAIDs scavenged OH directly in a dose-dependent manner.(3) M-5011 was the most potent drug among the NSAIDs tested regarding the scavenging activity of OH as follows; M-5011 > indomethacin > ketoprofen = suprofen > aspirin. The OH-scavenging activity of M-5011 was potent in comparison with that of oxidized glutathione (GSSG), an endogenous OH scavenger.(4) M-5011 did not scavenge O2; nor did GSSG. These results suggest that M-5011 ...

Hydroxyl Radical Scavenging Activity of Nonsteroidal Anti-Inflammatory Drugs

New 3- and 4-hydroxyfuranones as anti-oxidants and anti-inflammatory agents.

A foot-pad oedema model was used to investigate the presence of free radicals using a chemiluminescence method. This model is an example of a cell mediated hypersensitivity reaction. Male rats were inoculated in the scruff with Freund's Complete Adjuvant (FCA) on Day 0 and then challenged 6 days later with FCA in one hind paw. An acute inflammatory reaction was initiated over the following 96 hours and within 4 hours of induction, reactive oxygen species were detected in the inflamed tissue. A peak of chemiluminescence activity was seen 8 hours after the induction of the inflammatory reaction, well before maximum oedema was observed. Using mannitol, catalase and DABCO to elucidate the nature of the reactive oxygen species it was found that hydroxyl radicals, hydrogen peroxide and singlet oxygen all contributed to this burst of oxidative activity and are therefore probably involved with the process of lipid peroxidation and the severity of an inflammatory reaction.

Free radical production at the site of an acute inflammatory reaction as measured by chemiluminescence

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Free radical production at the site of an acute inflammatory reaction as measured by chemiluminescence