The quantitative free radical scavenging capacity of curcumin and its demethoxy derivatives (demethoxycurcumin (Dmc) and bisdemethoxycurcumin (Bdmc)) and hydrogenated derivatives (tetrahydrocurcumin (THC), hexahydrocurcumin (HHC) and octahydrocurcumin (OHC)) towards 1,1-diphenyl-2-picryl hydrazyl (DPPH), nitric oxide radical (NO), hydroxyl radical (HO · ) and superoxide anion radical (O 2 · ) were investigated by electron paramagnetic resonance (EPR) spectroscopy. One mole of the hydrogenated derivatives scavenged about 4 mol of the DPPH radical, while curcumin and Dmc scavenged about 3 mol of the DPPH radical. Curcumin and THC showed moderate scavenging activity towards NO, yielding 200 mmol of NO scavenged per 1 mol of the scavenger. In contrast, curcumin and its derivatives showed very low scavenging activity towards HO · and O 2 · , yielding approximately only 3-12 mmol scavenged per 1 mol of the tested compounds. Our results suggest that curcumin and its derivatives principally act as chain breaking antioxidants rather than as direct free radical scavengers. Furthermore, we showed that the ortho-methoxyphenolic group and the heptadione linkage of these molecules greatly contributed to their DPPH and NO scavenging activity.Key words curcumin; electron paramagnetic resonance; free radical scavenger; spin trapping Curcumin [1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] is the primary biologically active constituent that is isolated from the spice, turmeric (Curcuma longa LINN). It shows various therapeutically beneficial activities, including anti-oxidant, anti-inflammatory, anti-cancer, and anti-viral activities 1,2) mediated through its interactions with several molecular targets such as enzymes, receptors, and transcription factors.3,4) As a potent anti-oxidant, several mechanisms have been proposed which describe the direct interaction of curcumin with reactive oxygen species (ROS) as well as its involvement in ROS-independent mechanisms (i.e., induction of antioxidant enzymes). 5,6) The structure-antioxidant activity relationship of curcumin and the compound it reduces has been demonstrated in both in vitro and in vivo models, for example, 1,1-diphenyl-2-picrylhydrazyl (DPPH) kinetic analysis, γ-radiolysis of rat liver microsomes, 7) 2,2′-azobis(2-amidinopropane)dihydrochloride (AAPH)-induced low density lipoprotein (LDL) oxidation, 8) AAPH-induced linoleic oxidation. 9) Lastly, the protective effects of curcumin on oxidative injury have been demonstrated in vivo in several animal diseases models. [10][11][12] Free radicals are normally formed by the physiological processes of the cell. For example superoxide anion radical (O 2 −· ) is produced during the mitochondrial respiratory chain reaction and the nitric oxide radical (NO) is generated by the activation of nitric oxide synthase. In some circumstances, the overproduction of those radicals, as well as the formation of toxic radicals such as the hydroxyl radical (HO · ) leads to the damage of biological molecules, thus resulting in many ...

IntroductionOxidative stress has been demonstrated in malaria. The potential oxidative modification of lipoproteins derived from malaria patients was studied. These oxidized lipids may have role in pathogenesis of malaria.MethodThe plasma lipid profile and existence of oxidized forms of very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) were investigated in malaria (17 mild and 24 severe patients) and 37 control subjects. Thiobarbituric acid reactive substances (TBARs), conjugated dienes, tryptophan fluorescence and fluidity of lipoproteins were determined as markers of oxidation. The biological effect of malarial lipoproteins was assessed by the expression of adhesion molecules on endothelial cells.ResultsMalarial lipoproteins had decreased cholesterol (except in VLDL) and phospholipid. The triglyceride levels were unchanged. The cholesterol/phospholipid ratio of LDL was decreased in malaria, but increased in VLDL and HDL. TBARs and conjugate dienes were increased in malarial lipoproteins, while the tryptophan fluorescence was decreased. The fluidity of lipoproteins was increased in malaria. These indicated the presence of oxidized lipoproteins in malaria by which the degree of oxidation was correlated with severity. Of three lipoproteins from malarial patients, LDL displayed the most pronounced oxidative modification. In addition, oxidized LDL from malaria patients increased endothelial expression of adhesion molecules.ConclusionIn malaria, the lipoproteins are oxidatively modified, and the degree of oxidation is related with severity. Oxidized LDL from malarial patients increases the endothelial expression of adhesion molecules. These suggest the role of oxidized lipoproteins, especially LDL, on the pathogenesis of disease.

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The potential of free radical formation in serum of beta-thalassemia/Hb E patients receiving a single oral dose of 25 mg/kg body weight of deferiprone, a bidentate orally active iron chelator, was evaluated using EPR/spin trapping technique. In the presence of ascorbic acid and tert-butylhydroperoxide, EPR signals of ascorbyl radical (aH=0.18 mT) and DMPO-carbon centred adduct (aH=2.37 mT, aN=1.65 mT) were detected. Shortly after deferiprone administration, EPR signal intensities decreased concomitant with an increase in serum levels of deferiprone. Unfortunately, enhanced EPR signal intensities were observed at 300 min after dosing in patients with serum molar ratio of deferiprone to iron less than 3, suggesting the formation of incomplete iron-deferiprone complexes and consequently free radical formation. To avoid adverse effects of deferiprone, a dosage regimen should be designed according to iron status of the patients and aimed at maintaining an adequate ratio of serum chelator-to-iron concentration.

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