Antioxidant Effects Of Curcumin Research Articles

Hepatoprotective and Nephroprotective Effect of Curcumin Against Copper Toxicity in Rats.

Curcumin is a natural anti-inflammatory and antioxidant with several potential health benefits. Although it has been examined in several metals toxicity studies, but its role in the protection against copper toxicity has not been investigated. In this study; the detoxification and antioxidant effect of curcumin were examined to determine its prophylactic/therapeutic role experimentally in rats. Forty albino rats were divided into five groups; control, CuSO4 (4mg/kg body weight), curcumin (80mg/kg body weight), curcumin post-treatment (CuSO4 for 15days followed by curcumin for the next 15days) and curcumin co-treatment (CuSO4 plus curcumin for 30days). All rats were treated orally by stomach tube for 30days/once a day. Changes were observed in hepatic marker enzymes such as: aspartate aminotransferase (AST), alanine transaminase-(ALT), alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT), besides the serum total protein, urea and creatinine. Concentration of liver and kidney antioxidants such as: catalase (CAT), superoxide dismutase (SOD), reduced glutathione-(GSH) and malondialdehyde(MDA) were measured. An increased in the activities of liver marker enzymes, urea, creatinine and the MDA contents were detected after exposure to CuSO4. Meanwhile, the activities of serum total protein, hepatic and renal antioxidants were decreased. Changes in all biochemical parameters were alleviated by the post-treatment and co-treatment of curcumin. Our finding suggests that the curcumin showed protective effects on CuSO4-induced hepatotoxicity and nephrotoxicity.

Effect of curcumin on aging retinal pigment epithelial cells.

Age-related macular degeneration (AMD) is now one of the leading causes of blindness in the elderly population. The antioxidative effects of curcumin on aging retinal pigment epithelial (RPE) cells are still unclear. We conducted an in vitro study to investigate the effects of curcumin on aging RPE cells. A pulsed H2O2 exposure aging model was adopted. Aging RPE cells were treated with curcumin 20 µM, 40 µM, and 80 µM. Apoptosis of RPE cells was analyzed by flow cytometry. The intracellular reactive oxygen species concentration was detected using a specific probe and apoptosis-associated proteins were detected by Western blot. Expression of oxidative biomarkers, including superoxide dismutase, maleic dialdehyde, and glutathione, was detected commercially available assay kits. Compared with normal cells, lower cell viability, higher apoptosis rates, and more severe oxidation status were identified in the aging RPE cell model. Curcumin improved cell viability and decreased apoptosis and oxidative stress. Further, curcumin had a significant influence on expression of apoptosis-associated proteins and oxidative stress biomarkers. In conclusion, treatment with curcumin was able to regulate proliferation, oxidative stress, and apoptosis in aging RPE cells. Accordingly, application of curcumin may be a novel strategy to protect against age-related change in AMD.

Evolution of availability of curcumin inside poly-lactic-co-glycolic acid nanoparticles: impact on antioxidant and antinitrosant properties.

PurposeCurcumin exhibits antioxidant properties potentially beneficial for human health; however, its use in clinical applications is limited by its poor solubility and relative instability. Nanoparticles exhibit interesting features for the efficient distribution and delivery of curcumin into cells, and could also increase curcumin stability in biological systems. There is a paucity of information regarding the evolution of the antioxidant properties of nanoparticle-encapsulated curcumin.MethodWe described a simple method of curcumin encapsulation in poly-lactic-co-glycolic acid (PLGA) nanoparticles without the use of detergent. We assessed, in epithelial cells and in an acellular model, the evolution of direct antioxidant and antinitrosant properties of free versus PLGA-encapsulated curcumin after storage under different conditions (light vs darkness, 4°C vs 25°C vs 37°C).ResultsIn epithelial cells, endocytosis and efflux pump inhibitors showed that the increased antioxidant activity of PLGA-encapsulated curcumin relied on bypassing the efflux pump system. Acellular assays showed that the antioxidant effect of curcumin was greater when loaded in PLGA nanoparticles. Furthermore, we observed that light decreased, though heat restored, antioxidant activity of PLGA-encapsulated curcumin, probably by modulating the accessibility of curcumin to reactive oxygen species, an observation supported by results from quenching experiments. Moreover, we demonstrated a direct antinitrosant activity of curcumin, enhanced by PLGA encapsulation, which was increased by light exposure.ConclusionThese results suggest that the antioxidant and antinitrosant activities of encapsulated curcumin are light sensitive and that nanoparticle modifications over time and with temperature may facilitate curcumin contact with reactive oxygen species. These results highlight the importance of understanding effects of nanoparticle maturation on an encapsulated drug’s activity.

Curcumin-mediated oxidative stress resistance in Caenorhabditis elegans is modulated by age-1, akt-1, pdk-1, osr-1, unc-43, sek-1, skn-1, sir-2.1, and mev-1

Curcumin (diferuloylmethane), a pharmacologically active substance derived from turmeric, exhibits anti-inflammatory, anticarcinogenic, and antioxidant properties. We examined the modulation of oxidative-stress resistance and associated regulatory mechanisms by curcumin in a Caenorhabditis elegans model. Our results showed that curcumin-treated wild-type C. elegans exhibited increased survival during juglone-induced oxidative stress compared with the control treatment. In addition, curcumin reduced the levels of intracellular reactive oxygen species in C. elegans. Moreover, curcumin induced the expression of the gst-4 and hsp-16.2 stress response genes. Lastly, our findings from the mechanistic study in this investigation suggest that the antioxidative effect of curcumin is mediated via regulation of age-1, akt-1, pdk-1, osr-1, unc-43, sek-1, skn-1, sir-2.1, and mev-1. Our study elucidates the diverse modes of action and signaling pathways that underlie the antioxidant activity exhibited by curcumin in vivo.

Dichotomous effect of caffeine, curcumin, and naringenin on genomic DNA of normal and diabetic subjects.

Nutraceutical compounds show antioxidant and prooxidant properties under stress conditions like cancer, diabetes, and other diseases. The objective of this study is to find the dichotomic behavior of caffeine, curcumin, and naringenin on DNA of diabetic and normal subjects in the presence and absence of copper, hydrogen peroxide, and complex of copper-hydrogen peroxide. Hydrogen peroxide releases hydroxyl free radicals (•OH) on oxidation of Cu (I) to Cu (II) through Fenton-type reaction to cause DNA damage. In the results, agarose gel electrophoretic pattern speculates the prooxidant effect of caffeine and antioxidant effect of curcumin on DNA in the presence of copper and hydrogen peroxide. UV-Vis spectral analysis shows hyperchromism on addition of DNA to caffeine, hypochromism with curcumin, and subtle changes with naringenin. The chosen nutraceuticals act as inducers and quenchers of oxidative free radicals arising from diabetes.

Neuroprotective and antioxidant effects of curcumin in a ketamine-induced model of mania in rats

Bipolar disorder (BD) is a chronic and debilitating illness characterized by recurrent manic and depressive episodes. Our research investigates the protective effects of curcumin, the main curcuminoid of the Indian spice turmeric, in a model of mania induced by ketamine administration in rats. Our results indicated that ketamine treatment (25mg/kg, for 8 days) induced hyperlocomotion in the open-field test and oxidative damage in prefrontal cortex (PFC) and hippocampus (HP), evaluated by increased lipid peroxidation and decreased total thiol content. Moreover, ketamine treatment reduced the activity of the antioxidant enzymes superoxide dismutase and catalase in the HP. Pretreatment of rats with curcumin (20 and 50mg/kg, for 14 days) or with lithium chloride (45mg/kg, positive control) prevented behavioral and pro-oxidant effects induced by ketamine. These findings suggest that curcumin might be a good compound for preventive intervention in BD, reducing the episode relapse and the oxidative damage associated with the manic phase of this disorder.

Curcumin and resveratrol act by different ways on NADPH oxidase activity and reactive oxygen species produced by equine neutrophils

In neutrophils (PMNs), superoxide anion (O2−), the first reactive oxygen species (ROS) produced to kill pathogenic agents, is generated by NADPH oxidase, an enzymatic complex formed by the translocation of cytosolic subunits to the membrane flavocytochrome b558. In horses, excessive activation of PMNs is often associated with deadly pathologies and the modulation of their ROS production by acting on NADPH oxidase is a prime target to manage inflammation. We developed a cell-free assay to measure the activity of equine NADPH oxidase assembled in vitro, in order to test the effects of natural or synthetic compounds on the enzyme activity or assembly. The cell-free assay was validated with diphenyleneiodonium chloride and Gp91ds-tat, two inhibitors largely described for human NADPH oxidase. The anti-oxidant effects of curcumin and resveratrol at final concentration ranging from 10−4 to 10−6 M were studied on whole cells by chemiluminescence (CL) and by cell-free assay, in which the molecule was added before or after the enzyme assembly. The CL assay demonstrated that curcumin efficiently inhibited the O2− production and easily entered into PMNs or interacted with their membrane. Cell-free assay showed that curcumin acted on the reconstitution of NADPH oxidase even at 10−5M, while resveratrol appeared to be an O2− scavenger rather than an inhibitor of NADPH oxidase activity, since it acted from outside the cell in CL and after the complex assembly in cell-free assay. By acting directly on NADPH oxidase, curcumin should be a good candidate for the treatment of acute or inflammatory diseases involving an excessive ROS production.

Anti-inflammatory and anti-oxidative effect of curcumin in connective tissue type mast cell

Curcumin in turmeric from rhizome of plant Curcuma longa was investigated on its anti-inflammatory effect with canine cutaneous mastocytoma mast cells. Though the degranulation induced by neuropeptide substance P, specific mast cell secregtagogue Compound 48/80 and immunoglobulin IgG were reached above 10%, curcumin reduced the release below 4.6% at 10μM without cytotoxicity. Inhibitory effect of curcumin on [Ca2+]i elevation was also confirmed. ROS induced by Compound 48/80 were evaluated with dichlorodihydrofluorescein diacetate (DCFH-DA), and were lowered by curcumin in dose dependent manner. Cell membrane lipid peroxidation was monitored with diphenyl-1-pyrenylphosphine (DPPP). Curcumin decreased cell membrane lipid peroxidation induced by arachidonic acid in the concentration above 0.01μM. Curcumin also inhibited the protein tyrosine- and threonine-phosphorylations around 33 and 45kDa, respectively. Taking these findings into consideration with the inhibitory effects on connective tissue type mast cell, there is a potential use to ameliorate inflammation-related chronic diseases.

Hypolipidemic and antioxidative effects of curcumin on blood parameters, humoral immunity, and jejunum histology in Hy-line hens.

Turmeric (Curcuma Longa Linn) is a medicinal plant that contains curcumin. There is a growing interest in using curcumin powder (CP) as feed additives for antioxidative and antimicrobial properties to improve human health. This study was conducted to determine the appropriate levels of CP on blood parameters, immunity, and histology of jejunum in hens. A total of 200, 58-wk-old Hy-line hens were randomly distributed into 4 treatments (0%, 0.5%, 1.5%, and 2.5% CP or 0, 5, 15, and 25 g/kg feed, respectively) with 5 replicates (10 birds each) for 8 weeks using the completely randomized design. Blood samples were taken from 2 birds per replicate at weeks 61 and 65 to evaluate blood parameters. On weeks 63 and 65, two birds from each replicate received 0.5 ml SRBC (25%) injection in breast muscle and 7 days later, blood samples were collected to evaluate total Ig, IgG, and IgM titers in serum. Two hens were sacrificed at week 65 for the histological study of jejunum. Curcumin reduced triglycerides at 1.5% and 2.5% and cholesterol and LDL at 2.5% (p<0.05). Improvement of total Ig and IgG titers after the 1(st) and 2(nd) injections were observed. Muscle thickness in jejunum increased (p<0.05) at 1.5% curcumin and the length and surface area of villus were enhanced as well. Our results demonstrate that curcumin can be used as an antioxidant at 1.5% and antilipidemic agent at 2.5% in diet.

Antioxidant Effect of Curcumin Against Microcystin- LR-Induced Renal Oxidative Damage in Balb/c Mice

Purpose: To investigate the effect of curcumin on microcystin-LR (MC-LR)- induced renal oxidative damage in Balb/c mice.Methods: 40 male Balb/c mice were assigned randomly to 4 groups each having 10 mice. One group served as normal (saline treated) while another group was used as curcumin control. The third group was given MC-LR and used as toxin control. The fourth group was pre-treated with curcumin (300 mg/kg body wt) given orally once daily for 14 days before interperitoneal injection (i.p) of MC-LR (75 &#956;g/kg body wt). Biochemical assays including serum creatinine, blood urea nitrogen (BUN), urinary glucose, gamma-glutamyl transferase (GGT) and catalase (CAT) levels were measured. Renal biochemical tests such as protein carbonyl contents and DNA-protein cross-links, glutathione peroxidase (GSH-Px) activity, glutathione (GSH) and lipid hydroperoxide (LOOH) were evaluated.Results: Serum creatinine, BUN, urinary glucose, GGT increased in mice treated with MC-LR, while creatinine clearance decreased compared to controls (p &lt; 0.001), indicating occurrence of tubular damage. There was increased protein carbonyl content and DNA-protein cross-links in the kidney homogenates of these mice. Curcumin administration significantly reversed these effects and attenuated the MC-LR-induced reduction in the activities of CAT, GPH-Px, GSH as well as the MC-LR-induced increases in plasma and kidney lipid hydroperoxide.Conclusion: These results indicate that curcumin possesses natural antioxidant properties that renders it a potent protective agent against renal oxidative damage mediated by microcystin-LR.Keywords: Antioxidants, Curcumin, Microcystin, Renal oxidative damage

Curcumin attenuates testicular damage, apoptotic germ cell death, and oxidative stress in streptozotocin‐induced diabetic rats

The present study was designed to examine the protective and antioxidative effects of curcumin (Cur) on streptozotocin (STZ) induced testicular damage, apoptotic germ cell death, and oxidative stress. Diabetes was induced by a single intraperitoneal injection of STZ (50 mg/kg). The rats in the Cur-treated group were given Cur (100 mg/kg) once a day intragastrik for 8 weeks starting 3 days prior to STZ injection. Cur treatment significantly decreased the elevated tissue malondialdehyde levels and increased the reduced superoxide dismutase, and glutathione peroxidase enzyme activities in testis tissues samples. The Cur-treated rats in the diabetic group showed an improved histological appearance and serum testosterone levels. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end-labeling and there was a rise in the expression of proliferating cell nuclear antigen in testis tissues of Cur-treated rats in the diabetic group. These results demonstrate that Cur attenuated testicular damage in diabetic rats by decreasing oxidative stress.

Curcumin-supplemented diets increase superoxide dismutase activity and mean lifespan in Drosophila

Curcumin is a polyphenolic bioactive compound in turmeric. We examined if antioxidant effects of curcumin are associated with lifespan extension in Drosophila. In this experiment, females and males of Drosophila were fed diets either containing no curcumin (C0) or supplemented with curcumin at 0.5 (C1) and 1.0 (C2) mg/g of diet. The levels of malondialdehyde (MDA), enzyme activity of superoxide dismutase (SOD), and expression of seven age-related genes in females and males were analyzed. We found that C1 and C2 increased mean lifespan by 6.2 % and 25.8 % in females, and by 15.5 % and 12.6 % in males, respectively. Meanwhile, C1 and C2 significantly decreased MDA levels and increased SOD activity in both genders. Diets C1 in females and C2 in males are effective in extending mean lifespan and improving levels of two physiological and biochemical measures related to aging in Drosophila. Lifespan extension of curcumin in Drosophila was associated with the up-regulation of Mn-SOD and CuZn-SOD genes, and the down-regulation of dInR, ATTD, Def, CecB, and DptB genes. The present results suggest that curcumin increases mean lifespan of Drosophila via regulating gene expression of the key enzyme SOD and reducing accumulation of MDA and lipid peroxidation. This study provided new insights for understanding the anti-aging mechanism of curcumin in Drosophila.

Curcumin Attenuates Cardiopulmonary Bypass-Induced Lung Oxidative Damage in Rats

Acute lung injury is a common complication after cardiopulmonary bypass (CPB). Oxidative damage greatly impacts CPB-induced lung ischemic pathogenesis and may represent a target for treatment. We aimed to investigate whether curcumin upregulates heme oxygenase 1 (HO-1) expression and ameliorates lung injury in a rat CPB model. A total of 80 male Sprague-Dawley rats were divided into 2 sets of 5 groups (n = 8 per group): sham; control (CPB); vehicle; low-dose curcumin (L-Cur); and high-dose curcumin (H-Cur). Animals were pretreated with a single intraperitoneal injection of vehicle, L-Cur (50 mg/kg), or H-Cur (200 mg/kg) 2 hours prior to CPB. Lung tissue, serum, and bronchoalveolar lavage fluid was harvested 2 or 24 hours postoperatively. In the control group, CPB-induced lung injury was confirmed by histopathologic examination and a significantly increased wet-to-dry lung weight ratio and pulmonary permeability index value was observed (P < .05 vs sham group). Cardiopulmonary bypass was associated with a marked rise in the level of malondialdehyde and myeloperoxidase and a fall in superoxide dismutase 2 and 24 hours after surgery (P < .05 vs sham group). Administration of curcumin ameliorated lung damage and reversed the oxidative stress markers in a partially dose-dependent manner (P < .05 vs vehicle group). Furthermore, HO-1 gene transcription and protein expression were elevated to a greater extent in the lungs after curcumin pretreatment compared with the vehicle pretreatment. Curcumin has the potential to provide protection from CPB-induced lung damage reflected in the expression of oxidative stress markers. The antioxidant effect of curcumin may be partly related to upregulation of HO-1.

Spinal muscular atrophy: An oxidative stress response counteracted with curcumin

Spinal muscular atrophy (SMA) is an autosomal recessive neurodegenerative disorder with specific damage of motor neurons leading to progressive muscle weakness. The role of oxidative damage in the neurodegenerative process in SMA has been proposed. Polyphenols, with their antioxidant effects, may be used in SMA patients. In this study, the association between oxidative stress and SMA was examined in fibroblast cell lines derived from two different SMA type I patients, one SMA type I carrier and one healthy subject. Reactive oxygen species content of SMA type I, SMA type I carrier, and healthy fibroblasts was compared, and then the antioxidant effect of curcumin was analyzed. Expression differences of the antioxidant genes of SMA type I and healthy cell lines were evaluated with real-time PCR array before and after curcumin treatment. Collectively, our results led us to consider oxidative stress and neuronal development process together within the pathogenesis of SMA, The use of antioxidants, such as curcumin, as a supplement may be an alternative in SMA therapy.

Cytotoxic Effects of Curcumin At Various Concentrations and Role of Curcumin on Lipid Peroxidation and Activities of Antioxidant Enzymes of the Rat Peripheral Blood Lymphocytes

Abstract 4933 Background:Curcumin (diferuloylmethane) is an active ingredient of turmeric and has been suggested to have antiproliferative, pro-oxidant and cytotoxic effects (Das R, Apoptosis 2008). Curcumin has also been shown to have antioxidant effects (Rastogi M, Free Radic Res 2008). Our aim was to assess the cytotoxic, pro-oxidant and antioxidant effects of curcumin on rat peripheral blood lymphocytes (RPL) in culture. Methods:Different concentrations of curcumin (0.325 μM, 0.65 μM, 1.3 μM) were analyzed for cytotoxic effects on rat peripheral lymphocytes. The cytotoxic effect of curcumin was assessed by measuring cell viability using Trypan blue exclusion assay. DNA damage by curcumin (at 0.65 μM) was confirmed by the COMET assay. The effect of curcumin (at 0.65 μM) on oxidation was assessed by measuring the activity of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and lipid peroxidation (LP) by spectrophotometry. RPLs were cultured for 72 hr in vitro. The pro-oxidant effect of curcumin was determined by comparing LP induction in control (PBS treated) vs curcumin treated RPLs. Parameters were measured at 0, 24 and 48 hrs of curcumin exposure. Reactive oxygen species (ROS) generated by treatment with FeCl3 (10 mM) and H2O2 (5 mM) (Fe/H) were used to demonstrate the ROS scavenging effect of curcumin. Lymphocyte cultures were treated with either Fe/H alone or in combination with Curcumin. Oxidation levels were assessed as described above at 0, 24, 48 hrs following exposure. Results:Cytotoxic effects were seen at different curcumin concentrations (Table 1). Viability of RPLs were 42% at 0.64 μM concentration vs 72% at 0.325 μM. 30% decrease in cell viability of RPLs were seen at 0.65 μM concentration compared to 0.325 μM. Hence, 0.65 μM concentration was used for further experiments. There was a significant increase in DNA damage in curcumin exposed lymphocytes at 48hr (table 2). There was a significant increase in LP in curcumin exposed RPLs compared to control lymphocytes. By contrast, there was no significant change in LP values in presence of Fe/H at all time points compared to control. There was a significant decrease in LP when RPL cultures were incubated with curcumin for 48 hr compared to 0 hr of incubation. There was significant increase in activities of SOD, catalase and GPx in presence of curcumin and Fe/H (table 3 and 4).Table 1:Cytotoxic effect of curcumin as demonstrated Trypan blue viability assay Cnt=controlLymphocyte cultureLymphocyte cell viability at 48 hr (%)Cnt84Curcumin 0.325 μM72Curcumin 0.65 μM42Curcumin 1.3 μM35Table 2:Cytotoxic effect of curcumin (at 0.65 μM) as demonstrated by % Tail DNA. Two sample t-test was used to calculate p value% tail DNA (mean ± SD)Cnt (at 48 hr) (n= 6)0.53 ± 0.71Curcumin exposed lymphocyte (at 48 hr) (n=4)32.96 ± 17.97Difference in % tail DNA between control and Curcumin at 48 hrsp = 0.0019Table 3:Activities of antioxidant enzymes- SOD, catalase, GPx and LP level in optical density (OD- mean of 3 set of cultures)Lymphocyte culture (C) ODOD at 0hrOD at 24hrOD at 48hrProoxidant Activity (n=3)Only curcuminLP0.03100.11300.08500.05067Antioxidant activity (n=3)PBS+ FeCl3+H2O2Curcumin. + FeCl3+H2O2LP0.02200.02500.01600.01266SOD0.05600.02300.05400.13333Catalase0.02000.09330.22300.0936GPx0.01200.03630.12330.2170Table 4:Comparisons for enzyme activities between cnt and curcumin. One way ANOVA test was used to derive p values.NS= no significantComparison of enzyme activities between Cnt and Curcumin (at 0, 24, 48 hr)Comparison of enzymes activities (in presence of curcumin and Fe/H) at various time pointsCnt- 0hrcnt-24hrcnt-48hr0-24 hr0-48 hrPro-oxidant effectLP<0.0001<0.0001<0.0002NSNSAntioxidant effectCulture+ Fe/H (control) Vs Curcumin. + Fe/HComparison of enzymes activities (in presence of Curcumin and Fe/H) at various time pointsLPNSNSNSNS0.0392SODNSNS<0.00280.0015<0.0006Catalase<0.0053<0.0001<0.00510.0009NSGPx<0.0249<0.0001<0.0001<0.0001<0.0001 Conclusions:Dose dependent cytotoxic and DNA damage effects of curcumin are seen in RPLs. Treatment with curcumin alone increases lipid peroxidation, However in the presence of oxidative stress, curcumin may act as an antioxidant (ROS scavenging effect) by stimulating activities of antioxidant enzyme and preventing lipid peroxidation. Disclosures:No relevant conflicts of interest to declare.

Antioxidative Effects of Curcumin and its Analogues against the Free-radical-induced Peroxidation of Linoleic Acid in Micelles

Antioxidative Effects of Curcumin and its Analogues against the Free-radical-induced Peroxidation of Linoleic Acid in Micelles

Antioxidative effects of curcumin, β-myrcene and 1,8-cineole against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced oxidative stress in rats liver

The aim of this study was to investigate the effectiveness of curcumin, β-myrcene (myrcene) and 1,8-cineole (cineole) on antioxidant defense system in rats given a persistent environmental pollutant (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD). Rats (n = 112) were divided randomly into 8 equal groups. One group was kept as control and given corn oil as carrier. TCDD was orally administered at the dose of 2 μg/kg/week. Curcumin, myrcene and cineole were orally administered at the doses of 100 mg/kg/day, 200 mg/kg/day and 100 mg/kg/ day, respectively, by gavages dissolved in corn oil with and without TCDD. The liver samples were taken from half of all rats on day 30 and from the remaining half on day 60 for the determination of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), glutathione peroxidase (GSH-Px) and CuZn-SOD levels by spectrophotometric method. The results indicated that although TCDD significantly (p ≤ 0.01) increased formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GSH-Px and CuZn-SOD in rats. In contrast, curcumin, myrcene and cineole significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels but decreased formation of TBARS. Additionally, the antioxidative effects of curcumin, myrcene and cineole were increased at day 60 compared to day 30. In the TCDD groups given curcumin, myrcene and cineole, oxidative stress decreased by time. In conclusion, curcumin, myrcene and cineole showed antioxidant activity and eliminated TCDD-induced oxidative stress in rats in a time-dependent manner.

Antioxidant effects of curcumin in spinal cord injury in rats

This experimental study was performed to investigate the benefit of curcumin via its antioxidant effect on spinal cord injury (SCI) in rats. Twenty-four adult Wistar albino rats were randomized into three groups. SCI was performed by the weight-drop model. Group 1 underwent laminectomy followed by SCI and received no medication. Group 2 underwent laminectomy followed by SCI and received curcumin (200 mg/kg/day orally). Group 3 underwent laminectomy followed by SCI and received methylprednisolone (30 mg/kg intraperitoneally). Twenty-four hours later, blood samples were obtained from all rats; serum superoxide dismutase (SOD) and malondialdehyde (MDA) levels were determined, and the obtained results were compared. SOD level in the curcumin group was higher than in the control group (p < 0.000) and methylprednisolone group (p < 0.012). MDA level in the curcumin group was lower than in the control group (p < 0.042). Similarly, the MDA level in the methylprednisolone group was lower than in the control group (p < 0.001). The results of the present study show that curcumin effectively protects the spinal cord tissues against oxidative damage.

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl(2), 12 micromol kg(-1) b.w. single intraperitoneal injection). Curcumin treatment (80 mg kg(-1) b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure.

Antioxidative effects of curcumin and its analogues against the free‐radical‐induced peroxidation of linoleic acid in micelles

Curcumin (1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione, 1) is a yellow ingredient isolated from turmeric (curcumin longa). Many health benefits have been claimed for curcumin, and these have generally been ascribed to its radical-trapping antioxidant properties. In order to find more active antioxidants with 1 as the lead compound, we synthesized curcumin analogues, i.e., 1,7-bis(3,4-dihydroxyphenyl)-1,6-heptadiene-3,5-dione (2), 1-(3,4-dihydroxyphenyl)-7-(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione (3), 1-(4-hydroxy-3-methoxyphenyl)-7-(4-hydroxyphenyl)-1,6-heptadiene-3,5-dione (4), 1,7-bis (4-hydroxyphenyl)-1,6-heptadiene-3,5-dione (5), 1,7-bis(3,4-dimethoxyphenyl)-1,6-heptadiene-3,5-dione (6), 1,7-bis(4-methoxyphenyl)-1,6-heptadiene-3,5-dione (7), and 1,7-diphenyl-1,6-heptadiene-3,5-dione (8). Antioxidative effects of curcumin and these analogues against the peroxidation of linoleic acid were studied in sodium dodecyl sulfate (SDS) and cetyltrimethylammonium bromide (CTAB) micelles. The peroxidation was initiated thermally by a water-soluble initiator 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH), and reaction kinetics were monitored by the formation of linoleic acid hydroperoxides. Kinetic analysis of the antioxidation process demonstrates that these compounds, except 6, 7 and 8, are effective antioxidants in micelles by H-atom abstraction from the phenolic groups. Compounds 2 and 3, which bear ortho-diphenoxyl functionality, possess significantly higher antioxidant activity than curcumin and other analogues, and the 4-hydroxy-3-methoxyphenyl group also plays an important role in the antioxidative activity. In addition, the synergistic antioxidant effect of these compounds with alpha-tocopherol (vitamin E) in micelles was also studied by following the formation of linoleic acid hydroperoxides and the consumption of alpha-tocopherol. It was found that these compounds could not synergistically interact with alpha-tocopherol in micelles.