Antioxidant Effects Of Curcumin Research Articles

Antiviral, anti-inflammatory and antioxidant effects of curcumin and curcuminoids in SH-SY5Y cells infected by SARS-CoV-2

COVID-19, caused by SARS-CoV-2, affects neuronal cells, causing several symptoms such as memory loss, anosmia and brain inflammation. Curcuminoids (Me08 e Me23) and curcumin (CUR) are derived from Curcuma Longa extract (EXT). Many therapeutic actions have been linked to these compounds, including antiviral action. Given the severe implications of COVID-19, especially within the central nervous system, our study aims to shed light on the therapeutic potential of curcuminoids against SARS-CoV-2 infection, particularly in neuronal cells. Here, we investigated the effects of CUR, EXT, Me08 and Me23 in human neuroblastoma SH-SY5Y. We observed that Me23 significantly decreased the expression of plasma membrane-associated transmembrane protease serine 2 (TMPRSS2) and TMPRSS11D, consequently mitigating the elevated ROS levels induced by SARS-CoV-2. Furthermore, Me23 exhibited antioxidative properties by increasing NRF2 gene expression and restoring NQO1 activity following SARS-CoV-2 infection. Both Me08 and Me23 effectively reduced SARS-CoV-2 replication in SH-SY5Y cells overexpressing ACE2 (SH-ACE2). Additionally, all of these compounds demonstrated the ability to decrease proinflammatory cytokines such as IL-6, TNF-α, and IL-17, while Me08 specifically reduced INF-γ levels. Our findings suggest that curcuminoid Me23 could serve as a potential agent for mitigating the impact of COVID-19, particularly within the context of central nervous system involvement.

Protective and anti-oxidative effects of curcumin and resveratrol on Aβ-oligomer-induced damage in the SH-SY5Y cell line

Alzheimer's disease (AD) is a degenerative disorder characterized by the loss of synapses and neurons in the brain, and results in the accumulation of amyloid-based neurotic plaques. Amyloid-β oligomers (AβO) are widely accepted as the main neurotoxin that induces oxidative stress and neuronal loss in AD. In this study, an oxidative stress model of the neuroblastoma SH-SY5Y cell line exposed to AβO was established to simulate an AD cell model. Exposure to AβO significantly reduced the viability of cultured SH-SY5Y cells (p < 0.05) and significantly increased intracellular reactive oxygen species (ROS) (p < 0.01). AβO exposure also induced oxidative stress in SH-SY5Y cells. Furthermore, AβO significantly increased the level of hyperphosphorylation of tau at sites T181 and T205 in SH-SY5Y cells (p < 0.01). Using edaravone, a free radical scavenger with neuroprotective properties, as the control, the possible protective and anti-oxidative effects of curcumin (40 μM) and resveratrol (20 μM) were evaluated. The results suggest that curcumin and resveratrol decreased ROS generation, attenuated oxidative stress, inhibited tau hyperphosphorylation, and protected SH-SY5Y cells from AβO damage. Both curcumin and resveratrol are promising supplements or medicine as therapeutic agents for the treatment of AD.

Curcumin Blocks High Glucose-Induced Podocyte Injury via RIPK3-Dependent Pathway.

Podocyte loss is well known to play a critical role in the early progression of diabetic nephropathy. A growing number of studies are paying attention to necroptosis, a programmed form of cell necrosis as a mechanism of podocyte loss. Although necroptosis is a recently established concept, the significance of receptor interacting serine/threonine kinase 3 (RIPK3), a gene that encodes for the homonymous enzyme RIPK3 responsible for the progression of necroptosis, is well studied. Curcumin, a natural hydrophobic polyphenol compound responsible for the yellow color of Curcuma longa, has drawn attention due to its antioxidant and anti-inflammatory effects on cells prone to necroptosis. Nonetheless, effects of curcumin on high glucose-induced podocyte necroptosis have not been reported yet. Therefore, this study investigated RIPK3 expression in high glucose-treated podocytes to identify the involvement of necroptosis via the RIPK3 pathway and the effects of curcumin treatment on RIPK3-dependent podocytopathy in a hyperglycemic environment. The study discovered that increased reactive oxygen species (ROS) in renal podocytes induced by high glucose was improved after curcumin treatment. Curcumin treatment also significantly restored the upregulated levels of VEGF, TGF-β, and CCL2 mRNAs and the downregulated level of nephrin mRNA in cultured podocytes exposed to a high glucose environment. High glucose-induced changes in protein expression of TGF-β, nephrin, and CCL2 were considerably reverted to their original levels after curcumin treatment. Increased expression of RIPK3 in high glucose-stimulated podocytes was alleviated by curcumin treatment as well as N-acetyl cysteine (NAC, an antioxidant) or GSK′872 (a RIPK3 inhibitor). Consistent with this, the increased necroptosis-associated molecules, such as RIPK3, pRIPK3, and pMLKL, were also restored by curcumin in high glucose-treated mesangial cells. DCF-DA assay confirmed that such a result was attributed to the reduction of RIPK3 through the antioxidant effect of curcumin. Further observations of DCF-DA-sensitive intracellular ROS in NAC-treated and GSK′872-treated podocyte groups showed a reciprocal regulatory relationship between ROS and RIPK3. The treatment of curcumin and GSK′872 in podocytes incubated with high glucose protected from excessive intracellular superoxide anion production. Taken together, these results indicate that curcumin treatment can protect against high glucose-induced podocyte injuries by suppressing the abnormal expression of ROS and RIPK3. Thus, curcumin might be a potential therapeutic agent for diabetic nephropathy as an inhibitor of RIPK3.

Antioxidant Actions of Thymoquinone, Silymarin, and Curcumin on Experimental Aortic Ischemia-Reperfusion Model in Wistar Albino Rats.

Medical improvements are needed to prevent ischemia-reperfusion injury in thoracoabdominal aortic surgery. The aim of this study was to determine the antioxidant effects of thymoquinone, silymarin, and curcumin against ischemia-reperfusion injury associated with abdominal aorta. Twenty-five Wistar albino rats were included in the study. Sham, control, and treatment (thymoquinone, silymarin, and curcumin) groups were set in equal numbers. Ischemia-reperfusion was applied by clamping (120 minutes) and de-clamping (60 minutes) the infrarenal aorta of all groups, except the sham group. Before reperfusion, thymoquinone, silymarin, and curcumin were given intraperitoneally to the treatment groups. After reperfusion, blood samples were taken from the right ventricle. Total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were studied in serum samples and histopathological examination was performed on the gastrocnemius muscle. There was a significant difference in TOS and OSI values between the control and sham groups. Both values were found higher in the control group than in the sham group (P<0.05). OSI values were found to be lower in the thymoquinone group compared to the control group (P<0.05). All three parameters were found to be lower in the silymarin group than in the control group (P<0.05). TAS and TOS levels were found to be higher in the curcumin group than in the control group (P<0.05). There was no histopathological difference between the groups. Silymarin and thymoquinone administration decreases oxidative stress in experimental aortic ischemia-reperfusion injury. Antioxidant effect of curcumin was lower than silymarin and thymoquinone.

Effect of curcumin on sperm parameters after the cryopreservation

ObjectiveCryopreservation refers to the cooling of cells and tissues to sub-zero temperatures in order to stop all biologic activity and preserve them for future use. Human sperm cryopreservation is an important tool for assisted reproductive technology and male fertility preservation. However, cryopreservation significantly reduces the quality of spermatozoa. The antioxidant effects of curcumin on different cells have been widely reported. This study was aimed to evaluate changes in post-thaw viability, morphology, motility, chromatin condensation and DNA integrity in response to the addition of curcumin to human sperm freezing extender. Materials and methodsSemen of 23 normozoospermic men was collected and each sample was divided into three equal aliquots: Control, DMSO, Curcumin. The samples were analyzed freshly for viability (Eosin Y), morphology (Diff-Quick), motility (following WHO standarts), sperm chromatin packaging (aniline blue) and DNA integrity (acridine orange). The control group remained untreated and was mixed with cryopreservation medium (in-house 1:1). The DMSO group was mixed with cryopreservation medium containing 0.1% DMSO. The curcumin group was mixed with cryopreservation medium containing 10 µM curcumin. Samples stained with Diff-Quick and aniline blue were examined under light microscope, samples stained with Eosin Y were examined under phase-contrast microscope and samples stained with acridine orange were examined under fluorescence microscope. Ten days after cryopreservation, samples were thawed and pre-freeze analyses repeated. ResultsObtained results showed that cryopreservation significantly (P < 0.001) reduces sperm parameters. In Curcumin group, progressive motility, sperm chromatin condensation and DNA integrity significantly (P < 0.001) increased after the thawing process, as compared with the control and the DMSO group. ConclusionThese results suggest that the addition of curcumin to cryopreservation medium improves post-thaw progressive motility, sperm chromatin condensation and DNA integrity. It seems that curcumin ameliorates detrimental effects of cryopreservation on human spermatozoa. Further research is needed on the use of curcumin and other antioxidant substances in sperm cryopreservation.

Indispensable role of mitochondria in maintaining the therapeutic potential of curcumin in acute kidney injury

Acute kidney injury (AKI) is a serious disease for which effective therapeutic agents are required. The capacity of curcumin (CUR) to resolve renal inflammation/oxidative stress and mitochondrial damage has been reported, but crosstalk between these effects and the consequence of this crosstalk remain elusive. In this study, a hypoxia/reoxygenation (H/R)‐induced renal tubular epithelial cell (TEC) injury model and an ischaemia/reperfusion (I/R)‐induced mouse AKI model were treated with CUR with or without mitochondrial inhibitors (rotenone and FCCP) or siRNA targeting mitochondrial transcription factor A (TFAM). Changes in mitochondrial function, inflammation, the antioxidant system and related pathways were analysed. In vitro, CUR suppressed NFκB activation and cytokine production and induced NRF2/HO‐1 signalling in TECs under H/R conditions. CUR treatment also reduced mitochondrial ROS (mtROS) and mitochondrial fragmentation and enhanced mitochondrial biogenesis, TCA cycle activity and ATP synthesis in damaged TECs. However, the anti‐inflammatory and antioxidant effects of CUR in damaged TECs were markedly abolished upon mitochondrial disruption. In vivo, CUR treatment improved renal function and antioxidant protein (NRF2 and SOD2) expression and reduced oxidative stress (8‐OHdG), tubular apoptosis/death, cytokine release/macrophage infiltration and mitochondrial damage in the kidneys of AKI mice. In vitro, the anti‐inflammatory and antioxidant effects of CUR in damaged kidneys were impaired when mitochondrial function was disrupted. These results suggest mitochondrial damage is a driving factor of renal inflammation and redox imbalance. The therapeutic capacity of CUR in kidneys with AKI is primarily dependent on mitochondrial mechanisms; thus, CUR is a potential therapy for various diseases characterized by mitochondrial damage.

Antioxidant Effect of Curcumin on the Prevention of Oxidative Damage to the Cochlea in an Ototoxic Rat Model Based on Malondialdehyde Expression.

Introduction Aminoglycoside, as an antimicrobial medication, also has side-effects on the inner ears, bringing about hearing disorders. Curcumin has been proven to be a strong scavenger against various reactive oxygen species (ROS), and the increase in ROS production is considered to play an important role in the process of hearing disorder. Objective To prove that curcumin is an effective antioxidant to prevent cochlear damage based on malondialdehyde (MDA) expression. Methods The present research used 32 Rattus norvegicus , of the Wistar lineage, randomly divided into 8 groups: negative control, ototoxic control (a single dose of 40 mg/ml of gentamicin via intratympanic injection), 2 groups submitted to ototoxic control + curcumin treatment (100 mg/kg, 200 mg/kg), 2 groups who iunderwent ototoxic control + curcumin treatment for 7 days, and two groups submitted to curcumin treatment as prevention for 3 days + ototoxic induction. Results The results showed that the lowest dosage of curcumin (100 mg/kg) could decrease MDA expression on the cochlear fibroblastic wall of the ototoxic model; however using greater doses of curcumin (200 mg/kg) for 7 days would provide a better effect. Curcumin could also significantly decrease MDA expression when it was administered during the preototoxic exposure. Conclusion Curcumin can be used as a therapy for ototoxic prevention based on the decrease in MDA expression.

The Antioxidant Effect of Curcumin and Rutin on Oxidative Stress Biomarkers in Experimentally Induced Periodontitis in Hyperglycemic Wistar Rats.

Background: There is a growing interest in the correlation between antioxidants and periodontal disease. In this study, we aimed to investigate the effect of oxidative stress and the impact of two antioxidants, curcumin and rutin, respectively, in the etiopathology of experimentally induced periodontitis in diabetic rats. Methods: Fifty Wistar albino rats were randomly divided into five groups and were induced with diabetes mellitus and periodontitis: (1) (CONTROL)—control group, (2) (DPP)—experimentally induced diabetes mellitus and periodontitis, (3) (DPC)—experimentally induced diabetes mellitus and periodontitis treated with curcumin (C), (4) (DPR)—experimentally induced diabetes mellitus and periodontitis treated with rutin (R) and (5) (DPCR)—experimentally induced diabetes mellitus and periodontitis treated with C and R. We evaluated malondialdehyde (MDA) as a biomarker of oxidative stress and reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG and catalase (CAT) as biomarkers of the antioxidant capacity in blood harvested from the animals we tested. The MDA levels and CAT activities were also evaluated in the gingival tissue. Results: The control group effect was statistically significantly different from any other groups, regardless of whether or not the treatment was applied. There was also a significant difference between the untreated group and the three treatment groups for variables MDA, GSH, GSSG, GSH/GSSG and CAT. There was no significant difference in the mean effect for the MDA, GSH, GSSG, GSH/GSSG and CAT variables in the treated groups of rats with curcumin, rutin and the combination of curcumin and rutin. Conclusions: The oral administration of curcumin and rutin, single or combined, could reduce the oxidative stress and enhance the antioxidant status in hyperglycemic periodontitis rats.

Antioxidative Effects of Curcumin on the Hepatotoxicity Induced by Ochratoxin A in Rats.

Ochratoxin A (OTA) is a powerful mycotoxin found in various foods and feedstuff, responsible for subchronic and chronic toxicity, such as nephrotoxicity, hepatotoxicity, teratogenicity, and immunotoxicity to both humans and several animal species. The severity of the liver damage caused depends on both dose and duration of exposure. Several studies have suggested that oxidative stress might contribute to increasing the hepatotoxicity of OTA, and several antioxidants, including curcumin (CURC), have been tested to counteract the toxic hepatic action of OTA in various classes of animals. Therefore, the present study was designed to evaluate the protective effect of CURC, a bioactive compound with different therapeutic properties on hepatic injuries caused by OTA in rat animal models. CURC effects were examined in Sprague Dawley rats treated with CURC (100 mg/kg), alone or in combination with OTA (0.5 mg/kg), by gavage daily for 14 days. At the end of the experiment, rats treated with OTA showed alterations in biochemical parameters and oxidative stress in the liver. CURC dosing significantly attenuated oxidative stress and lipid peroxidation versus the OTA group. Furthermore, liver histological tests showed that CURC reduced the multifocal lymphoplasmacellular hepatitis, the periportal fibrosis, and the necrosis observed in the OTA group. This study provides evidence that CURC can preserve OTA-induced oxidative damage in the liver of rats.

Hypolipidemic and Anti-Oxidant Effects of Curcumin in Dexamethasone-Induced Dyslipidemia in Rats

Hypolipidemic and Anti-Oxidant Effects of Curcumin in Dexamethasone-Induced Dyslipidemia in Rats

Adaptogenic effects of curcumin on depression induced by moderate and unpredictable chronic stress in mice

Curcumin has been investigated for the prevention and treatment of diseases due to its anti-oxidant, anti-inflammatory, immunomodulatory, and neuroprotective actions. This current study evaluated the adaptogenic effects of a subchronic oral administration of curcumin to Swiss mice that were submitted to a chronic unpredictable mild stress (CUMS) model of depression. Four groups of mice (vehicle control, CO; curcumin control, COC; CUMS + vehicle, CUMS; CUMS + curcumin, CUMSC) were evaluated for the biochemical parameters. The CUMS model caused depressive-like and anxiety-like behavior in the animals when they were viewed in the Forced Swimming Test and in the Elevated Plus Maze Test. The treatments with curcumin prevented the depressive-like behavior in the Forced Swimming Test and they had anxiolytic effects on the non-stressed animals. This was confirmed by the Elevated Plus Maze Test. Curcumin showed antioxidant effects (IC50 of 38.86 ± 1.78 μg/mL) in the in vitro DPPH (2,2-diphenyl-1-picryl-hydrozole) test. The compound also showed antioxidant effects in vivo, increasing the catalase (CAT) levels in the brains of the stressed animals. The biochemical analyses did not reveal potential renal and hepatic damage. Together, these results have demonstrated the antidepressant and antioxidant effects of curcumin, highlighting in this mice model, the compound’s novel adaptogenic potential.

Curcumin as adjuvant therapy to Meloxicam in treatment of patients with knee Osteoarthritis; Evaluation of antioxidant activity

Osteoarthritis (OA) is a chronic degenerative joint disease that doubled in prevalence since the mid of 20th century most commonly due to obesity and aging. Osteoarthritis can affect any joint in the body. The pathogenesis of OA is multifactorial influenced by range of biochemical and mechanical factors.&#x0D; Oxidative stress is described to play an important role in many diseases including OA. Accumulating evidences suggested the beneficial effect of anti-oxidants for reducing OA severity. Curcumin is a well-known antioxidant agent that acts by different mechanisms in modulating oxidative stress status. This study was designed to evaluate the antioxidant effect of curcumin as adjuvent therapy to a non-steroidal anti-inflammatory drug, meloxicam, in the management of knee osteoarthritis. This prospective open-labelled randomized controlled study was carried out on forty-two eligible patients who were allocated in two groups, serum superoxide dismutase 3 (SOD3) and glutathione reductase (GR) were measured at baseline and after 3 months of the study. Pain and physical function assessment were evaluated by oxford knee score (OKS). Results illustrated highly significant improvement in pain and physical function scores when curcumin used as adjuvant to meloxicam, also curcumin supplementation resulted in significant increase in SOD3 serum level and only a modest decrease in GR serum level when compared to meloxicam alone. In conclusion, this study demonstrated benefit of curcumin when used in combination with meloxicam over using meloxicam alone in modulating antioxidant parameters in blood, in addition to significantly improving pain and physical function after 3 months of treatment.

Curcumin as adjuvant therapy to Meloxicam in treatment of patients with knee Osteoarthritis; Evaluation of antioxidant activity

Osteoarthritis (OA) is a chronic degenerative joint disease that doubled in prevalence since the mid of 20th century most commonly due to obesity and aging. Osteoarthritis can affect any joint in the body. The pathogenesis of OA is multifactorial influenced by range of biochemical and mechanical factors. Oxidative stress is described to play an important role in many diseases including OA. Accumulating evidences suggested the beneficial effect of anti-oxidants for reducing OA severity. Curcumin is a well-known antioxidant agent that acts by different mechanisms in modulating oxidative stress status. This study was designed to evaluate the antioxidant effect of curcumin as adjuvent therapy to a non-steroidal anti-inflammatory drug, meloxicam, in the management of knee osteoarthritis. This prospective open-labelled randomized controlled study was carried out on forty-two eligible patients who were allocated in two groups, serum superoxide dismutase 3 (SOD3) and glutathione reductase (GR) were measured at baseline and after 3 months of the study. Pain and physical function assessment were evaluated by oxford knee score (OKS). Results illustrated highly significant improvement in pain and physical function scores when curcumin used as adjuvant to meloxicam, also curcumin supplementation resulted in significant increase in SOD3 serum level and only a modest decrease in GR serum level when compared to meloxicam alone. In conclusion, this study demonstrated benefit of curcumin when used in combination with meloxicam over using meloxicam alone in modulating antioxidant parameters in blood, in addition to significantly improving pain and physical function after 3 months of treatment.

Fast-dissolving antioxidant curcumin/cyclodextrin inclusion complex electrospun nanofibrous webs

Curcumin/Hydroxypropyl-beta-Cyclodextrin (HP-β-CyD) and Curcumin/Hydroxypropyl-gamma-Cyclodextrin (HP-γ-CyD) inclusion complex nanofibrous webs were produced using electrospinning technique for the purpose of orally fast-dissolving antioxidant food supplement. Curcumin was totally preserved without any loss during the electrospinning process. The aqueous solutions of curcumin/HP-β-CyD and curcumin/HP-γ-CyD were yielded uniform fiber morphology with ~200 nm and ~900 nm average fiber diameter, respectively. Both Curcumin/CyD webs were produced in the form of free-standing and flexible character. Curcumin is a natural bioactive compound with poor water-solubility, however, the phase solubility test and dissolution/disintegration tests (water and artificial saliva) revealed that the water-solubility of curcumin was prominently improved by inclusion complexation with CyD. The antioxidant effect of curcumin in Curcumin/CyD webs was also enhanced due to higher solubility of curcumin by CyD inclusion complex. The results showed that HP-γ-CyD is significantly more effective than HP-β-CyD in order to enhance the solubility and antioxidant property of curcumin in Curcumin/CyD webs.

Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway.

Pregnancy complications are associated with oxidative stress induced by accumulation of trophoblastic ROS in the placenta. We employed the human trophoblast HTR8/SVneo cell line to determine the effect of curcumin pre-treatment on H2O2-induced oxidative damage in HTR8/Sveo cells. Cells were pretreated with 2.5 or 5 μM curcumin for 24 h, and then incubated with 400 μM H2O2 for another 24 h. The results showed that H2O2 decreased the cell viability and induced excessive accumulation of reactive oxygen species (ROS) in HTR8/Sveo cells. Curcumin pre-treatment effectively protected HTR8/SVneo cells against oxidative stress-induced apoptosis via increasing Bcl-2/Bax ratio and decreasing the protein expression level of cleaved-caspase 3. Moreover, curcumin pre-treatment alleviated the excessive oxidative stress by enhancing the activity of antioxidative enzymes. The antioxidant effect of curcumin was achieved by activating Nrf2 and its downstream antioxidant proteins. In addition, knockdown of Nrf2 by Nrf2-siRNA transfection abolished the protective effects of curcumin on HTR8/SVneo cells against oxidative damage. Taken together, our results show that curcumin could protect HTR8/SVneo cells from H2O2-induced oxidative stress by activating Nrf2 signaling pathway.

Antioxidant effects of curcumin on the blood tissue in rats

Curcumin is a pigment found in Indian saffron spices, also known as turmeric. The aim of this study is to investigate the antioxidant effect of curcumin, a phytochemical, on the blood tissue of rats. In the study, 24 Wistar rats were 8 weeks old, randomly divided into 2 groups which were the control group and the experimental group was fed with curcumin supplement. Curcumin supplemented group was fed at 300mg/kg/day curcumin dissolved in corn oil by oral gavage for 12 days. 24 hours after the last feeding, TAC (Total Antioxidant Capacity) and TOC (Total Oxidant Capacity) were analyzed in blood samples. In curcumin supplemented group TAC decreased significantly than control group (p&amp;lt;0,05). When the TOC is examined, in curcumin supplemented group TOC was evaluated statistically higher than in the control group (p&amp;lt;0,05). Results of the study show that curcumin strengthens the antioxidant defense system.

Immunomodulatory, anti-inflammatory, and antioxidant effects of curcumin

Turmeric is a widely used spice derived from the rhizomes of Curcuma longa. Having been used as a dietary spice, it has drawn scientists’ attention to the possible medicinal benefits of its active compounds called curcuminoids which consist of curcumin, demethoxycurcumin and bisdemethoxycurcmin. Considering wide range of pharmacological properties that curcumin offers, numerous studies have investigated its potency as a therapeutic agent in various diseases such as autoimmune, cardiovascular, neoplastic, pulmonary, neurodegenerative and metabolic diseases. With regard to its wide array of health benefits and published data on the underlying mechanisms of its action, a complex interaction between three main events including inflammation, oxidative stress, and immunity, seems to contribute to different therapeutic roles of this compound. Hence, this review discusses the current knowledge on the anti-inflammatory, antioxidant, and immunomodulatory roles of curcumin with the hope of recruiting curcumin as a therapeutic agent in future therapeutic regimen in order to enhance the efficacy of the treatment, as well as decreasing the adverse effects of synthetic chemical drugs.

Hepatoprotective and antioxidant effect of curcumin on sleep deprived albino rats.

Hepatoprotective and antioxidant effect of curcumin on sleep deprived albino rats.

Antioxidant effect of curcumin against exposure to malathion in Cyprinus carpio.

The aim of this study was to determine protective effects of curcumin on oxidant/antioxidant parameters in Cyprinus carpio exposed to malathion. The fish were exposed to two sublethal concentrations of malathion (0.5 and 1 mg/L), and curcumin (100 mg per kg of fish weight) was simultaneously administered for 14 days. Malondialdehyde level and superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase activities were monitored in liver, kidney and gills, which were collected at the end of the experiment. The results revealed a significant increase in the malondialdehyde levels of the groups that were exposed to malathion. Also, malathion exposure caused a significant increase in superoxide dismutase, catalase, and glutathione-S-transferase activities and a significant decrease in glutathione peroxidase activity. Treatment with curcumin attenuated the malathion-induced oxidative stress by significantly decreasing the levels of malondialdehyde in the tissues. In addition, curcumin reversed the superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase activities. In conclusion, this study demonstrated that malathion caused oxidative stress and negative alterations on the antioxidant enzyme activities of the fish. However, this toxic effect was neutralised by the administration of curcumin.

Anti-oxidative effects of curcumin on immobilization-induced oxidative stress in rat brain, liver and kidney.

Restraint stress has been indicated to induce oxidative damage in tissues. Several investigations have reported that curcumin (CUR) may have a protective effect against oxidative stress. The present study was designed to investigate the protective effects of CUR on restraint stress induced oxidative stress damage in the brain, liver and kidneys. For chronic restraint stress, rats were kept in the restrainers for 1h every day, for 21 consecutive days. The animals received systemic administrations of CUR daily for 21days. In order to evaluate the changes of the oxidative stress parameters following restraint stress, the levels of malondialdehyde (MDA), reduced glutathione (GSH), as well as antioxidant enzyme activities superoxide dismutase (SOD) glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CAT) were measured in the brain, liver and kidney of rats after the end of restraint stress. The restraint stress significantly increased MDA level, but decreased the level of GSH and activists of SOD, GPx, GR, and CAT the brain, liver and kidney of rats in comparison to the normal rats (P<0.001). Intraperitoneal administration of CUR significantly attenuated oxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in the tissues versus the control group (P<0.05). This study shows that CUR can prevent restraint stress-induced oxidative damage in the brain, liver and kidney of rats and propose that CUR may be useful agents against oxidative stress in the tissues.