Sensorimotor performance deficits induced by chronic chlorpyrifos exposure in Wistar rats: mitigative effect of vitamin C

This study was aimed at evaluating the ameliorative effect of vitamin C on chlorpyrifos-induced sensorimotor changes involving postural reflex, limb placing, and vibrissae touch in Wistar rats. Forty adult Wistar rats of either sex were divided into 4 groups of 10 animals in each group. Group I was administered soya oil (2?mL?kg^?1) while group II was given vitamin C (100?mg?kg^?1); group III was dosed with chlorpyrifos (10.6?mg?kg^?1, i.e. ～1/8th of the LD₅₀); group IV was administered vitamin C (100?mg?kg^?1) and then exposed to chlorpyrifos (10.6?mg?kg^?1), 30?min later. The regimens were administered by gavage once daily for a period of 17 weeks. Neurobehavioral parameters involving postural reflex, limb placing, and vibrissae touch responses measured at various intervals revealed a deficit in postural reflex, limb placing, and vibrissae touch responses in the CPF group, which was mitigated by vitamin C pretreatment. The neuronal and glial cell degeneration, increased brain malonaldehyde concentration, and decrease in superoxide dismutase, catalase, and acetylcholinesterase activities recorded in the group given chlorpyrifos were ameliorated by vitamin C. Therefore, vitamin C was shown to mitigate chlorpyrifos-induced sensorimotor deficits partly due to its antioxidant and acetylcholinesterase restoration properties.     

Comparative changes in absorption,distribution and toxicity of copper and cadmium chloride in toads during the hibernation and the role of vitamin C against their toxicity

The aim of this study was to determine the bioavailability and adverse effects of cadmium (Cd) and copper (Cu) on hibernating Egyptian toads and whether ascorbic acid (vitamin C) blocked Cd- and Cu-induced effects during hibernation. The oxidative status of liver, kidney, and intestine of Bufo regularis to Cd, Cu, and/or a combination of both metals administered orally for 2 weeks was determined. In the protection studies, vitamin C was given for 1?h prior to administration of Cu, Cd, and/or metal combination for 2 weeks. Treatment with Cu, Cd, and a combination of both metals produced a reduction in red blood count cells and hemoglobin content, while white blood count cells showed an increase in numbers during these treatments. After 2 weeks exposure, Cd and Cu increased significantly in all the tissues studied. Cu storage presented the following sequence: liver?>?intestine?>?kidney. Cd storage presented the following sequence: intestine?>?kidney?>?liver. When exposed to both metals, Cu and Cd storage presented the following sequence: liver?>?intestine?>?kidney. Histopathological examination of the liver revealed marked alterations including loss of hepatic cell architecture, and some cells exhibited distinct cytoplasmic vacuoles. The majority of blood vessels exhibited a marked dilatation and congestion with infiltration of blood cells, prominent hyperemia of hepatic veins, and significant proliferation of bile ductules. Histopathological changes in the kidney showed destruction and degeneration of both renal tubule cells and glomerular with infiltration of leukocytes and inflammatory cells. Histopathological alterations in the intestine were restricted to the innermost mucosal epithelium with marked degeneration of the villi and submucosa and an extensive fragmentation of mucosal epithelium as well as atrophy of goblet cells. The administration of vitamin C 1?h prior to administration of Cd, Cu, and metal combination did not protect against hepatic, renal, and intestinal damage. However, parental vitamin C given alone increased tissue toxicity.     

Protective effects of quercetin against sodium fluoride-induced oxidative stress in rat erythrocytes

Protective effects of quercetin against oxidative stress induced by sodium fluoride intoxication in rat erythrocytes were evaluated. Rats were divided into five groups consisting of 10 in each for this experiment. The animals of group I received water and standard diet to serve as control group, the animals of groups II and III were treated with quercetin (10 and 20?mg?kg^?1 body weight), administrated intraperitoneally for 7 days followed by sodium fluoride (600?ppm) in drinking water for the next 7 days. The animals of group IV were treated with vitamin C (10?mg?kg^?1) intraperitoneally for 7 days followed by sodium fluoride treatment for next 7 days serving as positive control group. The animals of group V were treated only with sodium fluoride (600?ppm) for the same time and were used as control group. Blood sample were collected via retro-orbital puncture. The antioxidant enzymes, superoxide dismutase, and catalase, as well as the levels of reduced glutathione and lipid peroxidation end products were measured in erythrocytes. There was a significant increase in lipid peroxidation along with a decrease in superoxide dismutase activity in the erythrocytes of sodium fluoride-treated animals. Quercetin treatment prior to fluoride administration normalized the levels of all parameters measured in the rat erythrocytes.     

Immunoprotective effect of curcumin on cypermethrin-induced toxicity in rats

Immunotoxicological effects of cypermethrin and their reversal by curcumin following oral administration were evaluated in rats. Mature male Wistar rats were orally administered cypermethrin (25?mg?kg^?1 body wt), curcumin (100?mg?kg^?1 body wt) or both daily for 4 weeks. At the end of fourth week, hematological, serum biochemical, and immunological parameters were studied. Subchronic exposure to cypermethrin significantly reduced body weight, total leukocyte count, lymphocyte count, serum total protein, serum albumin, serum globulin, antibody titer against sheep red blood cells, and cell-mediated immunity. Concomitant curcumin administration restored the changes in the body weight, hematological parameters, and serum biochemical indices and significantly increased the antibody titer, and cell mediated immunity. These results suggest that concurrent curcumin treatment has a beneficial role in mitigating immunotoxicological and other adverse effects of cypermethrin.     

Protective influence of antioxidant vitamins on hematological indices of rabbits fed crude-oil-contaminated diet

The effects of chronic exposure to petroleum on hematological parameters as well as the possible protective role of vitamins E and C were studied. The hematological parameters assessed were red blood cell (RBC) counts, hematocrit, hemoglobin concentration, and white blood cell (WBC) counts. The RBC and hemoglobin concentration were significantly decreased in the blood of petroleum-fed rabbits. However, there was a significant increase in WBC in rabbits exposed to crude-oil-contaminated feed. Pretreatment with the antioxidant vitamins E and C restored these parameters to normal.     

Protective role of epigallocatechin 3-gallate against lead-induced toxicity in human neuroblastoma cells

Lead (Pb) is a heavy metal, known to induce oxidative stress and produce damage to the antioxidant defence system ultimately leading to cell death. Antioxidants such as epigallocatechin 3-gallate (EGCG), a green tea polyphenol, was shown to play a protective role during Pb-exposure. In this study, human SH-SY5Y neuroblastoma cells were exposed to different concentrations (0.01–10?µM) of Pb for 48?h to determine effects on the viability of cells. It was observed that IC₅₀ was at 5?µM and at this concentration the cells exhibited a significant increase in caspase-3 activity, an indicator of apoptosis at least by 10-fold and the decrease of 59.4% in glutathione (GSH) content. The total cellular prostaglandin-E₂ (PGE₂) level was found to be elevated at least 10-fold upon Pb exposure. However, the effects of Pb on cells pre-incubated with 50?µM EGCG followed by 5?µM Pb showed 40% inhibition in cell viability, 17.3% decrease in caspase-3 activity, 23% increase in GSH content, and 11.4% fall in PGE₂ levels when compared with cells exposed to Pb only. Data suggest that EGCG exerted a significant protection to cell viability in preventing cell death and elevation in levels of GSH in cells exposed to Pb. However, EGCG did not elicit any significant effect on release of PGE₂ indicating the nature of EGCG as an effective anti-apoptotic, antioxidant, and anti-inflammatory agent.     

Protective role of L-ascorbic acid against cypermethrin-induced oxidative stress and lipid peroxidation in Wistar rats

Cypermethrin is a synthetic pyrethroid insecticide used for pest control in agriculture and as an acaricide in man and animals. This study was undertaken with the objective to investigate the propensity of cypermethrin to induce oxidative stress in rats following repetitive dermal exposure and its possible attenuation by L-ascorbic acid. Results obtained showed that cypermethrin significantly (p < 0.05) increased malonaldehyde levels, activity of catalase in rat erythrocytes and plasma protein levels. Whereas, activities of glutathione (GSH), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) were significantly (p < 0.05) reduced in the cypermethrin exposed rats as compared to the control. Supplementation of L-ascorbic acid in cypermethrin-exposed rats decreased lipid peroxidation of erythrocytes, total plasma protein and catalase activity significantly (p < 0.05) compared to non-cypermethrin-exposed group. However, L-ascorbic acid did not alleviate the negative effects of cypermethrin on the activities of SOD and GSH. This study revealed that the presence of L-ascorbic acid diminishes the adverse effects of cypermethrin on some oxidative stress parameters.     

三邻甲苯磷酸酯对大鼠C6星形胶质细胞的氧化损伤和细胞周期阻滞作用

三邻甲苯磷酸酯(tri-o-cresyl phosphate,TOCP)是一种有机磷酸酯类化合物,具神经毒性作用。研究表明星形胶质细胞是有机磷化合物(organophosphorus compounds,OPs)神经毒性作用的靶点之一。为了探讨TOCP对星形胶质细胞的毒性作用,采用大鼠C6星形胶质细胞分别经0.1、0.3、1.0和3.0 mmol·L-1TOCP染毒处理24 h,应用MTT比色法和乳酸脱氢酶(LDH)活力分析法检测细胞活力,在电子相差显微镜下观察细胞形态,二硫代二硝基苯甲酸(DNTB)比色法测定谷胱甘肽(GSH)含量和谷胱甘肽过氧化物酶(GSH-Px)活性,流式细胞仪检测分析细胞周期。结果显示,经TOCP处理24 h后,大鼠C6星形胶质细胞存活率降低,LDH释放增加,细胞形态也发生了明显的变化。GSH含量和GSH-Px活性降低,G1期细胞数量也逐渐增加。上述结果表明,TOCP对星形胶质细胞具有毒性作用,引起氧化损伤和细胞周期阻滞。     

Protective effects of curcumin on antioxidant status,body weight gain,and reproductive parameters in male rats exposed to subchronic 2,3,7,8-tetrachlorodibenzo-p-dioxin

The aim of this study was to investigate the effects of curcumin (CUR) on antioxidant status, body weight (BW) gains, and some reproductive parameters in male rats exposed to subchronic doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Thirty-two rats were divided into four groups. The first group was kept as control. The second group (TCDD group) was given TCDD at a dose of 50 ng·kg^?1 BW per day; the third group (CUR group) was treated with CUR at a dose of 80 mg·kg^?1 BW per day. The fourth group (TCDD + CUR group) was given TCDD and CUR at the same doses simultaneously. Malondialdehyde (MDA) levels were significantly increased in the TCDD group. In addition, TCDD exposure decreased liver superoxide dismutase (SOD) activity, catalase (CAT) activities of kidney and brain, glutathione peroxidase (GSH-Px) activities of liver, kidney, and brain, and glutathione levels of liver, kidney, and heart. However, CUR treatment with TCDD exposure decreased MDA levels in all tissues and increased SOD activities of liver, kidney, and brain, CAT activity of heart, and GSH-Px activities of heart and brain. TCDD caused a decrease in BW gain, and CUR partially eliminated this effect of TCDD. In addition, while reproductive organ weights, sperm concentration, and sperm motility tended to decrease with TCDD exposure, these effects tended to be close to normal levels by CUR treatment. In conclusion, CUR was seen to be effective in the treatment and prevention of toxicity induced by subchronic TCDD exposure.     

Cadmium sulfide nanoparticle induces oxidative stress and pro-inflammatory effects in human lung adenocarcinoma epithelial cells

Cadmium sulfide nanoparticles (CdSNP) are increasingly used in biological applications. This study was undertaken to understand the mechanisms underlying adverse effects of CdSNP using human lung adenocarcinoma epithelial (A549) cells. Cellular toxicity was evaluated by using 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide and neutral red assays. Results showed that CdSNP reduced mitochondrial function and induced lysosomal activity in concentration and time-dependent manner. CdSNP produced oxidative stress as evidenced by reduction of glutathione (GSH) levels and increase in reactive oxygen species and lipid peroxidation levels. Induction of caspase-3 enzymes and condensed, fragmented nuclei was observed in CdSNP-treated cells. Furthermore, the levels of interleukin-8, tumor growth factor and DNA fragmentation were significantly higher in CdSNP exposed cells. Data indicated that toxicity of CdSNP noted in A549 cells may be mediated through oxidative stress. This study warrants more comprehensive assessment of CdSNP prior to industrial applications.     

DNA fragmentation,apoptosis and cell cycle arrest induced by sodium arsenite in cultured murine Sertoli cells: prevention by curcumin

Arsenic is a significant environmental concern worldwide, primarily due to geo physiochemical contamination of drinking water, and a major public health hazard in both developing and developed countries. The present study was aimed to investigate ameliorative effects of curcumin (Cur) against sodium arsenite (SA)-induced toxicity in cultured murine Sertoli cells. The cells were treated with SA (5 μM) and Cur (5 μg/ml and 10 μg/ml) alone or in combination for 12 hr. The SA treatment decreased cell viability, produced oxidative stress, and induced apoptosis as reflected by reactive oxygen species (ROS) generation, loss of mitochondrial transmembrane potential, DNA fragmentation, and apoptotic cells. Moreover, the SA-induced cell cycle arrest in the cells is characterized by a rise in the number of cells in the sub G1 phase of the cell cycle. The Cur was found to be effective in reversing all these arsenic (As)-induced cellular events. Data suggest that Cur modulates As-mediated oxidative stress, apoptosis, DNA fragmentation, and cell cycle arrest through suppression of excessive ROS generation. Evidence indicates that Cur may emerge as a useful protective agent against As-induced Sertoli cells toxicity by inhibiting As-induced damage in testes.     

Nanosilica exerts cytotoxicity and apoptotic response via oxidative stress in mouse embryonic fibroblasts

Nanoscale silica is an important industrial material and extensively used in medicines. The objective of this study was to determine potential cytotoxicity and genotoxic effects attributed to nanosilica exposure in mouse embryonic fibroblasts (L929) cells. Nanosilica produced mild cytotoxicity in L929 cells. Results showed that nanosilica increased thiobarbituric acid reactive substance levels and enhanced superoxide dismutase activity but decreased levels of glutathione. This was accompanied by a concomitant generation of reactive oxygen species, loss of mitochondrial membrane potential, and activation of caspase-3 activity. In addition, in the single-cell gel test, nanosilica (50–300 μg/ml) at two treatment times 24 and 48 hr produced concentration- and time-dependent increase of DNA damage. Therefore, the obtained results indicate that nanosilica may induce genotoxic effects in cultured L929 cells associated with induction of oxidative stress.     

Protective role of Curcuma longa extract and curcumin on mercuric chloride-induced nephrotoxicity in rats: evidence by histological architecture

Mercury (Hg) is a potent nephrotoxin. The aim of this study was to investigate the protective role of Curcuma longa extract and curcumin against HgCl₂-induced nephrotoxicity. Male Sprague Dawley rats were administered HgCl₂ (12 μmol kg^?1, ip; once only) followed by treatment of Curcuma longa extract (200 mg kg^?1, po) and curcumin (80 mg kg^?1, po) for three days after 24 h of HgCl₂ administration. The present results showed that mercuric chloride administration caused an impairment of renal function system which was evident from significant increase in urea, creatinine, uric acid, and blood urea nitrogen concentration in serum. In addition, the swelling in glomerulus and degenerated renal tubules with obstructed lumen was also observed by acute mercuric chloride administration. Treatment with Curcuma longa extract and curcumin was effective in restoring all variables of kidney functions near to control group, which was consistent with kidney histoarchitecture. In conclusion, these results suggest that Curcuma longa extract and curcumin protect against HgCl₂-induced nephrotoxicity. This study could be important for the further understanding of mercury toxicity in renal tissues and in the development of better treatments for people and/or animals exposed to the metal.     

Hepatoprotective and antioxidant effects of Bridelia retusa against carbon tetrachloride-induced hepatotoxicity

The aim of present study was to validate hepatoprotective and antioxidant activities of the bark of Bridelia retusa. The aqueous ethanol extract of B. retusa exhibited highest in vitro hepatoprotective effects as evident from the significantly reduced serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) into the incubation medium of rat hepatocytes with carbon tetrachloride (CCl₄), over the other organic extracts (chloroform, ethylacetate, and methanol). CCl₄ administered through subcutaneous injection produced a marked elevation in the serum levels of GOT, GPT, lactate dehydrogenase, alkaline phosphatase, bilirubin, thiobarbituric acid reactive substances, and decreased in the levels of reduced glutathione, superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase, glutathione peroxidase, and total protein content. The biochemical activities were normalized in the pretreatment of rats induced by CCl₄ with different doses (250 and 500 mg kg^?1) of the aqueous ethanol extract of B. retusa. Histopathological changes induced by CCl₄ were also significantly attenuated by aqueous ethanol extract of B. retusa treatment. The activity of the aqueous ethanol extract of B. retusa at the dose of 500 mg kg^?1 was comparable to the standard drug, silymarin (25 mg kg^?1). The overall data indicated that B. retusa possesses a potent protective effect against CCl₄-induced hepatic damage and oxidative stress.     

Assessment of DNA damage and cytotoxicity of palmatine on human skin epithelial carcinoma cells

The present investigation was carried out to examine the cytotoxic and genotoxic effects of a Tinospora cordifolia crude methanolic extract (palmatine) on human skin epithelial carcinoma cells (A431). T. cordifolia is one of the indispensable medicinal plants used in Ayurvedic medicine for treatment of various diseases and recommended for improving the immune system. Cytotoxicity and genotoxicity evaluation was carried out using A431 cells treated with different concentrations of palmatine. The duration of the treatment was 24 and 48 hr. A cellular proliferative capacity test showed that palmatine produced cytotoxicity in concentration- and time-dependent manner. Further, palmatine induced significant intracellular reactive oxygen species generation and elevated lipid peroxidation, as well as activities of catalase and superoxide dismutase. DNA fragmentation analysis using the comet assay showed that palmatine induced genotoxicity in a concentration- and time-dependent manner. Evidence indicates palmatine is capable of induction of oxidative stress resulting in cell death and genomic instability.     

Efficiency of mercapto flavor compounds in removing acrylamide under high temperature and low humidity conditions

Acrylamide (AA) is a potential human carcinogen, genotoxicant, and neurotoxicant. Thus, the aim of this study was to examine the ability of mercapto flavor compounds to remove AA released from consumer packaging into food products. Four mercapto flavor compounds including 1,2-ethanedithiol, 1-butanethiol, 2-methyl-3-furanthiol, and 2-furanmethanethiol were employed to extract AA in model system using high temperature and low humidity. Our study showed that mercaptans were effective in eliminating AA in our model system. In order to remove 0.2 μmol AA, the optimal conditions in the reaction system were mercaptan flavor chemicals at 5 μmol, temperature 180 °C, and reaction time 25 min. In the presence of a higher pH, the greater was the amount of AA eliminated. Evidence indicates that employment of mercapto flavor chemicals under certain temperature and pH conditions is a reliable method to remove any unwanted AA from food products.     

The relations of antioxidant vitamins A,E, and C with MDA levels in serum and liver of rats treated with nitrosamines

In this study, we investigated the levels of vitamins A, E, and C in serum and liver, and malondialdehyde (MDA) were followed by long-term administration of some nitrosamines. Sprague-Dawley rats were divided into four groups. N-Nitrosodiethylamine (NDEA), 1-Nitrosopiperidine (NPip), and N-Nitrosopyrrolidine (NPyr) were administered 200 ppb, orally with water for 30 consecutive days to experimental groups. Animals were decapitated at 3rd, 7th, 15th, and 30th days of the administrations. Significant increases were observed in MDA levels treated with nitrosamines at all times. Serum MDA levels were found to be significantly higher in NDEA-treated animals than in control and other groups at 30th day. Liver MDA levels were highly increased in NPyr-treated group. Significant decreases were observed in the levels of vitamins A, E, and C in rats treated with nitrosamines at all times. There were also significantly negative correlations at present changes among the serum or liver MDA levels and vitamin A, E, and C levels in all nitrosamines-treated groups. These findings demonstrate that exposure at low levels of nitrosamines decreased vitamin A, E, and C levels while it attributed lipid peroxidation. Therefore, maintaining an adequate level of antioxidant vitamins in serum and liver may be necessary for the prevention or protection of long-term nitrosamine exposures.     

Evaluation of vitamin E and calcium effects on fluoride toxicity-induced fertility impairment

Chronic fluoride (Fl) toxicity is a serious public health problem globally where drinking water contains more than 1 ppm of Fl. Sodium fluoride (NaF) produced male reproductive system toxicity. The aim of the present study was to evaluate the amelioration of Fl toxicity-induced fertility impairment by vitamin E and calcium during the withdrawal period. The study was carried out on 70 adult male albino rats divided into five main groups: group I control; subdivided into group Ia (maintained on standard diet and water ad libitum for 60 days) and group Ib (maintained on standard diet and water ad libitum for 120 days), group II was administered NaF and subdivided into group IIa (administered NaF for 60 day and sacrificed) and group IIb (administered NaF for 60 day then maintained on standard diet and water ad libitum for a further 60 days), and treated groups III, IV, and V were administered NaF. Rats were maintained during withdrawal from NaF, on vitamin E (10 mg kg^?1 day^?1 for 60 days), calcium (50 mg kg^?1 day^?1 orally for 60 days), and both vitamin E and calcium, respectively. The duration of NaF administration was 60 days at a dose 20 mg kg^?1 day^?1 for all treated groups. The following parameters were determined: body and organ weights, sperm motility, sperm morphology, sperm viability, fertility test, and hormone assays: testosterone, in vitro testosterone production, luteinizing hormone, and follicular stimulating hormone. The combined administration of vitamin E and calcium during withdrawal from NaF showed significant improvement from chronic FL-induced toxicity on male reproductive organs.     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.     

Therapeutic effect of melatonin against aluminum-induced neurotoxicity in cerebellum of albino mice

The therapeutic effect of melatonin (MEL) against aluminum (Al)-induced neurotoxicity was investigated in mouse cerebellum. Two groups of male albino mice were intraperitoneally injected with Al acetate or MEL alone, at doses of 3.5 or 7?mg?kg^?1?day^?1, respectively, for 6 weeks. During this period, another group of animals received a combination of both Al and MEL (3.5?+?7?mg?kg^?1?day^?1). At the end of the treatment cerebellum was removed and processed to examine the oxidative stress markers: superoxide dismutase (SOD), catalase (CAT), and thiobarbituric acid-reactive substances (TBA-RS). Oxidative stress increased significantly with administration of Al which was estimated by increased TBA-RS and reduction in the activities of SOD and CAT. However, these alterations were significantly reversed significantly following MEL treatment which was observed in co-administered group. Protective effects of MEL were also observed at electron microscopic level. Ultrastructural studies revealed an increase in vacuolization, chromatin condensation within the nucleus, degenerated purkinje cell, degenerated axon and degenerated granule cells in the cerebellum of Al-treated mice group whereas concurrent administration of MEL with Al reduced these changes. The results of the present investigation emphasize the potential use of MEL as a supplement in therapy of free radical based neurological disorders in which oxidative stress is involved.