Pluchea lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity in Swiss albino mice

Cadmium intoxication induces lipid peroxidation and causes oxidative damage to various tissues by altering antioxidant defence system enzymes. At 24 h after treatment with a single intraperitoneal dose of cadmium chloride (5 mg kg-1), Swiss albino mice showed a significant increase in the levels of malanodialdehyde and xanthine oxidase (P<0.001), and a concomitant depletion of renal glutathione, catalase (P<0.001) and other antioxidant enzymes. CdCl2 also led to a simultaneous increase in micronuclei formation (P<0.001) and chromosomal aberrations (P<0.05) in mouse bone marrow cells. Oral pre-treatment with Pluchea lanceolata extract at doses of 100 and 200 mg kg-1 for 7 consecutive days before CdCl2 intoxication caused a significant reduction in malanodialdehyde formation and xanthine oxidase activity (P<0.001). A significant restoration of the activity of antioxidant defence system enzymes such as catalase, glutathione peroxidase (P<0.05), glutathione-S-transferase and glutathione reductase (P<0.001) was observed. A significant dose-dependent decrease in chromosomal aberrations and micronuclei formation was also observed (P<0.05). The results indicate that pre-treatment with P. lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity by altering antioxidant enzymes and reducing chromatid breaks and micronuclei formation.     

Vetiver oil (Java) attenuates cisplatin-induced oxidative stress,nephrotoxicity and myelosuppression in Swiss albino mice

Clinical efficacy of the widely used anticancer drug cisplatin is limited due to its adverse side effects in normal tissues mediated by oxidative stress. This study was aimed to investigate the protective effects of vetiver acetate oil, Java (VO) against cisplatin-induced toxicity in Swiss albino mice. The ameliorating potential was evaluated by orally priming the animals with VO at doses 5, 10 or 20 mg/kg bw for 7 days prior to cisplatin treatment. Acute toxicity in mice was induced by injecting cisplatin (3 mg/kg bw) intraperitoneally for 5 consecutive days. Significant attenuation of renal toxicity was confirmed by histopathological examination, lowered levels of serum blood urea nitrogen, creatinine and reduced DNA damage. VO also compensated deficits in the renal antioxidant system. VO intervention significantly inhibited DNA damage, clastogenic effects, and cell cycle arrest in the bone marrow cells of mice. Hematological parameters indicated attenuation of cisplatin-induced myelosuppression. Overall, this study provides for the first time that VO has a protective role in the abatement of cisplatin-induced toxicity in mice which may be attributed to its antioxidant activity.     

Reproductive toxicity of piperine in Swiss albino mice

Piperine (CAS 94-62-2) is a constituent of various spices which are used as common food additives all over the world. The reproductive toxicity of piperine was studied in Swiss albino mice. Relevant short-term tests were employed to assess the effect on estrous cycle, mating behaviour, toxicity to male germ cells, fertilization, implantation and growth of pups. Piperine (10 and 20 mg/kg b.w.) increased the period of the diestrous phase which seemed to result in decreased mating performance and fertility. Post-partum litter growth was not affected by the piperine treatment. Sperm shape abnormalities were not induced by piperine at doses up to 75 mg/kg b.w. Considerable anti-implantation activity was recorded after five days post-mating oral treatment with piperine. The sex ratio and post-implantation loss were unaffected after treatment with piperine. Intrauterine injection of piperine caused the total absence of implants in either of the uterine horns (16.66%) or one of the horns (33%) of treated females. No histopathological changes were detected in the ovary and the uterus at the cellular level. Prostaglandin E1-induced acute inflammation of rat paw was significantly reduced after piperine treatment. Our results show that piperine interferes with several crucial reproductive events in a mammalian model.     

Antioxidant potential of tea reduces arsenite induced oxidative stress in Swiss albino mice

Environmental arsenic (As) is a potent human carcinogen and groundwater As contamination is a major health concern in West Bengal, India. Oxidative stress has been one of the prime factors in As-induced carcinogenicity. Generation of reactive oxygen species (ROS), beyond the body’s endogenous antioxidant balance cause a severe imbalance of the cellular antioxidant defence mechanism. Tea, a popular beverage has excellent chemopreventive and antioxidant properties. In this study it was investigated whether these flavonoids could ameliorate the arsenite (As III) induced oxidative stress in Swiss albino mice. Bio-monitoring with comet assay elicited that the increase in genotoxicity caused by As III was counteracted by both black tea and green tea. Elevated levels of lipid peroxides and protein carbonyl by As III were effectively reduced with green as well as black tea. They also exhibited protective action against the As III induced depletion of antioxidants like catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione (GSH) in mice liver tissue. Thus the tea polyphenols by virtue of their antioxidant potential may be used as an effective agent to reduce the As III induced oxidative stress in Swiss albino mice.     

Protective effect of Plumbago zeylanica against cyclophosphamide-induced genotoxicity and oxidative stress in Swiss albino mice

Plumbago zeylanica, commonly known as white leadwort, found abundantly in the plains of Bengal and southern India, was tested for its possible in vivo protective effect against cyclophosphamide-induced genotoxicity and oxidative stress in Swiss albino mice. Pretreatment with the alcoholic root extract of Plumbago zeylanica (250 and 500 mg/kg body weight orally for 5 days) significantly reduced the frequency of micronucleated polychromatic erythrocytes (MnPCEs), increased the PCE/NCE (normochromatic erythrocyte) ratio in the bone marrow, and decreased the levels of lipid peroxidation products with concomitant changes in the status of antioxidants. Both doses of Plumbago zeylanica were effective in exerting a protective effect against cyclophosphamide-induced genotoxicity and oxidative stress.     

Spirulina fusiformis provides protection against mercuric chloride induced oxidative stress in Swiss albino mice

Oxidative stress induced by mercuric chloride (5 mg/kg body weight i.p.) in mice substantially increases the lipid peroxidation level along with corresponding decrease in the reduced glutathione and various antioxidant enzymes in liver and increase in serum transaminases activity. Supplementation of Spirulina (800 mg/kg body weight orally, in olive oil, along with mercuric chloride) for 40 days resulted in decreased LPO level, serum glutamate oxaloacetate and serum glutamate pyruvate transaminase activity along with increase in liver GSH level. The activities of antioxidants enzymes superoxide dismutase, catalase and glutathione-S-transferase were also concomitantly restored to near normal level by Spirulina supplementation to mercuric chloride intoxicated mice. The results clearly demonstrate that Spirulina treatment augments the antioxidants defense mechanism in mercuric chloride induced toxicity and provides evidence that it may have a therapeutic role in free radical mediated diseases.     

Metoclopramide attenuates iminodipropionitrile-induced oxidative stress and neurobehavioral toxicity in rats

Metoclopramide (MET) has long been used as a neuroleptic and antiemetic drug in clinical practice. Motor impairment and dyskinesia have been reported in some patients following chronic treatment with MET. Occasionally, the adverse symptoms may appear even after acute exposure to MET in more susceptible population (such as elderly individual) or due to concomitant exposure to MET and certain neurotoxins. Iminodipropionitrile (IDPN), a prototype nitrile toxin, has been shown to produce dyskinetic syndrome in rodents. This study reports the effect of concomitant exposure of rats to MET and IDPN on behavioral abnormalities in rats namely excitation, circling and chorea (ECC) syndrome. Four groups of female Wistar rats (aged 3 months) were given MET (0, 10, 40 and 80 mg/kg, i.p., for 11 days) 30 min before IDPN (100 mg/kg, i.p. for 8 days). Two additional groups of rats were treated with either saline (control group) or 80 mg/kg of MET (drug alone group). The animals were observed for neurobehavioral abnormalities including dyskinetic head movement, circling, tail hanging, air righting reflex and contact inhibition of righting reflex. Horizontal and vertical locomotor activities and fore limbs grip strength were also measured. On day 12, the animals were sacrificed and brains were collected for biochemical analysis. MET significantly and dose-dependently protected the animals against IDPN-induced ECC syndrome, motor impairment and deficiency in grip strength. MET also protected the animals against IDPN-induced oxidative stress.     

Zoledronic acid induces cytogenetic toxicity in male germline cells of Swiss albino mice

This study mainly focuses on the cytogenetic toxicity induction by zoledronic acid (ZA), a nitrogen containing bisphosphonate (N-BPs) in the male germline cells of Swiss albino mice. A single intraperitoneal exposure with three different doses of ZA (2, 4, and 8?mg/kg body weight), toxicity was assessed by analyzing spermatogonial metaphase chromosome aberrations at 24?h, aberrant primary spermatocytes at week 4, and abnormal spermatozoa at week 8 posttreatment. Cyclophosphamide (40?mg/kg) and 0.9% NaCl were used as positive and vehicle controls respectively in the study. The results showed that there was a significant induction in the number of chromosomal aberrations especially at two doses of ZA (4 and 8?mg/kg) after 24?h in the spermatogonial cells (p?<?0.001) compared to vehicle control. The transmission genetic damages were noticed as aberrant spermatocytes with atypical bivalents (X-Y/autosomal asynapsis) at 4?mg/kg of ZA (p?<?0.01) and at 8?mg/kg of ZA (p?<?0.001) at week 4 posttreatment. A statistically significant higher number of abnormal spermatozoa (sperm) were also noticed at week 8 posttreatment of both at 4 and 8?mg/kg of ZA (p?<?0.001). Hence, from these genotoxicity studies, it can be concluded that ZA is genotoxic in male germline cells and has the potential of transmitting the genotoxic effects from spermatogonial cells to sperm in male Swiss mice.     

Myrica nagi Attenuates Cumene Hydroperoxide‐Induced Cutaneous Oxidative Stress and Toxicity in Swiss Albino Mice

In recent years, considerable efforts have been made to identify new chemopreventive agents which could be useful for man. Myrica nagi, a subtropical shrub, has been shown to possess significant activity against hepatotoxicity and other pharmacological and physiological disorders. We have shown a chemopreventive effect of Myrica nagi on cumene hydroperoxide‐induced cutaneous oxidative stress and toxicity in mice. Cumene hydroperoxide treatment at a dose level of 30 mg/animal/0.2 ml acetone enhances susceptibility of cutaneous microsomal membrane for iron‐ascorbate‐induced lipid peroxidation and induction of xanthine oxidase activity which are accompanied by decrease in the activities of cutaneous antioxidant enzymes such as catalase, glutathione peroxidase, glutathione reductase, glucose‐6‐phosphate dehydrogenase and depletion in the level of cutaneous glutathione. Parallel to these changes a sharp decrease in the activities of phase II metabolizing enzymes such as glutathione S‐transferase and quinone reductase has been observed. Application of Myrica nagi at doses of 2.0 mg and 4.0 mg/kg body weight in acetone prior to that of cumene hydroperoxide (30 mg/animal/0.2 ml acetone) treatment resulted in significant inhibition of cumene hydroperoxide‐induced cutaneous oxidative stress and toxicity in a dose‐dependent manner. Enhanced susceptibility of cutaneous microsomal membrane for lipid peroxidation induced by iron ascorbate and xanthine oxidase activities were significantly reduced (P<0.05). In addition the depleted level of glutathione, the inhibited activities of antioxidants, and phase II metabolizing enzymes were recovered to a significant level (P<0.05). The protective effect of Myrica nagi was dose‐dependent. In summary our data suggest that Myrica nagi is an effective chemopreventive agent in skin and capable of ameliorating cumene hydroperoxide‐induced cutaneous oxidative stress and toxicity.     

Protective effect of Mentha piperita against arsenic-induced toxicity in liver of Swiss albino mice

The protective role of leaves of Mentha piperita Linn (Mint) was studied in adult Swiss albino mice against arsenic-induced hepatopathy. The animals were divided into four groups. Group I: only vehicle (0.9% NaCl) was administered. Group II: the animals received Mentha leaf extract (1 g/kg body weight per day) orally for 30 days. Group III: animals were treated with sodium arsenite (4 mg/kg body weight) intraperitoneally in 0.9% NaCl. Group IV: animals were given Mentha extract for 10 consecutive days prior to sodium arsenite treatment and continuously for 30 days after sodium arsenite treatment. The animals from the above groups were killed at various time-points, and body weight and liver weight were measured. The biochemical estimation of lipid peroxidation (LPO), reduced glutathione (GSH), lactate dehydrogenase (LDH), acid phosphatase (ACP), and alkaline phosphatase (ALP) in liver and serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) in serum were done. In the arsenic-treated group there was a significant increase in ACP, ALP, SGOT, SGPT and LPO content, whereas a significant decrease was recorded in body weight, liver weight, GSH and LDH activity in liver. Pre- and post-treatment of Mentha with arsenic significantly alters the biochemical parameters in liver. A significant decline in ACP, ALP, SGOT, SGPT and LPO content was observed. However, a significant increase in body weight, liver weight, GSH content and LDH activity in liver was estimated. The results indicate that the Mentha extract may be useful in reducing the side effects of arsenic-induced hepatopathy.     

Phytol ameliorated benzo(a)pyrene induced lung carcinogenesis in Swiss albino mice via inhibition of oxidative stress and apoptosis

In the present study, the modulatory effect of phytol against benzo(a)pyrene [B(a)P] induced lung carcinogenesis was investigated in Swiss albino mice. During the experimental period, phytol treatment showed no adverse toxic effect and mortality to the experimental animals. Lung tumor was observed in B(a)P treated group and also in animals post‐treated with low concentration (50 mg/kg) of phytol. No neoplastic changes were observed in the lung tissue of the animals treated with the maximum dose of phytol (100 mg/kg). An elevated level of antioxidant enzymes combined with macromolecular damage (lipid peroxidation, protein carbonyl content) was observed upon B(a)P treatment whereas, phytol restored the level of antioxidant enzymes which were comparable to the vehicle control group. Moreover, administration of B(a)P induced apoptosis, as observed by the highest expression of Bax, caspase‐3, and caspase‐9 proteins in lung tissue of B(a)P alone treated animals. However, phytol treatment reduced the expression of Bax, caspase‐3, and caspase‐9 protein and maintained the constant expression of anti‐apoptotic protein Bcl‐2. These observations positively reveal that phytol regulates the antioxidant enzymes and thereby protects the cells against B(a)P induced carcinogenesis without showing any adverse toxic effect to the animals.     

Role of leptin on alcohol-induced oxidative stress in Swiss mice.

Previous studies suggest a possible link between leptin and hepatic inflammation; however, the role of leptin on liver disease remains unclear. The purpose of the present study was to evaluate the effect of leptin on tissue lipid peroxidation and the antioxidant status in experimental hepatotoxicity. Administering ethanol (6.32 g/kg body weight) to 4-week-old healthy mice for 45 days resulted in significantly elevated levels of tissue thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and lowered activities of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glutathione related enzymes such as glutathione peroxidase (GPx) and glutathione S-transferase (GST) as compared with those of the control mice. subsequent to the experimental induction of hepatotoxicity (i.e. after the initial period of 30 days) exogenous leptin was simultaneously administered (230 microg/kg body weight) every alternate day for 15 days along with the daily dose of alcohol. Leptin administration to control and alcohol-treated mice significantly reduced the weight gain, significantly elevated the liver and kidney levels of TBARS and CD, and significantly lowered the levels of enzymic and non-enzymic antioxidants as compared with the untreated control and alcohol supplemented mice. It is postulated that the increase in systemic leptin levels enhance the oxidative stress, and lower the antioxidant defence, leading to augmented hepatic inflammation in alcoholic liver disease.     

Tumourigenic studies on deltamethrin in Swiss albino mice

Deltamethrin, an alpha-cyano type II synthetic pyrethroid insecticide is used to control a wide range of insects on a variety of crops. Deltamethrin is reported to cause many adverse effects on non-target species. Deltamethrin is reported to cause DNA damage and micronuclei induction in human lymphocytes. It is highly toxic for other organisms such as aquatic invertebrates, fish and Daphnia. About the tumorigenic risk (both tumour initiating and promoting) associated with deltamethrin exposure, very few reports are available in literature. In the present set of investigations, deltamethrin has been evaluated for its tumorigenic and co-carcinogenic (tumour initiating and tumour promoting) potential following long term dermal exposure in Swiss albino mice. The results revealed that deltamethrin has only tumour initiating potential in both the sexes of Swiss albino mice, initiated with deltamethrin and promoted by standard tumour promoter, 12-O-tetra decanoyl phorbol-13-acetate (TPA). In the single dose initiated mice (deltamethrin 4 mg/kg body weight, once only), 44% males and 43% females developed benign skin tumours. A much higher incidence of tumorigenesis was recorded in multiple dose initiated animals (deltamethrin 4 mg/kg body weight, three times per week for 3 weeks), where 71% male and 75% female mice developed tumours at the site of application of deltamethrin. Deltamethrin exposure failed to show any tumour promoting and complete tumorigenic potential at all the three tested dose levels.     

Fisetin, a novel flavonol attenuates benzo(a)pyrene-induced lung carcinogenesis in Swiss albino mice

Lung cancer is the foremost cause of cancer mortality and is a growing economic burden worldwide. Fisetin (3,7,3′,4′-tetrahydroxyflavone), a naturally occurring flavonoid is found in vegetables and fruits possesses anti-oxidative, anti-inflammatory and anti-proliferative effects in a wide variety of cancer. In the present study it is hypothesized that fisetin may provide chemopreventive as well as chemotherapeutic effects against experimental lung carcinogenesis. The present study was designed to investigate whether fisetin confers anti-cancer action against benzo(a)pyrene [B(a)P] induced lung carcinogenesis. Treatment with fisetin significantly reduced the degree of histological lesions, restored the levels of lipid peroxidation (LPO), enzymic and non-enzymic anti-oxidants in B(a)P-induced mice. Anti-proliferative efficacy of fisetin was assessed by immunohistochemical analysis of proliferating cell nuclear antigen (PCNA) in B(a)P induced mice showed increased PCNA expression which is restored upon fisetin administration. Together, our results depicts that fisetin can be used as chemopreventive agent against lung cancer.     

Ascorbic acid attenuates cognitive impairment and brain oxidative stress in ovariectomized mice

Background

Menopause is associated with increased oxidative stress and memory impairment. Based on the antioxidant property of ascorbic acid (AA), It’s effect on cognitive function, the serum level of the brain-derived neurotrophic factor (BDNF) and the activity of antioxidant enzymes within the brain in ovariectomized (OVX) mice was investigated.

Cyto-genotoxicity and oxidative stress induced by zinc oxide nanoparticle in human lymphocyte cells in vitro and Swiss albino male mice in vivo

ZnO-np has immense potential and application in cosmetic and health care sectors. Hence it was imperative to assess the toxicity/safety of these nanoparticles. In this study, we have evaluated the effects of ZnO-np in human peripheral blood mononuclear cells (PBMCs) in vitro and in Swiss albino male mice in vivo for cyto-genotoxicity and oxidative damage. In vitro results showed that ZnO-nps were weakly genotoxic, induced significant decrease in mitochondrial membrane potential and was capable of ROS generation, leading to apoptosis. In bone marrow cells in vivo, reduction of mitochondrial membrane potential (MMP), increased oxidative stress and G0/G1 cell cycle arrest was observed along with chromosome aberrations and micronuclei formation. In liver cells DNA damage and induction of oxidative stress with concurrent decrease in inhibition of antioxidant enzymes were noted. These in vitro and in vivo results demonstrated that ZnO-np induced genotoxic response and ROS production leading to apoptotic cell death and established a good co-relation between the two biological systems. More importantly, the results stress on the need of multiple endpoint assay-approaches, with an in vitro-in vivo study design to assess nanoparticle toxicology.     

Chicoric acid regulates behavioral and biochemical alterations induced by chronic stress in experimental Swiss albino mice

The present study was taken up to see the effect of chicoric acid (CA) on behavioral and biochemical alterations induced by chronic restraint stress in experimental Swiss albino mice. CA at 1 mg/kg dose level exhibited considerable antidepressant activity as shown by significant decrease in immobility period in the Porsolt's swim stress-induced behavioral despair test and escape failures in Learned “helplessness test”. The antidepressant activity shown by CA can be attributed to its modulating effect on nor-adrenaline (NA), dopamine (DA) and 5- hydroxy tryptamine (5-HT) as shown by their quantification in CA treated chronically stressed mice. Further, a significant antioxidant effect was exhibited by CA as shown by estimation of lipid peroxidation, glutathione (GSH) and glycogen in liver of chronically stressed mice. It also normalized altered values of serum glucose, triglycerides, aspartate aminotransferase (AST) alanine aminotransferase (ALT) and alkaline phosphatase (ALP) in a dose dependent manner. The stress busting potential of CA was further confirmed by its regulating effect on raised plasma corticosterone levels and significant attenuation of the depleted ascorbic acid, cholesterol and corticosterone levels in adrenal glands. Thus, our results suggest that CA possesses considerable stress busting potential, and that anti-oxidation may be one of the mechanisms underlying its antistress action.     

A teratogenic study of carbaryl in Swiss albino mice

To study the teratogenicity of carbaryl, groups of 10 pregnant mice were dosed, by gavage, with 0, 100, 150 or 200 mg carbaryl/kg body weight, in corn oil, on day 8 or day 12 of pregnancy or daily (as daily doses) from day 6 to day 15. The two higher doses were toxic to both dams and foetuses regardless of the timing of treatment. Treated dams generally showed reduced weight gains but total weight gain was significantly reduced only for dams given 200 mg carbaryl on day 8 or day 12 of gestation. Maternal mortality was increased in most groups given 150 or 200 mg carbaryl. Carbaryl treatment tended to reduce litter size, to increase the percentage of resorbed foetuses, and to reduce foetal weight. There were increased incidences of open eye, of certain visceral abnormalities, and of reduced ossification in virtually all treated groups. The variety of abnormalities in treated foetuses reflected the dysmorphogenic potential of the pesticide. More aberrations were seen in foetuses from dams treated throughout organogenesis than in those from dams given a single dose.     

Protective effects of fruit extracts of Hippophae rhamnoides L. against arsenic toxicity in Swiss albino mice

Seabuckthorn (Hippophae rhamnoides L.) berry has a long history of applications as a food and medicinal ingredient in eastern countries. The present study was carried out to investigate the effect of different fruit extracts of H. rhamnoides on altered biochemical parameters indicative of haematological alterations, tissue oxidative stress, and arsenic concentration in arsenic-exposed mice (2.5 mg/kg body weight, intraperitoneally). Two aqueous extracts (at room temperature and under reflux condition) and an ethanolic extract of H. rhamnoides at a dose of 500 mg/kg body weight were co-administered daily during arsenic exposure in mice for 3 weeks. Exposure to arsenic led to a significant inhibition of blood delta-aminolevulinic acid dehydratase (ALAD) activity, suggesting disturbed haem synthesis pathway. Arsenic also caused significant depletion of reduced hepatic glutathione (GSH) level, glutathione S-transferase (GST) and glutathione peroxidase and catalase activities, while it increased the level of thiobarbituric acid reactive substance (TBARS), suggesting liver oxidative stress. Most of the altered biochemical variables responded favorably to the co-supplementation of H. rhamnoides, particularly the aqueous fruit extract, extracted at room temperature (HF-WRT). However, arsenic concentration in blood and tissues remained unchanged, suggesting the lack of chelating property of fruit extract of H. rhamnoides. The present study, thus, led us to conclude that the fruit extract of H. rhamnoides has a significant protective role against arsenic-induced oxidative injury. However, it lacks the ability to remove arsenic from the binding sites, suggesting that the herbal extract could be co-administered with a chelating agent of known efficacy during treatment of arsenic to achieve the optimum effect of chelation treatment.     

Piroxicam attenuates 3-nitropropionic acid-induced brain oxidative stress and behavioral alteration in mice

3-Nitropropionic acid (3-NP) is a fungal toxin that produces Huntington’s disease like symptoms in both animals and humans. Piroxicam, a non-selective cyclooxygenase (COX) inhibitor, used as anti-inflammatory agent and also known to decrease free oxygen radical production. In this study, the effect of piroxicam was evaluated against 3-NP-induced brain oxidative stress and behavioral alteration in mice. Adult male Swiss albino mice were injected with vehicle/piroxicam (10 and 20?mg/kg, i.p.) 30?min before 3-NP challenge (15?mg/kg, i.p.) regularly for 14 days. Body weights of the mice were measured on alternative days of the experiment. At the end of the treatment schedule, mice were evaluated for behavioral alterations (movement analysis, locomotor test, beam walking test and hanging wire test) and brain homogenates were used for the estimation of oxidative stress markers (lipid peroxidation, reduced glutathione and catalase). Administration of 3-NP significantly altered the behavioral activities and brain antioxidant status in mice. Piroxicam, at both the tested doses, caused a significant reversal of 3-NP-induced behavioral alterations and oxidative stress in mice. These findings suggest piroxicam protects the mice against 3-NP-induced brain oxidative stress and behavioral alteration. The antioxidant properties of piroxicam may be responsible for the observed beneficial actions.