Brain Antioxidant Defense Research Articles

Naringenin-induced enhanced antioxidant defence system meliorates cholinergic neurotransmission and consolidates memory in male rats

AimsFree radical mediated neurotoxicity is a leading cause of neurodegenerative disorders. Neurodegeneration due to oxidative stress can produce cognitive dysfunctions. Flavonoids and curcuminoids are naturally occurring polyphenolic compounds that display a variety of therapeutic importance against oxidative stress. Main methodsThis study was designed to assess potential role of polyphenolic compounds in neurocognitive functions and prevention against oxidative stress. For this purpose, young rats were orally treated with naringenin (NAR), curcumin (CUR) and quercetin (QUE) at a dose of 50mg/kg, 200mg/kg and 50mg/kg respectively for 16days. At 4th day of drug administration cognitive functions were monitored by Morris water maze (MWM) test. In MWM cognitive functions in terms of learning acquisition (1h after training), retention (24h after training), memory extinction (4days after training), and reconsolidation (8 and 12days after training) were monitored. Biochemical and neurochemical analysis were done in whole brain. Key findingsTreatment of NAR, CUR and QUE significantly enhanced learning acquisition, memory retention and reconsolidation and prevented memory extinction. Treatment of NAR and QUE prevented the alteration of brain antioxidant defence system by enhancing antioxidant enzyme activities and increasing antioxidant compound concentration. Oxidative stress in terms of lipid peroxidation was significantly prevented in treated rats. Serotonergic and cholinergic improvement was also found in treated rats. SignificanceThe present study therefore provides biological evidence supporting the usefulness of these polyphenolic compounds in daily life for improvement of cognitive abilities and hence may have a potential role in the management of dementia and related disorders.

Hydroalcoholic extract of Dorema aucheri leaves prevents weakening of the brain antioxidant defense system and inhibits oxidative damage in rat model of ischemic stroke

Hydroalcoholic extract of Dorema aucheri leaves prevents weakening of the brain antioxidant defense system and inhibits oxidative damage in rat model of ischemic stroke

Dietary supplementation with acetyl-l-carnitine counteracts age-related alterations of mitochondrial biogenesis, dynamics and antioxidant defenses in brain of old rats

We previously reported the ability of dietary supplementation with acetyl-l-carnitine (ALCAR) to prevent age-related decreases of mitochondrial biogenesis in skeletal muscle and liver of old rats. Here, we investigate the effects of ALCAR supplementation in cerebral hemispheres and cerebellum of old rats by analyzing several parameters linked to mitochondrial biogenesis, mitochondrial dynamics and antioxidant defenses.We measured the level of the coactivators PGC-1α and PGC-1β and of the factors regulating mitochondrial biogenesis, finding an age-related decrease of PGC-1β, whereas PGC-1α level was unvaried. Twenty eight-month old rats supplemented with ALCAR for one and two months showed increased levels of both factors. Accordingly, the expression of the two transcription factors NRF-1 and TFAM followed the same trend of PGC-1β. The level of mtDNA, ND1 and the activity of citrate synthase, were decreased with aging and increased following ALCAR treatment. Furthermore, ALCAR counteracted the age-related increase of deleted mtDNA. We also analyzed the content of proteins involved in mitochondrial dynamics (Drp1, Fis1, OPA1 and MNF2) and found an age-dependent increase of MFN2 and of the long form of OPA1. ALCAR treatment restored the content of the two proteins to the level of the young rats. No changes with aging and ALCAR were observed for Drp1 and Fis1. ALCAR reduced total cellular levels of oxidized PRXs and counteracted the age-related decrease of PRX3 and SOD2.Overall, our findings indicate a systemic positive effect of ALCAR dietary treatment and a tissue specific regulation of mitochondrial homeostasis in brain of old rats. Moreover, it appears that ALCAR acts as a nutrient since in most cases its effects were almost completely abolished one month after treatment suspension. Dietary supplementation of old rats with this compound seems a valuable approach to prevent age-related mitochondrial dysfunction and might ultimately represent a strategy to delay age-associated negative consequences in mitochondrial homeostasis.

Brain region- and sex-specific alterations in mitochondrial function and NF-κB signaling in the TgCRND8 mouse model of Alzheimer’s disease

Alzheimer’s disease (AD) is the most common late onset neurodegenerative disorder with indications that women are disproportionately affected. Mitochondrial dysfunction has been one of the most discussed hypotheses associated with the early onset and progression of AD, and it has been attributed to intraneuronal accumulation of amyloid β (Aβ). It was suggested that one of the possible mediators for Aβ-impaired mitochondrial function is the nuclear factor kappa B (NF-κB) signaling pathway. NF-κB plays important roles in brain inflammation and antioxidant defense, as well as in the regulation of mitochondrial function, and studies have confirmed altered NF-κB signaling in AD brain. In this study, we looked for sex-based differences in impaired bioenergetic processes and NF-κB signaling in the AD-like brain using transgenic (Tg) CRND8 mice that express excessive brain Aβ, but without tau pathology. Our results show that mitochondrial dysfunction is not uniform in affected brain regions. We observed increased basal and coupled respiration in the hippocampus of TgCRND8 females only, along with a decreased Complex II-dependent respiratory activity. Cortical mitochondria from TgCRND8 mice have reduced uncoupled respiration capacity, regardless of sex. The pattern of changes in NF-κB signaling was the same in both brain structures, but was sex specific. Whereas in females there was an increase in all three subunits of NF-κB, in males we observed increase in p65 and p105, but no changes in p50 levels. These results demonstrate that mitochondrial function and inflammatory signaling in the AD-like brain is region- and sex-specific, which is an important consideration for therapeutic strategies.

P 051 - Intracerebroventricular injection of glycine alters enzymatic antioxidant defenses in rat striatum: prevention by bezafibrate

Non-ketotic hyperglycinemia (NKH) is an inborn error of metabolism caused by deficiency in the glycine (GLY) cleavage system and characterized by a high cerebrospinal fluid / plasma GLY ratio. NKH often results in early death, and therapeutical approaches are limited to controlling the symptoms, mainly seizures and hypotonia, and detoxifying GLY. Therefore, we evaluated antioxidant defenses in striatum, cerebral cortex and hippocampus of young rats following an intracerebral administration of GLY, as well as the beneficial effects of a pre-treatment with bezafibrate (BEZ), a potential neuroprotective compound, on the alterations caused by GLY. GLY administration increased the activities of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase in striatum, and decreased reduced glutathione concentrations in hippocampus. No significant alterations were verified in cerebral cortex. BEZ totally prevented GLY-induced increase of SOD and GR activities, and attenuated the increase of GPx activity. Our data show that GLY intracerebral administration disturbs antioxidant defenses in brain. In addition, since some alterations caused by GLY were prevented by BEZ, this compound may be considered as adjuvant therapy for NKH.

Fullerol potentiates the brain antioxidant defense system and decreases γ-glutamyl transpeptidase (GGT) mRNA during cerebral ischemia/reperfusion injury

AbstractFullerol compounds have potent antioxidant effects on biological systems. Therefore, we examined whether fullerol pretreatment potentiates the brain antioxidant defense system and decreases

Acute and Subchronic Toxicity Study of the Median Septum of Juglans regia in Wistar Rats.

Purpose: Median septum of Juglans regia L. (Juglandaceae) with anti-diabetic effects has been used in Iranian traditional medicine. The present study estimates both oral acute and subchronic toxicities. Methods: In the oral acute toxicity study, female Wistar rats were treated with doses of 10, 100, 1000, 1600, 2900 and 5000 mg/ kg of the Juglans regia septum of methanol extract (JRSME), and were monitored for 14 days. In subchronic study, JRSME was administered by gavage at dose of 1000 mg/kg daily in Wistar rats for 28 days. Antioxidant status and biochemical examinations were fulfilled, and the vital organs were subjected to pathological analyses. Results: The extract did not produce any toxic signs or deaths; the medium lethal dose must be higher than 5000 mg/kg. In subchronic study, No significant morphological and histopathological changes were observed in the studied tissues. There was a significant increase in serum malondialdehyde (MDA) level in treated group compared to control after 4 weeks of JRSME intake. The treatment of rats resulted in a significant reduction of serum urea level (p<0.05), kidney's xanthine dehydrogenase (XDH) activity (p<0.001) and elevation of aldehyde oxidase (AO) activity (p<0.05) in kidney. In the treated group, the mean diameter of glomerulus and proximal urine tube epithelium stature was slightly greater than control group. A significant increase in serum MDA level is subject for further studies. Conclusion: This study showed that the extract has no acute or subacute adverse effects with dose of 1000 mg/kg. The administration of JRSME may improve kidney structure and function and help in treatment of some chronic diseases.

Serum metabolites from walnut-fed aged rats attenuate stress-induced neurotoxicity in BV-2 microglial cells

The shift in equilibrium towards excess reactive oxygen or nitrogen species production from innate antioxidant defenses in brain is a critical factor in the declining neural function and cognitive deficit accompanying age. Previous studies from our laboratory have reported that walnuts, rich in polyphenols, antioxidants, and omega fatty acids such as alpha-linolenic acid and linoleic acid, improve the age-associated declines in cognition and neural function in rats. Possible mechanisms of action of these effects include enhancing protective signaling, altering membrane microstructures, decreasing inflammation, and preventing accumulation of polyubiquitinated protein aggregates in critical regions of the brain. In the current study, we investigated whether the serum collected from aged animals fed with walnut diets (0, 6, and 9%, w/w) would enhance protection on stressed BV-2 microglia in vitro. In the growth medium, fetal bovine serum was substituted with the serum collected from 22-month-old rats fed per protocol for 12 weeks. Walnut diet serum (6 and 9%) significantly attenuated lipopolysaccharide-induced nitrite release compared to untreated control cells and those treated with serum from rats fed 0% walnut diets. The results also indicated a significant reduction in pro-inflammatory tumor necrosis factor-alpha, cyclooxygenase-2, and inducible nitric oxide synthase. These results suggest antioxidant and anti-inflammatory protection or enhancement of membrane-associated functions in brain cells by walnut serum metabolites.

Neuroprotective potential of antioxidant potent fractions from Convolvulus pluricaulis Chois. in 3-nitropropionic acid challenged rats

Objective: To isolate the neuroprotective component from Convolvulus pluricaulis Chois. (Convolvulaceae) which can be used as a lead molecule in the treatment of Huntington's disease (HD).Methods: The methanolic extract of whole plant was fractionated into four fractions; chloroform, ethyl acetate, n-butanol, and aqueous fraction. The chloroform and ethyl acetate fractions were pooled on the basis of antioxidant activity and TLC profile and charged into silica gel column. Four subfractions were collected from column (FrA, FrB, FrC, and FrD) and further assessed for antioxidant potential by 2,2-diphenyl-1-picrylhydrazyl in vitro assay. 3-Nitropropionic acid (3-NP) was administered to Wister rats for induction of HD. Different fractions were administered for 14 days. Different behavioral alterations were assessed in between study period. Animals were euthanized immediately following the last behavioral session, and biochemical parameters were measured.Result and discussion: Systemic administration of 3-NP showed marked motor deficits and oxidative damage in rats. Only FrB showed significant antioxidant activity and on further purification gave pure compound (scopoletin). Our study showed that FrB (20 mg/kg) pre-treatment significantly attenuated the loss in body weight, improved the locomotor activity, grip strength, and gait abnormalities. It also has attenuated the increased malondialdehyde and nitrite levels, and restored superoxide dismutase and reduced GSH enzyme activity in the striatum and cortex in 3-NP-treated groups. These results suggest that C. pluricaulis Chois. exhibits a neuroprotective effect by accelerating brain antioxidant defense mechanisms in 3-NP-treated rats.

Ceftriaxone mediated rescue of nigral oxidative damage and motor deficits in MPTP model of Parkinson's disease in rats

Parkinson's disease is a neurodegenerative disorder characterized by the loss of dopamine neurons in the substantia nigra pars compacta along with decreased striatal dopamine levels, and consequent extra pyramidal motor dysfunctions occur. It has been reported that Ceftriaxone, a β-lactam antibiotic recently had shown to have neuroprotective effects in various neurodegenerative disorder. Therefore the present study was designed to investigate the effects of Ceftriaxone (CFX) in a MPTP model of Parkinson in rats. MPTP was administered intranigrally for the induction of PD in Male Wistar rats. Ceftriaxone (100 and 200mg/kg) and Ropinirole (1.5 and 3mg/kg) were given intraperitonially, after induction of Parkinson's disease for 14 days. Different behavioral performance was carried on 1st, 14th, 21st, 28th consecutive days and biochemical parameters were estimated on 28th day. Central administration of MPTP showed significant impairment of motor behavior and marked increase of oxidative damage and neuro-inflammmation in rats. However, post treatment with Ceftriaxone (100 and 200mg/kg) significantly improved the motor deficits and attenuated the oxidative damage indicating decreased rise of LPO and nitrite concentration and restored the decreased activities of endogenous antioxidant enzyme (Glutathione, Catalase, SOD). In addition Ceftriaxone also attenuates the pro-inflammatory cytokines like TNF-α and IL-β in striatum region of MPTP induced PD in rats. Ropinirole (1.5mg/kg) pretreatment with sub-effective dose of a Ceftriaxone (100mg/kg) had significantly enhanced the protective effect of Ceftriaxone as compare to its effect with per se group. These results suggested that Ceftriaxone exhibit Neuroprotective effect by mediating brain antioxidant defense mechanism and by up regulating of dopaminergic pathway and down regulation of glutamatergic pathway.

Lycopene protects against memory impairment and mito-oxidative damage induced by colchicine in rats: An evidence of nitric oxide signaling

Oxidative–nitrosative stress and mitochondrial dysfunction plays an important role in the onset of various neurodegenerative diseases. Lycopene, a carotenoid antioxidant, has received considerable scientific interest in recent years. Present study was designed to evaluate the possible nitric oxide mechanism in protective effects of lycopene against the colchicine induced cognitive impairment and mito-oxidative damage in rats. Wistar rats were received i.c.v. colchicine (15µg/5µl). Lycopene (2.5 and 5mg/kg), NO modulators e.g. l-Arginine (50mg/kg) l-NAME (5mg/kg) administered for 21 days. Behavioural alterations were assessed in between study period. Animals were killed immediately following the last behavioral session, and mitochondrial enzymes, oxidative parameters, inflammatory mediators (TNF-α, IL-6) and caspase-3 activity were measured. I.C.V. administration of colchicine impaired memory performance in Morris water maze, oxidative defense and mitochondrial complex enzymes activities as compared to sham group. A significant increase of TNF-α, IL-6 and caspase-3 activity in hippocampus and cortex was also noted. Chronic treatment lycopene significantly improved memory retention and attenuated mito-oxidative damage parameters, inflammatory markers and apoptosis in colchicine treated rats. Further, l-arginine pretreatment with sub effective dose of lycopene significantly reversed the protective effect of lycopene. However, l-NAME pretreatment with sub effective dose of lycopene significantly potentiated the protective effect of lycopene which was significant as compared to their effect per se. These results suggest that lycopene exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating nitric oxide pathways. Thus, lycopene may be used as therapeutic agent in preventing complications in memory dysfunction.

Effect of Hyperoxia on Resuscitation of Experimental Combined Traumatic Brain Injury and Hemorrhagic Shock in Mice

Hypotension and hypoxemia worsen traumatic brain injury outcomes. Hyperoxic resuscitation is controversial. The authors proposed that hyperoxia would improve hemodynamics and neuronal survival by augmenting oxygen delivery despite increased oxidative stress and neuroinflammation in experimental combined controlled cortical impact plus hemorrhagic shock in mice. Adult C57BL6 mice received controlled cortical impact followed by 35 min of hemorrhagic shock (mean arterial pressure, 25-27 mmHg). The resuscitation phase consisted of lactated Ringer's boluses titrated to mean arterial pressure greater than 70 mmHg. Definitive care included returning shed blood. Either oxygen or room air was administered during the resuscitation phases. Brain tissue levels of oxidative stress and inflammatory markers were measured at 24 h and hippocampal neuronal survival was quantified at 7 days. Hyperoxia markedly increased brain tissue oxygen tension approximately four- to fivefold (n = 8) and reduced resuscitation fluid requirements approximately 15% (n = 53; both P < 0.05). Systemic and cerebral physiologic variables were not significantly affected by hyperoxia. Hippocampal neuron survival was approximately 40% greater with oxygen versus room air (n = 18, P = 0.03). However, ascorbate depletion doubled with oxygen versus room air (n = 11, P < 0.05). Brain tissue cytokines and chemokines were increased approximately 2- to 20-fold (n = 10) after combined controlled cortical impact injury plus hemorrhagic shock, whereas hyperoxia shifted cytokines toward a proinflammatory profile. Hyperoxic resuscitation of cortical impact plus hemorrhagic shock reduced fluid requirements and increased brain tissue oxygen tension and hippocampal neuronal survival but exacerbated ascorbate depletion and neuroinflammation. The benefits of enhanced oxygen delivery during resuscitation of traumatic brain injury may outweigh detrimental increases in oxidative stress and neuroinflammation.

Maternal exercise improves antioxidant defenses in brain of young Wistar rats

Maternal exercise improves antioxidant defenses in brain of young Wistar rats

Disruption of redox homeostasis in cerebral cortex of developing rats by acylcarnitines accumulating in medium-chain acyl-CoA dehydrogenase deficiency

Medium-chain fatty acids and acylcarnitines accumulate in medium-chain acyl-CoA dehydrogenase deficiency (MCADD), the most frequent fatty acid oxidation defect clinically characterized by episodic crises with vomiting, seizures and coma. Considering that the pathophysiology of the neurological symptoms observed in MCADD is poorly known and, to our knowledge, there is no report on the involvement of acylcarnitines in the brain damage presented by the affected patients, the objective of the present study was to investigate the in vitro effects of hexanoylcarnitine (HC), octanoylcarnitine, decanoylcarnitine (DC) and cis-4-decenoylcarnitine (cDC) at concentrations varying from 0.01 to 1.0mM on important oxidative stress parameters in cerebral cortex of young rats. HC, DC and cDC significantly induced lipid peroxidation, as determined by increased thiobarbituric acid-reactive substances (TBA-RS) values. In addition, carbonyl formation was significantly augmented and sulfhydryl content diminished by DC, reflecting induction of protein oxidative damage. HC, DC and cDC also decreased glutathione (GSH) levels, the most important brain antioxidant defense. Furthermore, DC-induced elevation of TBA-RS values and decrease of GSH levels were prevented by the free radical scavengers melatonin and α-tocopherol, indicating the involvement of reactive oxygen species in these effects. We also found that l-carnitine itself did not induce lipid and protein oxidative damage, neither reduced the antioxidant defenses. Our present data show that the major medium-chain acylcarnitines accumulating in MCADD elicit oxidative stress in rat brain. It is therefore presumed that these compounds may be involved to a certain extent in the pathogenesis of the neurologic dysfunction of MCADD.

Antioxidant and bioenergetic coupling between neurons and astrocytes

Oxidative and nitrosative stress underlie the pathogenesis of a broad range of human diseases, in particular neurodegenerative disorders. Within the brain, neurons are the cells most vulnerable to excess reactive oxygen and nitrogen species; their survival relies on the antioxidant protection promoted by neighbouring astrocytes. However, neurons are also intrinsically equipped with a biochemical mechanism that links glucose metabolism to antioxidant defence. Neurons actively metabolize glucose through the pentose phosphate pathway, which maintains the antioxidant glutathione in its reduced state, hence exerting neuroprotection. This process is tightly controlled by a key glycolysis-promoting enzyme and is dependent on an appropriate supply of energy substrates from astrocytes. Thus brain bioenergetic and antioxidant defence is coupled between neurons and astrocytes. A better understanding of the regulation of this intercellular coupling should be important for identifying novel targets for future therapeutic interventions.

Long-term consumption of aspartame and brain antioxidant defense status

The present study investigated the effect of long-term intake of aspartame, a widely used artificial sweetener, on antioxidant defense status in the rat brain. Male Wistar rats weighing 150–175 g were randomly divided into three groups as follows: The first group was given aspartame at a dose of 500 mg/kg body weight (b.w.); the second group was given aspartame at dose of 1,000 mg/kg b.w., respectively, in a total volume of 3 mL of water; and the control rats received 3 mL of distilled water. Oral intubations were done in the morning, daily for 180 days. The concentration of reduced glutathione (GSH) and the activity of glutathione reductase (GR) were significantly reduced in the brain of rats that had received the dose of 1,000 mg/kg b.w. of aspartame, whereas only a significant reduction in GSH concentration was observed in the 500-mg/kg b.w. aspartame-treated group. Histopathological examination revealed mild vascular congestion in the 1,000 mg/kg b.w. group of aspartame-treated rats. The results of this experiment indicate that long-term consumption of aspartame leads to an imbalance in the antioxidant/pro-oxidant status in the brain, mainly through the mechanism involving the glutathione-dependent system.

Influence of Punica granatum L. on region specific responses in rat brain during Alloxan-Induced diabetes

ObjectiveThe present study was carried out to investigate the effects of Punica granatum peel methanolic extract (PGPE) on cerebral cortex (CC) and Hippocampus (HC) brain antioxidant defense system and markers of lipid and protein oxidation in alloxan induced diabetic rats. MethodsOral administration of PGPE (75 and 150 mg of kg body weight) for 45 days resulted in significant reduction in blood glucose levels. ResultsSupplementation of diabetic rats with PGPE showed increased activities of SOD and GPx with concomitant decrease in MDA and PC content. Region-specific changes were more evident in the HC when compared to CC. ConclusionsThe present study indicated that PGPE can ameliorate brain oxidative stress in alloxan induced diabetic rats by up regulating antioxidant defense mechanism by attenuating lipid and protein oxidation. PGPE thus may be used as a potential therapeutic agent in preventing diabetic complications in the brain.

Microsomal Lipid Peroxidation, Antioxidant Enzyme Activities in Brain of Male Rats during Long-Term Exposure to Isoniazid

Isoniazid, a broad-spectrum antibiotic employed clinically in the treatment of bacterial infections, is known to cause a number of biochemical dysfunctions and suspected to induce memory decline with age to animals and humans. The present study therefore evaluates the oxidative damage in brain albino male rats. Isoniazid was administered orally at the dose regimen level of 5.0 mg/kg body weight per day in three equal divided doses of 10, 20, 30mg/kg (12 h interval) for 60 days. Control rats were given distilled water for the same period. Administration of Isoniazid significantly decreased the activity of superoxide dismutase. The activity of gamma-glutamyltranspeptidase, the activity of alanine-amino transferase (ALT) and alkaline phosphatase (ALP) as well as the formation of malondialdehyde (MDA) increased (p<0.05) compared to the corresponding control. The toxic effects of Isoniazid to the brain antioxidant defence systems were significantly increased. Collectively, the results suggest that therapeutic dose of Isoniazid elicits brain lesions in male rats through induction of oxidative damage and via the inhibitory effect on protein synthesis.

Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats

Alzheimer’s disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.

The effects of Feijoa sellowiana fruits on the antioxidant defense system, lipid peroxidation, and tissue morphology in rats

Context: The fruits of Feijoa sellowiana Berg. (Myrtaceae) have been used to treat goiter in traditional Turkish medicine.Objective: To evaluate the in vivo antioxidant activities of different polarities of the fruit extracts in blood and tissue (liver, kidney, brain, and heart) antioxidant defense systems in standard pellet diet and in high fat diet consumed, male rats were assessed.Materials and methods: The extracts (methanol, n-hexane, chloroform, ethyl acetate, n-butanol, and aqueous) were administered orally to male rats at 50 mg/kg doses daily for 4 weeks. The blood and tissue malondialdehyde (MDA), reduced glutathione (GSH) levels, plasma nitrate (NOx) level, total triiodothyronine (T3), thyroxine, cholesterol, triglyceride, protein, and glucose levels were determined, and erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities; plasma antioxidant activity (AOA) were experimentally studied.Results: Blood MDA level (7.81 ± 0.4) was significantly decreased; GSH level (29.65 ± 1.21) and AOA (1.52 ± 0.08) were increased in ethyl acetate extract as compared with control and the other extracts. In addition, all the extracts decreased MDA levels and increased GSH levels (except brain tissue homogenate) in the tissue homogenates. Erythrocyte SOD and CAT activity levels were unchanged in F. sellowiana extracts. However, the extracts had no effect on plasma NOx. In the histopathological examinations, any changes or damage in the vital organs were seen in animals.Conclusion: The experimental data demonstrated that F. sellowiana extracts displayed remarkable antioxidant activity and decreased lipid peroxidation in rats; furthermore, no histopathological changes or damage have been observed in the vital organs of rats.