Acrylamide-induced Neurotoxicity Research Articles

Investigation of Neuroprotective Activity of Extracts of Asparagus racemosus Wild. in Acrylamide Induced Neurotoxicity in Adult Zebrafish

The efficacy of an extract from Asparagus racemosus seeds in protecting zebrafish neurons from acrylamide-induced neurotoxicity was the focus of this investigation. ACR treatment induced neurotoxicity in zebrafish by reducing glutathione reductase levels by a factor of 3, increasing lipid peroxidation activity by a factor of 3.4, elevating nitrite levels by a factor of 1.7, raising acetylcholinesterase levels by a factor of 3.9, and decreasing total protein levels by a factor of 1.4, when compared to wild-type zebrafish. Vinpocetine demonstrated neuroprotective properties in ACR-induced zebrafish. These results indicate a 2.7-fold increase in glutathione reductase, a 3.4-fold reduction in lipid peroxidation activity, a 1.5-fold decrease in nitrite levels, a 3.2-fold decrease in acetylcholinesterase levels, and a 1.4-fold increase in total protein levels. Zebrafish with inherent genetic traits had similar outcomes. Treatment with solvent seed extracts from A. racemosus effectively reduced the damage caused by ACR. Following this intervention, levels of glutathione reductase, lipid peroxides, nitrite, protein, and acetylcholinesterase activity reverted back to levels seen in control group. The ethanolic extract exhibited superior neuroprotective effects compared to the solvent extract in zebrafish treated with ACR. After administering an ethanolic seed extract therapy at a concentration of 440 mg/l, the levels of glutathione reductase rose by a factor of 2.7. Simultaneously, there was a decrease in lipid peroxidation activity by 3.1, nitrite by 1.4, and acetylcholinesterase by 2.7. The protein content of zebrafish exposed to ACR rose by a factor of 1.3. Wild zebrafish had comparable results

Blood RNA-sequencing analysis in acrylamide-induced neurotoxicity and depressive symptoms in rats.

Acrylamide (ACR) is a by-product of the Maillard reaction, which occurs when food reacts at high temperatures. Occupational exposure is a risk factor for chronic ACR toxicity. ACR may cause neurotoxicity and depressive symptoms with high concentration in the blood; however, the underlying mechanism remains unknown. We showed the rats developed neurotoxic symptoms after being fed with ACR for 28 days, such as reduced activity and hind limb muscle weakness. We investigated whether ACR exposure causes gene expression differences by blood RNA sequencing and analyzed the differential expression of depressive symptoms-associated genes. The result indicated that IFN-γ the key regulator of neurotoxicity and depressive symptoms was induced by ACR. ACR induced the ubiquitin-mediated proteolysis pathway and JAK/STAT pathways gene expression. ACR upregulated the expression of IFN-γ, inducing neuroinflammation and neurotoxicity. ACR also upregulated the expression of JAK2, STAT1, PI3K, AKT, IκBα, UBE2D4, NF-κB, TNF-α, and iNOS in rat brain tissues and Neuro-2a cells. Thus, IFN-γ induction by ACR may induce depressive symptoms, and the ubiquitin-mediated proteolysis pathway and JAK/STAT pathways may involve in ACR neurotoxicity and depressive symptoms.

High-fat diet exacerbated motor dysfunction via necroptosis and neuroinflammation in acrylamide-induced neurotoxicity in mice

Health risks associated with acrylamide (ACR) or high-fat diet (HFD) exposure alone have been widely concerned in recent years. In a realistic situation, ACR and HFD are generally co-existence, and both are risk factors for the development of neurological diseases. The purpose of the present study was to investigate the combined effects of ACR and HFD on the motor nerve function. As a result, neurobehavioral tests and Nissl staining disclosed that long-term HFD exacerbated motor dysfunction and the damage of spinal cord motor neurons in ACR-exposed mice. Co-exposure of ACR and HFD resulted in morphological changes in neuronal mitochondria of the spinal cord, a significantly reduced mitochondrial subunits NDUFS1, UQCRC2, and MTCO1, released the mitochondrial DNA (mtDNA) into the cytoplasm, and promoted the production of reactive oxygen species (ROS). Combined exposure of HFD and ACR activated the calpain/CDK5/Drp1 axis and caused the mitochondrial excessive division, ultimately increasing MLKL-mediated necroptosis in spinal cord motor neurons. Meanwhile, HFD significantly exacerbated ACR-induced activation of NFkB, NLRP3 inflammasome, and cGAS-STING pathway. Taken together, our findings demonstrated that combined exposure of ACR and HFD aggravated the damage of spinal cord motor neurons via neuroinflammation and necroptosis signaling pathway, pointing to additive effects in mice than the individual stress effects.

Protective effect of Punica granatum peel extract and its alginate-encapsulated nanoparticles against acrylamide-induced neurotoxicity in rats

Protective effect of Punica granatum peel extract and its alginate-encapsulated nanoparticles against acrylamide-induced neurotoxicity in rats

Preventive and therapeutic effects of azithromycin on acrylamide-induced neurotoxicity in rats

BackgroundAcrylamide (ACR) can induce neurotoxicity through different pathways, including oxidative stress and apoptosis. Azithromycin is well-known for its antioxidant and anti-apoptotic properties. ObjectiveTo evaluate the potential neuroprotective effect of azithromycin in an in vivo model of ACR-induced neurotoxicity, by investigating its impact on oxidative stress and apoptosis pathways. MethodsMale rats were divided into eleven groups at random (n = 6). 1:control (vehicle), 2:ACR (50 mg/kg, 11 days, I.P.), 3–7:ACR+ azithromycin (3.1, 6.25, 12.5, 25, 50 mg/kg, 11 days, I.P.), 8–9:ACR+ azithromycin (3.1, 6.25 mg/kg, from day 3–11), 10: ACR+ vitamin E (200 mg/kg, every other day, I.P.), 11. Azithromycin (50 mg/kg). Following the treatment period, a gait score examination was performed, and malondialdehyde (MDA), glutathione (GSH), Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio and caspase-3 levels in the cerebral cortex were measured. ResultsGait abnormality, a drop in GSH, and an increase in lipid peroxidation, Bax/Bcl-2 ratio, and caspase-3 levels were all significantly triggered by ACR in the cerebral cortex versus the control group. Azithromycin 3.1 and 6.25 mg/kg with ACR and azithromycin 6.25 mg/kg with ACR from day 3–11 ameliorated movement disorders caused by ACR. Azithromycin in all doses and both protocols along with ACR decreased the MDA level. Azithromycin (3.1, 6.25 mg/kg) along with ACR in both protocols increased the level of GSH, reduced the Bax/Bcl-2 ratio and caspase-3 amounts in the brain tissue versus the ACR group. ConclusionsAdministration of azithromycin had both preventive and therapeutic effects on ACR-induced neurotoxicity through its antioxidant and antiapoptotic properties.

Transcriptome analysis of the cerebral cortex of acrylamide-exposed wild-type and IL-1β-knockout mice.

Acrylamide is an environmental electrophile that has been produced in large amounts for many years. There is concern about the adverse health effects of acrylamide exposure due to its widespread industrial use and also presence in commonly consumed foods and others. IL-1β is a key cytokine that protects the brain from inflammatory insults, but its role in acrylamide-induced neurotoxicity remains unknown. We reported recently that deletion of IL-1β gene exacerbates ACR-induced neurotoxicity in mice. The aim of this study was to identify genes or signaling pathway(s) involved in enhancement of ACR-induced neurotoxicity by IL-1β gene deletion or ACR-induced neurotoxicity to generate a hypothesis mechanism explaining ACR-induced neurotoxicity. C57BL/6J wild-type and IL-1β KO mice were exposed to ACR at 0, 12.5, 25mg/kg by oral gavage for 7days/week for 4weeks, followed by extraction of mRNA from mice cerebral cortex for RNA sequence analysis. IL-1β deletion altered the expression of genes involved in extracellular region, including upregulation of PFN1 gene related to amyotrophic lateral sclerosis and increased the expression of the opposite strand of IL-1β. Acrylamide exposure enhanced mitochondria oxidative phosphorylation, synapse and ribosome pathways, and activated various pathways of different neurodegenerative diseases, such as Alzheimer disease, Parkinson disease, Huntington disease, and prion disease. Protein network analysis suggested the involvement of different proteins in related to learning and cognitive function, such as Egr1, Egr2, Fos, Nr4a1, and Btg2. Our results identified possible pathways involved in IL-1β deletion-potentiated and ACR-induced neurotoxicity in mice.

Effect of royal jelly on acrylamide-induced neurotoxicity in rats

Royal Jelly (RJ) is a natural product made by nurse bees known for its multiple therapeutic properties. The research aims to discover the ability of RJ to improve the hematological alterations and neurotoxicity caused by acrylamide (AA). The study rats were separated equally into four groups (6 in each group), the control group, the AA (38.27 mg/kg bw) group, the RJ (150 mg/kg bw) + AA group, and the RJ (300 mg/kg bw) + AA group. Blood and brain samples were collected after 10 days to evaluate haematological and biochemical parameters and to examine histopathological and immunohistochemistry. The administration of AA increased the level of malondialdehyde (MDA), decreases levels of haematological parameters, superoxide dismutase (SOD), reduced glutathione (GSH), brain-derived neurotrophic factor (BDNF), neurotransmitters (serotonin, dopamine, and acetylcholine), and cleaved caspase-3, as well as increase the damage to the brain tissues. Meanwhile, RJ improved levels of haematological parameters, oxidative stress parameters (MDA, SOD, and GSH), BDNF, neurotransmitters, cleaved caspase-3, and brain tissue damage induced by AA. The study demonstrated the protective impact of RJ against the haematological alterations and neurotoxicity caused by AA.

The ameliorative effects of aqueous allium sativum on acrylamide-induced neurotoxicity in drosophila melanogaster model

The ameliorative effects of aqueous allium sativum on acrylamide-induced neurotoxicity in drosophila melanogaster model

The ameliorative effects of aqueous allium sativum on acrylamide-induced neurotoxicity in drosophila melanogaster model

The ameliorative effects of aqueous allium sativum on acrylamide-induced neurotoxicity in drosophila melanogaster model

Neuroprotective Effect of Ethanolic Extract of Scoparia dulcis on Acrylamide-Induced Neurotoxicity in Zebrafish Model.

All herbal medicines are reported to be safe and have better results in curing disabilities. Scoparia dulcis is known for its anti-inflammatory and antioxidant properties. This study has been executed to explore the neuroprotective effects of ethanolic extract of Scoparia dulcis (EESD) against acrylamide using adult zebrafish. The experimental period was 72h. After fixing the optimum acrylamide concentration and EESD, the healthy adult fish were grouped into control, induction, and treatment. During the experimental period, behavioural changes such as memory and locomotion were observed in control and experimental groups using the T-maze experiment. After 72h, the neuronal tissues were isolated from the grouped fishes and analysed for various biochemical and enzymatic assays. The mRNA of the HSP-70 gene in control and experimental groups was expressed using RT-PCR. The optimum dosages for acrylamide and EESD were found to be 0.75mM and 20µg/mL, respectively. Memory improvement was observed in S. dulcis-treated fish, compared to the acrylamide-treated group using the T-maze assay. The extract reduced the toxicity induced by acrylamide from the various biochemical and histopathological parameters. The result shows the potential neuroprotective effects of ethanolic extract of Scoparia dulcis (EESD) against acrylamide-induced neurotoxicity in adult zebrafish. Therefore, Scoparia dulcis is a potent neuroprotective agent.

Deletion of IL-1β exacerbates acrylamide-induced neurotoxicity in mice.

Acrylamide is a neurotoxicant in human and experimental animals. Interleukin-1β (IL-1β) is a proinflammatory cytokine known as a critical component of brain reaction to any insult or neurodegenerative pathologies, though its role in electrophile-induced neurotoxicity remains elusive. The aim of this study was to investigate the role of IL-1β in acrylamide-induced neurotoxicity in mice. Ten-week-old male wild-type and IL-1β knock-out mice were allocated into 3 groups each and exposed to acrylamide at 0, 12.5, 25 mg/kg body weight by oral gavage for 28 days. Compared with wild-type mice, the results showed a significant increase in landing foot spread test and a significant decrease in density of cortical noradrenergic axons in IL-1β KO mice exposed to acrylamide at 25 mg/kg body weight. Exposure to acrylamide at 25 mg/kg significantly increased cortical gene expression of Gclc, Gpx1, and Gpx4 in wild-type mice but decreased them in IL-1β KO mice. The same exposure level significantly increased total glutathione and oxidized glutathione (GSSG) in the cerebellum of wild-type mice but neither changed total glutathione nor decreased GSSG in the cerebellum of IL-1β KO mice. The basal level of malondialdehyde in the cerebellum was higher in IL-1β KO mice than in wild-type mice. The results suggest that IL-1β protects the mouse brain against acrylamide-induced neurotoxicity, probably through suppression of oxidative stress by glutathione synthesis and peroxidation. This unexpected result provides new insight on the protective role of IL-1β in acrylamide-induced neurotoxicity.

Protective effect and mechanism of Lycium ruthenicum polyphenols against acrylamide-induced neurotoxicity.

This study aimed to investigate the potential neuroprotective effects of Lycium ruthenicum polyphenols (LRP) against acrylamide (ACR)-induced neurotoxicity and the mechanism of action in vitro and in vivo. LRP treatment significantly attenuated ACR-induced cytotoxicity in SH-SY5Y cells in a dose-dependent manner. LRP treatment increased the nuclear factor erythroid-2-related factor 2 (Nrf2) protein and subsequent activation of downstream proteins in SH-SY5Y cells. LRP treatment down-regulated the expression of relevant apoptotic proteins, including JNK, P-JNK, P38, P-P38, and caspase 3 in ACR-induced cells. In vivo, LRP improved exploratory and locomotor deficits in ACR-induced rats. LRP activated the Nrf2 pathway in the striatum and substantia nigra. LRP treatment attenuated striatal ROS levels and increased GSH and SOD in ACR-induced rats. Immunohistochemistry, western blot, and ELISA revealed a significant increase in tyrosine hydroxylase (TH) neurons and dopamine and its metabolites in the striatum and substantia nigra under the protective effect of LRP. Therefore, LRP can be a protective agent against ACR-induced brain damage.

Palliative effect of Moringa olifera-mediated zinc oxide nanoparticles against acrylamide-induced neurotoxicity in rats.

Repeated acrylamide (ACR) exposure in experimental animals and humans causes variable degrees of neuronal damage. Because of its unique features, several green synthesized nanomaterials are explored for neuromodulatory activity. Hence, this study investigated the effect of green synthesized zinc oxide nanoparticles using Moriga olifera leaves extract (MO-ZnONP) against acrylamide (ACR)-induced neurobehavioral and neurotoxic impacts in rat. Forty male Sprague Dawley rats were distributed into four groups orally given distilled water, MO-ZnONP (10mg/kg b.wt), ACR (20mg/kg b.wt), or MO-ZnONP+ACR for 60 days. Gait quality and muscular, motor, and sensory function were assessed. Acetylcholinesterase (AChE), dopamine, catalase, malondialdehyde (MDA), and Zn brain contents were determined. Brain histopathology and immunohistochemical localization of the amyloid-β protein and abnormal Tau were performed. The results revealed that MO-ZnONP significantly reduced ACR-induced sensory dysfunctions, hind limb abnormality, and motor deficits. Additionally, the ACR-induced increase in dopamine and AChE were significantly supressed by MO-ZnONP. Besides, MO-ZnONP significantly restored catalase and Zn content but reduced increased MDA brain content resulting from ACR. Furthermore, the ACR-induced neurodegenerative changes and increased amyloid-β and phosphorylated Tau immunoexpression was significantly abolished by MO-ZnONP. Conclusively, MO-ZnONP could be used as a biologically effective compound for mitigating ACR's neurotoxic and neurobehavioral effects.

Investigating the effect of telmisartan on acrylamide-induced neurotoxicity through in vitro and in vivo methods.

Acrylamide (ACR) is an environmental contaminant and neurotoxin. Telmisartan is an AT1 blocker that has neuroprotective properties basically through its anti-oxidant effect. The effect of telmisartan on ACR-induced neurotoxicity was investigated in this study. Male Wistar rats were randomly assigned to eight groups (n=6): 1:Control (normal saline), 2:ACR (50 mg/kg, 11 days, IP), 3:ACR+vitamin E (200 mg/kg, every other day, 11 days), 4-6:ACR+telmisartan (0.6, 1.25, and 2.5 mg/kg, 11 days, IP), 7:ACR+telmisartan (0.6 mg/kg, days 3-11), 8:Telmisartan (2.5 mg/kg, 11 days). The behavioral test and blood pressure were assessed after 11 days. Then, the levels of MDA and GSH in brain tissue were measured. The MTT assay was used to evaluate the effect of telmisartan on ACR-induced cytotoxicity. Exposing PC12 cells to ACR decreased cell viability versus the control group. Pretreating PC12 cells with telmisartan (0.0125, 0.025 µM) enhanced cell viability compared with the ACR group. Compared with control samples, ACR significantly caused motor impairment, elevated MDA, and reduced GSH levels. Locomotor abnormalities were significantly ameliorated by telmisartan (0.6, 1.25 mg/kg, 11 days) and vitamin E versus the ACR group. Receiving telmisartan (0.6, 1.25, and 2.5 mg/kg) and vitamin E along with ACR decreased MDA levels and enhanced GSH content compared with the ACR group. There was no significant difference in animal blood pressure between the groups. Oxidative stress has a chief role in the neurotoxicity of ACR. Telmisartan (in doses that do not affect blood pressure) ameliorated ACR-induced toxicity by inhibiting oxidative stress.

The Mechanism of Acrylamide-Induced Neurotoxicity: Current Status and Future Perspectives.

Acrylamide (ACR), a potential neurotoxin, is produced by the Maillard reaction between reducing sugars and free amino acids during food processing. Over the past decade, the neurotoxicity of ACR has caused increasing concern, prompting many related studies. This review summarized the relevant literature published in recent years and discussed the exposure to occupational, environmental, and daily ACR contamination in food. Moreover, ACR metabolism and the potential mechanism of ACR-induced neurotoxicity were discussed, with particular focus on the axonal degeneration of the nervous system, nerve cell apoptosis, oxidative stress, inflammatory response, and gut-brain axis homeostasis. Additionally, the limitations of existing knowledge, as well as new perspectives, were examined, specifically regarding the connection between the neurotoxicity caused by ACR and neurodegenerative diseases, NOD-like receptor protein 3 (NLRP3) inflammasome-related neuroinflammation, and microbiota-gut-brain axis signaling. This review might provide systematic information for developing an alternative pathway approach to assess ACR risk.

AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity.

Acrylamide (ACR) is present in high-temperature-processed high-carbohydrate foods, cigarette smoke, and industrial pollution. Chronic exposure to ACR may induce neurotoxicity from reactive oxygen species (ROS); however, the mechanisms underlying ACR-induced neurotoxicity remain unclear. We studied 28-day subacute ACR toxicity by repeatedly feeding ACR (0, 15, or 30 mg/kg) to rats. We conducted RNA sequencing and Western blot analyses to identify differences in mRNA expression in the blood and in protein expression in the brain tissues, respectively, of the rats. AQP4 transient transfection was performed to identify potential associations with protein regulation. The rats treated with 30 mg/kg ACR exhibited hind-limb muscle weakness. Matrix metalloproteinase (MMP9) expression was higher in the ACR-treated group than in the control group. ACR induced MMP-9 and AQP4 protein expression in the brain tissues of the rats, which subsequently presented with neurotoxicity. In the in vitro study, Neuro-2a cells were transiently transfected with AQP4, which inhibited MMP-9 and TNF receptor-associated factor 6 (TRAF6) expression, and inhibited ACR induced expression of TRAF6, IκBα, and nuclear factor κB (NFκB). Using a combination of in vivo and in vitro experiments, this study revealed that depressive symptoms associated with ACR-induced neurotoxicity are associated with downregulation of AQP4 and induction of the TRAF6 pathway.

The involvement of oxidative stress, neuronal lesions, neurotransmission impairment, and neuroinflammation in acrylamide-induced neurotoxicity in C57/BL6 mice

The involvement of oxidative stress, neuronal lesions, neurotransmission impairment, and neuroinflammation in acrylamide-induced neurotoxicity in C57/BL6 mice

Protective effect of aqueous and ethanolic extracts of Lippia citriodora Kunth. on acrylamide-induced neurotoxicity.

Objective:Acrylamide (ACR) neurotoxicity is induced by different mechanisms such as oxidative stress and apoptosis. Scientific researchs have indicated the antioxidative properties of Lippia citriodora. The protective effect of L. citriodora aqueous and ethanolic extracts on ACR-induced neurotoxicity was investigated.Materials and methods:Male Wistar rats were randomly divided into 13 groups: (1) control, (2) ACR (50 mg/kg, i.p.), (3-6) ACR+aqueous extract (12.5, 25, 50, and 100 mg/kg, i.p.), (7-10) ACR+ethanolic extract (12.5, 25, 50, and 100 mg/kg, i.p.), (11) aqueous extract (100 mg/kg), (12) ethanolic extract (100 mg/kg), and (13) ACR+Vitamin E (200 mg/kg, every other day, i.p.). After 11 days, gait score, MDA, and GSH levels in brain cortical tissue were measured. In the in vitro test, the viability of PC12 cells (using MTT test), the amount of reactive oxygen species (ROS; using DCFH-DA method), and the protein levels of Bax, Bcl2 and caspase 3 (by western blotting) were measured. Results:In the in vitro study, the IC50 for the treatment of PC 12 cells with ACR after 24 hr was 6 mM. ACR decreased cell viability, but increased ROS level, Bax/Bcl-2 ratio, and caspase-3 protein level. Pre-treatment by L. citriodora extracts (15-120 µg/ml) ameliorated the toxic effects of ACR on PC12 cells. In the in vivo experiment, ACR-induced movement disorders increased MDA but decreased GSH content. The extracts of L. citriodora improved ACR toxic effects. Conclusion:Aqueous and ethanolic extracts of L. citriodora were found to reduce ACR-induced neurotoxicity via inhibiting oxidative stress and apoptosis.

The effects of acrylamide-mediated dorsal root ganglion neurons injury on ferroptosis.

Acrylamide (ACR) is a water-soluble chemical applied in industrial and laboratory processes. The neurotoxicity induced by acrylamide involves both peripheral and central nervous system. Hence, there is a growing urgency to investigate the mechanisms of acrylamide-induced neurotoxicity and search novel therapeutic target for the nerve repair. The effects of ACR on the proliferation, reactive oxygen species (ROS) and iron production of dorsal root ganglia (DRG) neurons and Schwann cells were determined. 5-Ethynyl-2'-deoxyuridine (EDU) staining and transwell assay were applied to detect the proliferation and migration capacity of DRG cells. Ferrostatin-1 (Fer-1) was used to suppress ferroptosis induced by ACR. RT-PCR analysis was performed to examine the expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), vascular endothelial growth factor (VEGF) and glial cell line-derived neurotrophic factor (GDNF). Moreover, Iron, ROS, malondialdehyde (MDA) and glutathione (GSH) contents were measured to reveal the regulation of ferroptosis in ACR-related nerve injury. ACR inhibited the proliferation and migration of DRG neurons and the supplementation of Fer-1 reversed the effects induced by ACR. Besides, the treatment of Fer-1 effectively increased the expression of NGF, BDNF, VEGF and GDNF. Furthermore, ACR increased the iron level, MDA and ROS contents while inhibited the level of GSH. It was unveiled that ACR attenuated the proliferation, migration and neuron repair of DRG neurons through regulating ferroptosis. The modulation of ferroptosis might be a promising therapeutic strategy and provide references for future treatment of acrylamide-induced nerve damage.

Ameliorative activity of medicinal plant fraction for neuroprotection against acrylamide-induced neurotoxicity in Drosophila melanogaster\u2014a comparative study

BackgroundMedicinal plant extracts used in folk medicine seem to be crucial since those are generally accepted by people without worrying about the toxicity. In our present study, we have compared the neuroprotective role of the rhizome of Curculigo orchioides Gaertn. and leaf extracts of Olea dioica Roxb., against acrylamide-induced neurotoxicity in Drosophila melanogaster.ResultsIn-vivo neurotoxic study was carried out using 7-day-old flies (wild-type D. melanogaster). Prior to co-after exposing the flies with acrylamide (8 mM) along with or without OLE-2 and CU-3 fractions (0.2, 0.4 and 0.6% w/v), the heads of flies of both the control and treated groups were homogenized for biochemical assay. ACR-treated groups have shown higher elevation in AChE, SOD, LPO, and CAT activity when compared to control and treated (plant fraction) groups. Biochemical and histopathology studies show that both the plant fractions (OLE-2 and CU-3) have neuroprotective action against acrylamide.ConclusionThe present study has demonstrated that dietary supplementation with plant fraction of OLE-2 and CU-3 has increased antioxidant enzymes and decreased AChE activity in D. melanogaster. This activity could be part of the probable mechanisms of action by which OLE-2 and CU-3 fractions have extended the lifespan and locomotory activity in fruit flies. These fruit flies continue to provide an exciting system for metabolic studies and should be more extensively exploited. Based on these results, further studies on the identified bioactive compounds from these two plants are being planned.