Abelmoschus moschatus extract reverses altered pain and neurohistology of a rat with developmental exposure of fluoride

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Fluoride causes major human health complications and evidence suggests that exposure of fluoride during developmental periods adversely affect neurodevelopment, behavior, and maturity of the brain as these periods are critical for developing stages for CNS. The present study aimed to assess the mechanically induced pain sensitivity, cell morphology, circuitry in terms of neural connections and networks and maturation of neurons under fluorideinduced toxicity with concurrent treatment of protective effects of Abelmoschus moschatus seed extract from day 1 of pregnancy to post-natal day (PND) of a rat with age 30th day. Timed pregnant wistar rats (30) were segregated into six groups, viz. control, sodium fluoride (NaF) (20 ppm), NaF + A. moschatus aqueous extract (AMAE), NaF + A. moschatus ethanolic extract (AMEE), AMAE, and AMEE and treated for 51 days (21 gestational and 30 postnatal days). On postnatal days 1, 7, 14, 21 and 30, rats were assessed for oxidative stress markers (GSH and GSSG) and neurohistology of the brain. Increased threshold levels to the mechanical stimulus were observed in fluoridetreated rats. Brain stained with Congo red, Cresyl violet and Golgi cox for β-amyloid, Nissl substance and synaptic connections respectively showed cells become amyloidosis with decreased Nissl substance and decreased number of neuronal connections in NaF exposed rats. Reduced content of GSH and increased GSSG levels (P < 0.001) were also recorded in NaF treated rats. These alterations were associated with increased production of free radicals and the effect of fluoride on the brain is inversely proportional with age. These changes were ameliorated by supplementation with AMAE and AMEE with anti-oxidant properties, which reduce the production of free radicals from fluoride. Thus, the seed extract of A. moschatus had a protective effect over fluoride induced alteration in neural cell maturation, and the establishment of circuitry, mechanical pain sensitivity, and oxidative stress.

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Fluoride is an ineluctable environmental pollutant and its chronic exposure causes nociception and inflammation. Alpha-tocopherol and Selenium (Se) are widely available compounds that are safe if taken in moderation and exert a wide range of antioxidant, analgesic and anti-inflammatory activities. This study examined the protective activity of dietary supplements, alpha-tocopherol (2 mg/kg BW) and Selenium (05 µg/kg BW), by using thermal (Hot plate test, Tail-flick test), chemical (writhing test, formalin test) and neuropathic (allodynia test) tests in fluoride (20mg/kg BW) induced pain models. In addition, anti-inflammatory activity was also assessed with paw oedema assay. The obtained data suggest that hyperalgesia in fluoride exposure group was significantly (p<0.05) exhibited in hot plate, tail flick, writhing response, formalin and allodynia tests. Moreover, inflammation in fluoride exposure group was also significantly (p<0.05) increased in paw oedema tests in comparison with the control group. The combined administration of Se and alpha-tocopherol significantly (p<0.05) increased response latency in hot plate and tail flick tests, reduced writhing responses in the writhing test, increased withdrawal duration in allodynia test, inhibited formalin induced pain response in both phases but it was more pronounced in the second phase and attenuated formalin induced paw oedema in comparison with independent treatment of Se and alpha-tocopherol against NaF suggesting their analgesic and anti-inflammatory activities. These findings conclude the synergistic effects of selenium and alpha-tocopherol against fluoride induced nociception and inflammation.
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Objective: This study reports protective effect of Abelmoschus moschatus seed extract against sodium fluoride-induced neurodegeneration through oxidative stress, neurohistological, and behavioral observations in Wistar rats.Methods: A total of 20 Wistar rats (around 250 g) were randomly classified into four groups, namely, control, fluoride (NaF), fluoride + A. moschatus seed aqueous extract (AMAE), and fluoride + A. moschatus seed ethanol extract (AMEE). The control group animals received normal tap water, fluoride group received fluoridated water at the rate of 40 mg/kg b. wt., 3rd group rats treated with fluoride (40 mg/kg b. wt.) + AMAE (300 mg/kg b. wt.), and 4th group rats treated with fluoride (40 mg/kg b. wt.) + AMEE (300 mg/kg b. wt.). Neurobehavioral responses of rotarod, hot plate, and maze learning tests and oxidantive stress markers including lipid peroxidation (LPO), GSH levels, superoxide dismutase, CAT, and GSH peroxidase (GPx) activities, and also histology with H and E as well as congo red staining were studied in control, fluoride, and A. moschatus seed extract treated against fluoride groups.Results: Decreased neurobehavioral responses with rotarod, hot plate, and maze and enhanced LPO (p<0.05) levels were found in fluoride received animals. Whereas, the superoxide dismutase (SOD), CAT, GSH, and GPx were decreased (p<0.05) in NaF treatment. The rats received seed extract along with NaF showed significant reversal of behavioral and oxidative stress markers and the effect of ethanol extract was more pronounced than aqueous extract. The fluoride-treated group showed disturbed cell structure and reduced number of cells in H and E as well as congo red staining which was reversed in cell morphology and restored cell number in seed extract against NaF-treated group. As a result of increased LPO, decreased antioxidant system, and decreased number of cells, neurodegeneration was observed resulting in the disturbance in functions associated with reported behavior.Conclusion: Okra with high antioxidants activity, seed extract showed reversal of LPO levels and antioxidant status in the brain tissue. And also plant extract administered rats displayed normal cell structure and number of cells than only fluoride received group. Therefore, the aqueous and ethanolic extract of A. moschatus plant seeds has neuroprotective effects against fluoride-induced motor, nociceptive, learning behavior, and on histological structure of brain through antioxidant mechanism. The ethanol extract has shown more efficacy than aqueous extract.
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The antioxidant activities and protective effects of total phenolic extracts (TPE) and their major components from okra seeds on oxidative stress induced by carbon tetrachloride (CCl4) in rat hepatocyte cell line were investigated. The major phenolic compounds were identified as quercetin 3-O-glucosyl ( 1 → 6 ) glucoside (QDG) and quercetin 3-O-glucoside (QG). TPE, QG, and QDG from okra seeds exhibited excellent reducing power and free radical scavenging capabilities including α, α-diphenyl-β-picrylhydrazyl (DPPH), superoxide anions, and hydroxyl radical. Overall, DPPH radical scavenging activity and reducing power of QG and QDG were higher than those of TPE while superoxide and hydroxyl radical scavenging activities of QG and TPE were higher than those of QDG. Furthermore, TPE, QG, and QDG pretreatments significantly alleviated the cytotoxicity of CCl4 on rat hepatocytes, with attenuated lipid peroxidation, increased SOD and CAT activities, and decreased GPT and GOT activities. The protective effects of TPE and QG on rat hepatocytes were stronger than those of QDG. However, the cytotoxicity of CCl4 on rat hepatocytes was not affected by TPE, QG, and QDG posttreatments. It was suggested that the protective effects of TPE, QG, and QDG on rat hepatocyte against oxidative stress were related to the direct antioxidant capabilities and the induced antioxidant enzymes activities.
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Wistar albino rats were exposed to 30 or 100 ppm fluoride (as NaF) in drinking water during their fetal, weanling, and post-weaning stages until the age of ten weeks. Rats exposed to 30 ppm fluoride did not show any notable alterations in brain histology, whereas rats exposed to 100 ppm fluoride showed significant neurodegenerative changes in the hippocampus, amygdala, motor cortex, and cerebellum. Changes included decrease in size and number of neurons in all the regions, decrease in the number of Purkinje cells in the cerebellum, and signs of chromatolysis and gliosis in the motor cortex. These histological changes suggest a toxic effect of high-fluoride intake during the early developing stages of life on the growth, differentiation, and subcellular organization of brain cells in rats.
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A method for measurement of both oxidized (GSSG) and reduced (GSH) glutathione has been developed, with use of o-phthalaldehyde (OPT) as a fluorescent reagent. The method takes advantage of the reaction of GSH with OPT at pH 8 and of GSSG with OPT at pH 12; GSH can be complexed to N-ethylmaleimide to prevent interference of GSH with measurement of GSSG. The method gave “recoveries” of 91 to 110% for both GSH and GSSG and was quite specific for glutathione; and none of the manipulations appeared to influence the amount of glutathione present in the tissue. Results for GSH levels agreed well with earlier reports but levels of GSSG estimated here were higher than earlier reported values. The reasons for the apparently higher levels of GSSG are discussed.
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Long-term habituation to a novel environment is one of the most elementary forms of nonassociative learning. Here we studied the effect of pre- or posttraining intrahippocampal administration of drugs acting on specific molecular targets on the retention of habituation to a 5-min exposure to an open field measured 24 h later. We also determined whether the exposure to a novel environment resulted in the activation of the same intracellular signaling cascades previously shown to be activated during hippocampal-dependent associative learning. The immediate posttraining bilateral infusion of CNQX (1 microg/side), an AMPA/kainate glutamate receptor antagonist, or of muscimol (0.03 microg/side), a GABA(A) receptor agonist, into the CA1 region of the dorsal hippocampus impaired long-term memory of habituation. The NMDA receptor antagonist AP5 (5 microg/side) impaired habituation when infused 15 min before, but not when infused immediately after, the 5-min training session. In addition, KN-62 (3.6 ng/side), an inhibitor of calcium calmodulin-dependent protein kinase II (CaMKII), was amnesic when infused 15 min before or immediately and 3 h after training. In contrast, the cAMP-dependent protein kinase (PKA) inhibitor Rp-cAMPS, the mitogen-activated protein kinase kinase (MAPKK) inhibitor PD098059, and the protein synthesis inhibitor anisomycin, at doses that fully block memory formation of inhibitory avoidance learning, did not affect habituation to a novel environment. The detection of spatial novelty is associated with a sequential activation of PKA, ERKs (p44 and p42 MAPKs) and CaMKII and the phosphorylation of c-AMP responsive element-binding protein (CREB) in the hippocampus. These findings suggest that memory formation of spatial habituation depends on the functional integrity of NMDA and AMPA/kainate receptors and CaMKII activity in the CA1 region of the hippocampus and that the detection of spatial novelty is accompanied by the activation of at least three different hippocampal protein kinase signaling cascades.
Sesamin, a major lignan derived from sesame seeds, has been reported to have many benefits and medicinal properties. However, its protective effects against fluoride-induced injury in kidney of fish have not been clarified. Previously we found that fluoride exposure caused damage and apoptosis in the kidneys of the common carp, Cyprinus carpio. In this study, the effects of sesamin on renal oxidative stress and apoptosis in fluoride-exposed fish were determined. The results showed that sesamin alleviated significantly fluoride-induced renal damage and apoptosis of carp in a dose-dependent manner, indicated by the histopathological examination and ultrastructural observation. Moreover, treatment with sesamin also inhibited significantly fluoride-induced remarkable enhancement of reactive oxygen species (ROS) production and oxidative stress, such as the increase of lipid peroxidation level and the depletion of intra-cellular reduced glutathione (GSH) level in kidney. To explore the underlying mechanisms of sesamin action, we found that activities of caspase-3 were notably inhibited by treatment with sesamin in the kidney of fluoride-exposed fish. Sesamin decreased the levels of p-JNK protein in kidney, which in turn inactivated pro-apoptotic signaling events by restoring the balance between mitochondrial pro-and anti-apoptotic Bcl-2 and Bax proteins and by decreasing the release of mitochondrial cytochrome c in kidney of fluoride-exposed fish. JNK was also involved in the mitochondrial extrinsic apoptotic pathways of sesamin effects against fluoride-induced renal injury by regulating the levels of p-c-Jun, necrosis factor-alpha (TNF-) and Bak proteins. These findings indicated that sesamin could protect kidney against fluoride-induced apoptosis by the oxidative stress downstream-mediated change in the inactivation of JNK signaling pathway. Taken together, sesamin plays an important role in maintaining renal health and preventing kidney from toxic damage induced by fluoride.
Aluminum is a light weight and toxic metal present ubiquitously on earth, which has gained considerable attention due to its neurotoxic effects. It also has been linked ecologically and epidemiologically to several neurological disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Guamanian–Parkinsonian complex and Amyotrophic lateral sclerosis (ALS). The mechanism of aluminum neurotoxicity is poorly understood, but it is well documented that aluminum generates reactive oxygen species (ROS). Enhanced ROS production leads to disruption of cellular antioxidant defense systems and release of cytochrome c (cyt-c) from mitochondria to cytosol resulting in apoptotic cell death. Quercetin (a natural flavonoid) protects it from oxidative damage and has been shown to decrease mitochondrial damage in various animal models of oxidative stress. We hypothesized that if oxidative damage to mitochondria does play a significant role in aluminum-induced neurodegeneration, and then quercetin should ameliorate neuronal apoptosis. Administration of quercetin (10 mg/kg body wt/day) reduced aluminum (10 mg/kg body wt/day)-induced oxidative stress (decreased ROS production, increased mitochondrial superoxide dismutase (MnSOD) activity). In addition, quercetin also prevents aluminum-induced translocation of cyt-c, and up-regulates Bcl-2, down-regulates Bax, p53, caspase-3 activation and reduces DNA fragmentation. Quercetin also obstructs aluminum-induced neurodegenerative changes in aluminum-treated rats as seen by Hematoxylin and Eosin (H&E) staining. Further electron microscopic studies revealed that quercetin attenuates aluminum-induced mitochondrial swelling, loss of cristae and chromatin condensation. These results indicate that treatment with quercetin may represent a therapeutic strategy to attenuate the neuronal death against aluminum-induced neurodegeneration.
In human body, several categories of degenerative processes are largely determined by free radicals originating in cell. Free radicals are also known to have correlated with a variety of cognitive disorders (CDs) resulting in neuronal injury and eventually to death. Alzheimer's disease (AD) and Parkinson's disease (PD) are such kind of killer CDs that occur due to dysfunction of cholinergic and dopaminergic neurons. Plant parts of Ginkgo biloba, Bacopa monnieri etc. are being used for the treatment of cognitive disorders in several countries. The present study was aimed to explore the detailed antioxidant and anti-cholinesterase activity of Acaciacatechu leaf (ACL) over CDs. Gas chromatography-Mass spectroscopy (GC-MS) analysis and Nuclear Magnetic Resonance (NMR) were employed to identify the bioactive components present in ACL. Furthermore, the extract was evaluated to check the cytotoxic effects of ACL on normal cells. Amongst several antioxidant assays, DPPH assay, hydroxyl radical, nitric oxide radical and hypochlorous acid inhibitory activities were found to be greater in ACL than that of the respective standards while other assays exhibited a moderate or at per inhibitory activity with standards. Total phenolic and flavonoid content were also found to be present in decent amount. In addition, we found, a greater acetylcholinesterase (AChE) inhibitory activity of ACL when compared to other medicinally important plants, indicating its positive effect over CDs. Forty one bioactive components were explored through GC-MS. Of these, gallic acid, epicatechin, catechin, isoquercitrin etc. were found, which are potent antioxidant and a few of them have anti-neurodegenerative properties. Eventually, ACL was found to be nontoxic and safer to consume. Further studies with animal or human model however, would determine its efficacy as a potential anti-schizophrenic drug.
Decreased learning and memory ability in rats with fluorosis: increased oxidative stress and reduced cholinesterase activity Gao, Liu, Guan SUMMARY: The aim of this research was to study the mechanism of the decreased learning and memory of rats with chronic fluorosis. Compared with controls, decreased learning and memory ability, lower levels of total antioxidant capacity (T-AOC), and increased content of malondialdehyde (MDA) in brain tissues were observed in both male and female young adult rats after 6 months with either 5 or 50 mg NaF/L in their drinking water. Interestingly, the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in the brain were reduced more in the rats with the lower NaF concentration than in those with the higher concentration, thereby suggesting a paradoxical dose-response effect of F on these enzymes. The results indicate that the reduced learning capacity and memory ability of rats induced by F may be connected with increased oxidative stress and diminished cholinergic nervous system responses.
This study describes alterations in the nervous system resulting from chronic administration of the fluoroaluminum complex (AlF3) or equivalent levels of fluoride (F) in the form of sodium-fluoride (NaF). Twenty seven adult male Long-Evans rats were administered one of three treatments for 52 weeks: the control group was administered double distilled deionized drinking water (ddw). The aluminum-treated group received ddw with 0.5 ppm AlF3 and the NaF group received ddw with 2.1 ppm NaF containing the equivalent amount of F as in the AlF3 ddw. Tissue aluminum (Al) levels of brain, liver and kidney were assessed with the Direct Current Plasma (DCP) technique and its distribution assessed with Morin histochemistry. Histological sections of brain were stained with hematoxylin & eosin (H&E), Cresyl violet, Bielschowsky silver stain, or immunohistochemically for beta-amyloid, amyloid A, and IgM. No differences were found between the body weights of rats in the different treatment groups although more rats died in the AlF3 group than in the control group. The Al levels in samples of brain and kidney were higher in both the AlF3 and NaF groups relative to controls. The effects of the two treatments on cerebrovascular and neuronal integrity were qualitatively and quantitatively different. These alterations were greater in animals in the AlF3 group than in the NaF group and greater in the NaF group than in controls.
The measure of antioxidant capacity (AC) considers the cumulative action of all the antioxidants present in plasma and body fluids, thus providing an integrated parameter rather than the simple sum of measurable antioxidants. The capacity of known and unknown antioxidants and their synergistic interaction is therefore assessed, thus giving an insight into the delicate balance in vivo between oxidants and antioxidants. Measuring plasma AC may help in the evaluation of physiological, environmental, and nutritional factors of the redox status in humans. Determining plasma AC may help to identify conditions affecting oxidative status in vivo (e.g., exposure to reactive oxygen species and antioxidant supplementation). Moreover, changes in the plasma AC after supplementation with galenic antioxidants or with antioxidant-rich foods may provide information on the absorption and bioavailability of nutritional compounds. Consequently, this review discusses the rationale, interpretation, confounding factors, measurement limits, and human applications of the measure of plasma AC.
The mechanisms underlying the neurotoxicity of endemic fluorosis still remain unknown. To investigate the expression level of neural cell adhesion molecules (NCAM), oxidative stress, and apoptosis induced by fluoride, the primary rat hippocampal neurons were incubated with 20, 40, and 80 mg/l sodium fluoride for 24 h in vitro. The results showed that the cell survival rate in the 80 mg/l fluoride-treated group was significantly lower than that of the control group. Forty and 80 mg/l of fluoride induced significantly increased lactate dehydrogenase release, intracellular reactive oxygen species, and the percentage of apoptosis. Compared with control group, the malondialdehyde levels were significantly elevated while glutathione levels and glutathione peroxidase activities were decreased in all fluoride-treated groups, accompanied by the markedly reduced superoxide dismutase activity in 80 mg/l fluoride-treated group. With respect to NCAM mRNA expression levels, a significant dose-dependent decrease was observed in 40 and 80 mg/l fluoride-treated groups against the control group. In addition, as compared to the control group, the protein expression levels of NCAM-180 in 40 and 80 mg/l fluoride-treated groups, NCAM-140 in all fluoride-treated groups, and NCAM-120 in the 80 mg/l fluoride-treated group were significantly decreased. Our study herein suggested that fluoride could cause oxidative stress, apoptosis, and decreased mRNA and protein expression levels of NCAM in rat hippocampal neurons, contributing to the neurotoxicity induced by fluoride.
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