ascorbic-acid and Encephalitis

Topics: Amantadine; Antiviral Agents; Ascorbic Acid; Dosage Forms; Drug Evaluation; Encephalitis; Hepatitis; Herpes Simplex; Herpes Zoster; Humans; Idoxuridine; Influenza, Human; Inosine Pranobex; Interferons; Levamisole; Rimantadine; Subacute Sclerosing Panencephalitis; Trifluridine; Virus Diseases

Sodium benzoate (SB) is a widely used food preservative. However, excessive intake of a high dose of SB poses a risk of neurotoxicity. Ascorbic acid (AA) is a naturally occurring antioxidant found in fruits with reported neuroprotective properties. The present study investigated the neurobehavioral and biochemical alterations in SB-treated rats and the ameliorative effect of AA in rats.. Forty-two male Wistar rats were divided into six groups (n = 7). Group 1 (vehicle, 10 ml/kg), Groups 2-4 rats SB (150, 300, and 600 mg/kg), Group 5 AA (100 mg/kg) and Group 6 (SB 600 mg/kg + AA 100 mg/kg). Treatment was daily administered for 28 days by oral route. Anxiogenic behavior, locomotor, and exploratory activities were evaluated in the open field monitored with a camera, and memory performance in Y-maze. Brain oxidative stress, inflammatory, apoptosis, and cholinergic markers were determined. The cortico-hippocampal tissues were examined histologically.. SB-treated rats showed significant anxiogenic-like behavior and impairment in locomotor, exploratory, and memory performance. This was reversed in SB (600 mg/kg)-treated rats coadministered with AA. SB-treated rats showed a decrease in antioxidant enzyme activities, increase malondialdehyde (MDA), nitrite, tumor necrosis factor-alpha, caspase-3, and acetylcholinesterase activity in the striatum, hippocampus, frontal cortex, and cerebellum. These biochemical changes were reversed in AA-treated rats. Reduced cortico-hippocampal neuronal cell count and the pyknotic index were found in SB-treated rats, which was also reversed in AA-treated rats.. Conclusively, sodium-benzoate-induced neurobehavioral deficits and brain biochemical changes were ameliorated by ascorbic acid probably via antioxidant, anti-inflammatory, and apoptotic mechanisms.

Topics: Acetylcholinesterase; Animals; Antioxidants; Ascorbic Acid; Behavior, Animal; Brain; Encephalitis; Male; Oxidative Stress; Rats; Rats, Wistar; Sodium Benzoate

Ethanol induces oxidative stress and its exposure during early developmental age causes neuronal cell death which leads to several neurological disorders. We previously reported that vitamin C can protect against ethanol-induced apoptotic cell death in the developing rat brain. Here, we extended our study to understand the therapeutic efficacy of vitamin C against ethanol-induced oxidative stress, neuroinflammation mediated neurodegeneration in postnatal day 7 (PND7) rat. A single episode of ethanol (5g/kg) subcutaneous administration to postnatal day 7 rat significantly induced the production of reactive oxygen species (ROS), and activated both microglia and astrocytes followed by the induction of different apoptotic markers. On the other hand, due to its free radical scavenging properties, vitamin C treatment significantly reduced the production of reactive oxygen species, suppressed both activated microglia and astrocytes and reversed other changes including elevated level of Bax/Bcl-2 ratio, cytochrome c and different caspases such as caspase-9 and caspase-3 induced by ethanol in developing rat brain. Moreover, vitamin C treatment also reduced ethanol-induced activation of Poly [ADP-Ribose] Polymerase 1(PARP-1) and neurodegeneration as evident from Flouro-Jade-B and Nissl stainined neuronal cell death in PND7 rat brain. These findings suggest that vitamin C mitigated ethanol-induced oxidative stress, neuroinflammation and apoptotic neuronal loss and may be beneficial against ethanol damaging effects in brain development.

Topics: Animals; Animals, Newborn; Apoptosis; Ascorbic Acid; bcl-2-Associated X Protein; Brain; Caspase 3; CREB-Binding Protein; Disease Models, Animal; Encephalitis; Ethanol; Fluoresceins; Glial Fibrillary Acidic Protein; Neurodegenerative Diseases; Neuroprotective Agents; Poly (ADP-Ribose) Polymerase-1; Proto-Oncogene Proteins c-bcl-2; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species

In this study, lipid peroxidation and antioxidant status were investigated in children with acute bacterial meningitis and encephalitis. The aim was to determine whether there was a possible role of free radicals in meningitis and encephalitis in childhood. Our study included 16 children with acute bacterial meningitis, 13 with encephalitis, and 17 control subjects. Serum malondialdehyde (MDA), reduced glutathione (GSH), vitamin C, vitamin E, beta-carotene, and retinol levels were studied in all subjects within 6 h of admission. There was a statistically significant difference for serum MDA, GSH, and vitamin C between the groups. Serum MDA and vitamin C levels were higher, and serum GSH levels were lower in the study groups compared to the control group. Vitamin C levels were similar in both the encephalitis and control groups, but they were significantly lower in the children with encephalitis than the meningitis group. In conclusion, our study showed that serum MDA and GSH levels were affected in children with both meningitis and encephalitis, but vitamin C level was affected only in children with meningitis. Serum vitamin E, beta-carotene, and retinol levels were not changed in childhood meningitis and encephalitis.

Topics: Analysis of Variance; Antioxidants; Ascorbic Acid; beta Carotene; Case-Control Studies; Chi-Square Distribution; Child; Child, Preschool; Encephalitis; Female; Glutathione; Humans; Lipid Peroxidation; Male; Malondialdehyde; Meningitis, Bacterial; Spectrophotometry; Vitamin A

Free radicals, such as superoxide and nitric oxide, are known to play a role in a number of inflammatory and degenerative brain diseases, in which resident microglia upregulate the inducible nitric oxide synthase (iNOS) and thus produce large amounts of nitric oxide. Simultaneously, microglia generate superoxide mainly via NADPH-oxidase, which reacts at a diffusion-limited rate with nitric oxide to form the powerful oxidant peroxynitrite. We used mixed astroglial/microglial cultures to study the effects of iNOS induction by lipopolysaccharide and interferon-gamma on free radical formation. Using the fluorogenic compound 2,7-dihydrodichlorofluorescein diacetate, we monitored cellular peroxynitrite formation by confocal laser microscopy. Peroxynitrite formation in continuously nitric oxide-producing microglial cells was rather limited. However, activation of the superoxide-generating enzyme NADPH-oxidase dramatically increased DCF fluorescence within a few minutes. We conclude that superoxide is the limiting factor for peroxynitrite formation. Since the formation and oxidant activity of peroxynitrite depends strongly on the availability of cellular antioxidants, we investigated the capacity of several compounds to influence peroxynitrite formation. Among the substances under investigation in this study, glutathione and the synthetic compound ebselen had a major effect on preventing peroxynitrite formation, whereas ascorbate failed to decrease peroxynitrite levels.

Topics: Animals; Animals, Newborn; Antioxidants; Ascorbic Acid; Astrocytes; Cells, Cultured; Encephalitis; Enzyme Inhibitors; Fluorescent Antibody Technique; Fluorescent Dyes; Glutathione; Interferon-gamma; Lipopolysaccharides; Microglia; NADPH Oxidases; Neurodegenerative Diseases; Nitric Oxide; Nitric Oxide Synthase; Oxidative Stress; Peroxynitrous Acid; Rats; Rats, Wistar; Superoxides; Tetradecanoylphorbol Acetate

Topics: Adrenal Insufficiency; Ascorbic Acid; Autonomic Nervous System Diseases; Blood Circulation; Communicable Diseases; Cortisone; Desoxycorticosterone; Encephalitis; Flavonoids; Humans; Liver; Pathology; Pulmonary Edema; Rutin; Water-Electrolyte Balance

Topics: Ascorbic Acid; Athetosis; Chorea; Encephalitis; Extrapyramidal Tracts; Humans; Hyperkinesis; Movement Disorders; Myoclonus; Reserpine; Spasm; Tics; Torticollis

Topics: Adenosine; Adenosine Triphosphate; Albumins; Ascorbic Acid; Autonomic Nervous System Diseases; Diencephalon; Encephalitis; Humans; Influenza, Human; Polyphosphates