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1.
Ayyildiz M  Coskun S  Yildirim M  Agar E 《Epilepsia》2007,48(7):1388-1395
PURPOSE: Epileptic seizure results from excessive discharge in a population of hyperexcitable neurons. A number of studies help to document the effects of active oxygen free radical scavengers such as alpha-tocopherol or ascorbic acid (vitamin C). In the present study, we examined the effects of ascorbic acid, at the six different doses, on penicillin-induced epileptiform activity. METHODS: A single microinjection of penicillin (2.5 microl, 500 units, intracortically) into the left sensorimotor cortex induced epileptiform activity within 2-5 min, progressing to full seizure activity lasting approximately 3-5 h. In the first set of experiments, 30 min after penicillin injection, six different doses of ascorbic acid (25, 50, 100, 200, 400, or 800 mg/kg) were administered intraperitoneally (IP). The other group of animals received the effective dose of ascorbic acid (100 mg/kg, IP) for 7 days. Ascorbic acid administration was stopped 24 h before penicillin treatment. Another group of rats received the effective dose of ascorbic acid (100 mg/kg, IP) 30 min before penicillin treatment. In the second set of experiments, the lipid peroxidation (MDA) and reduced glutathione (GSH) levels of brain were measured in the control, control + ascorbic acid, penicillin, and penicillin + ascorbic acid groups. RESULTS: Ascorbic acid, at the low dose (50, 100 mg/kg, 30 min after penicillin injection), decreased both the frequency and amplitude of penicillin-induced epileptiform activity in rats. Ascorbic acid, at intermediate doses (200, 400 mg/kg, 30 min after penicillin injection), decreased the frequency of epileptiform activity without changing the amplitude. Ascorbic acid, at the lowest dose (25 mg/kg) and highest dose (800 mg/kg) (30 min after penicillin injection), did not change either the frequency or amplitude of epileptiform activity. Ascorbic acid, at the low dose (100 mg/kg) was the most effective dose in changing the frequency and amplitude of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) 30 min before penicillin treatment caused a significant delay in the onset of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) for 7 days did not change the latency of epileptiform activity. The most effective dose of ascorbic acid (100 mg/kg) prevented both the decrease in GSH level and the increase in lipid peroxidation level (MDA) occurring after penicillin-induced epileptiform activity. CONCLUSIONS: These data indicate that ascorbic acid has neuroprotective activity against penicillin-induced epileptiform electrocorticogram activity.  相似文献
2.
The pathogenesis of Menkes disease seems to be linked to metallothionein which binds to copper trapped within cells in some tissues. The only known therapy for this disease is parenteral administration of copper, but the effects are equivocal. We treated a patient with Menkes disease by giving vitamin C orally. The clinical manifestation and bone changes improved and the plasma copper and ceruloplasmin levels gradually increased. Vitamin C may prevent the binding of copper and metallothionein by its reducing effect, and excess copper would be released from the cells. Vitamin C treatment is a simple and physiological method, and should aid in clarifying the pathogenesis of the disease.  相似文献
3.
Microdialysis was used to measure extracellular ascorbic and uric acid concentrations in the lateral hypothalamus of water-restricted rats as they drank distilled water or 1.5% NaCl. Other water-restricted rats, not implanted with microdialysis probes, were decapitated 2 h after beginning to drink these fluids. Rats were inverted and their blood was collected for measurements of plasma osmolality and percent hematocrit. Results showed that drinking distilled water produced a significant increase in the ascorbic acid concentration but not in the uric acid concentration. Drinking 1.5% NaCl produced a significant decrease in the uric acid concentration but not in the ascorbic acid concentration. Drinking distilled water decreased mean osmolality from 306.0 to 291.5 mOsm/kg, whereas drinking 1.5% NaCl maintained mean osmolality at water-restricted levels. These results indicate that the extracellular fluid concentration of ascorbic acid in the lateral hypothalamus rises in response to a fall in plasma osmolality.  相似文献
4.
The neuronal damage induced by systemic administration of kainic acid reproduces the cellular and regional pattern of damage produced by repeated seizures, The ability of kainic acid to induce lipid peroxidation, and the ability of free radical inhibitors to prevent ischaemically-induced cell death, has led us to examine the possible role of free radicals in kainate-induced injury, Ascorbic acid was able to reduce kainate-induced damage of the rat hippocampus, measured by means of the gliotic marker ligand [3H]PK1 1195. Ascorbate was significantly effective at doses of 30 mg kg−1 and above, with total protection against kainate at 50 mg kgt-1. Histologically, ascorbate at 50 mg kg−1 was able to prevent kainate-induced neuronal loss in the hippocampal CAI and CA3a cell layers. The antioxidant was also effective when administered simultaneously with, or l h before the kainate. Protection was also obtained by allopurinol, 175 mg kg−1 and by oxypurinol, 40 mg kg−1. Ascorbate did not modify synaptically evoked potentials or long-term potentiation in hippocampal slices, ruling out any blocking activity at glutamate receptors. It is concluded that the neuronal damage produced by systemically administered kainate involves the formation of free radicals.  相似文献
5.
为探讨帕金森病(PD)患者体内抗氧化系统水平及其在PD发病中的作用,对70例PD患者血浆维生素C(P-VC)、维生素E(P-VE)、血浆及红细胞超氧化物歧化酶(P-SOD,E-SOD)、血浆与红细胞过氧化脂质(P-LPO,E-LPO)的水平进行了检测并与正常对照组比较。结果表明:PD组P-VC、P-VE水平及P-SOD、E-SOD活性均比正常对照组显著降低,而P-LPO、E-LPO则显著增高,并且P-VC、P-VE、E-SOD与病情和病程呈负相关,提示抗氧化系统缺陷及内源性氧自由基堆积与PD发病有密切关系。  相似文献
6.
Summary. 24-Hydroxycholesterol, the main cholesterol elimination product of the brain is increased in serum of Alzheimer patients. This oxysterol behaves neurotoxic towards the human neuroblastoma cell line, SH-SY5Y. Here we demonstrate, that 24-hydroxycholesterol-induced neurotoxicity in differentiated SH-SY5Y cells was due to apoptosis, as indicated by DNA-fragmentation, caspase-3 activation and a decrease of the mitochondrial membrane potential. Free radicals were generated, resulting in the death of 75% of the cells within 48 h; neurotoxicity in differentiated SH-SY5Y cells was partially prevented by physiological concentrations of vitamin E (50–100 μM) in that 75% of the cells survived. Physiological concentrations of estradiol-17β (1–100 nM) elicited a protective effect in differentiated cells, which was not significant; however, in undifferentiated cells a significant protection was noted by this steroid hormone. Vitamin C and melatonin did not prevent 24-hydroxycholesterol-induced neurotoxicity. These in vitro data support the in vivo observed beneficial effects reported as circumstantial evidence of vitamin E and estradiol-17β treatment in the prevention and therapy of neurodegenerative disease. Received June 19, 2000; accepted November 20, 2000  相似文献
7.
Korcok J  Dixon SJ  Lo TC  Wilson JX 《Brain research》2003,993(1-2):201-207
Skeletal muscle and brain are major sites of glucose transport and ascorbate (vitamin C) storage. Ascorbate is oxidized to dehydroascorbic acid (DHAA) when used as an enzyme cofactor or free radical scavenger. We evaluated the hypothesis that glucose regulates DHAA uptake and reduction to ascorbate (i.e., recycling) by skeletal muscle cells and cerebral astrocytes. DHAA uptake was inhibited partially by glucose added simultaneously with DHAA. Comparison of wild type L6 skeletal muscle cells with an L6-derived cell line (D23) deficient in facilitative hexose transporter isoform 3 (GLUT3), indicated that both GLUT3 and facilitative hexose transporter isoform 1 (GLUT1) mediate DHAA uptake. Preincubation of muscle cells with glucose inhibited the rates of glucose and DHAA uptake, and decreased the intracellular concentration of ascorbate derived from recycling of DHAA. In contrast, glucose preincubation did not depress GLUT1 protein and activity levels or DHAA recycling in astrocytes. These results establish that glucose downregulates subsequent recycling of DHAA by skeletal muscle cells but not astrocytes.  相似文献
8.
9.
目的探讨维生素C治疗脑胶质瘤的作用机制,为胶质瘤的临床治疗提供实验室依据。方法制作大鼠C6脑胶质瘤模型。荷瘤7d后将Wistar大鼠随机分为5组,每组10只,即对照组;维生素C低剂量组(2.0g/kg);维生素C中剂量组(4.0g/kg);维生素C高剂量组(8.0g/kg);5-Fu组(20mg/kg)。于用药结束后次日处死各组小鼠,计算肿瘤体积和抑瘤率;流式细胞术检测各组肿瘤组织细胞凋亡率;免疫组化法检测各组肿瘤组织Ki-67蛋白表达情况。结果维生素C可抑制大鼠肿瘤生长,且呈剂量依赖性,实验组肿瘤体积与对照组相比有显著差异(P〈0.05),维生素C高剂量组与5--Fu组肿瘤体积比较无统计学差异(P〉0.05)。维生素C可诱导大鼠肿瘤细胞凋亡,维生素C各组与对照组相比均有极显著性差异(P〈0.01),维生素C高剂量组凋亡率高于5-Fu组(P〈0.05)。免疫组化法检测肿瘤组织细胞Ki-67蛋白表达中,维生素C各组与对照组相比均有极显著性差异(P〈0.01),维生素C高剂量组与5-Fu组细胞凋亡率比较无统计学差异(P〉0.05)。结论维生素C在-定剂量范围内可抑制C6大鼠脑胶质瘤的生长,诱导肿瘤细胞发生凋亡是其机制之一;药理剂量的维生素C能降低C6大鼠脑胶质瘤细胞增殖活性,具有-定的抗肿瘤作用。  相似文献
10.
Free radicals induced by traumatic brain injury have deleterious effects on the function and antioxidant vitamin levels of several organ systems including the brain. Melatonin possesses antioxidant effect on the brain by maintaining antioxidant enzyme and vitamin levels. We in-vestigated the effects of melatonin on antioxidant ability in the cerebral cortex and blood of traumatic brain injury rats. Results showed that the cerebral cortex β-carotene, vitamin C, vita-min E, reduced glutathione, and erythrocyte reduced glutathione levels, and plasma vitamin C level were decreased by traumatic brain injury whereas they were increased following melatonin treatment. In conclusion, melatonin seems to have protective effects on traumatic brain inju-ry-induced cerebral cortex and blood toxicity by inhibiting free radical formation and supporting antioxidant vitamin redox system.  相似文献
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