• Journal of The Korean Society of Clinical Toxicology
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• v.4 no.2
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• pp.147-150
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• 2006

Neurotoxic shellfish poisoning (NSP) can result from eating filter-feeding shellfish carrying brevetoxins produced by the marine dinoflagellate Krenia brevis (formally Gymnodinium breve). Brevetoxins enhance sodium entry into cells via voltage-sensitive sodium channels and have an excitatory effect. The incubation period is three hours (range 15 minutes-18 hours). NSP is characterized by gastroenteritis combined with neurologic symptoms. Gastrointestinal (GI) symptoms include abdominal pain, nausea, diarrhea and burning pain in the rectum. Neurologic symptoms are paresthesia, reversal of hot and cold temperature sensation, myalgia, headache, vertigo, and ataxia. Other symptoms may include malaise, tremor, dysphagia, bradycardia, decreased reflexes, dilated pupils, seizure, and coma. The health problem caused by K. breviscan be associated with a red tide bloom. We encountered 3 cases of neurotoxic shellfish poisoning. They all presented with GI and neurologic symptoms andrecovered after conservative treatment.

• Journal of Dental Anesthesia and Pain Medicine
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• v.20 no.2
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• pp.55-61
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• 2020

During dental treatment, a dentist usually applies the local anesthesia. Therefore, all dentists should have expertise in local anesthesia and anesthetics. Local anesthetics have a neurotoxic effect at clinically relevant concentrations. Many studies have investigated the mechanism of neurotoxicity of local anesthetics but the precise mechanism of local anesthetic-induced neurotoxicity is still unclear. In addition, it is difficult to demonstrate the direct neurotoxic effect of local anesthetics because perioperative nerve damage is influenced by various factors, such as the anesthetic, the patient, and surgical risk factors. This review summarizes knowledge about the pharmacology of local anesthetics, nerve anatomy, and the incidence, risk factors, and possible cellular mechanisms of local anesthetic-induced neurotoxicity.

• Archives of Pharmacal Research
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• v.27 no.11
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• pp.1154-1160
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• 2004

We investigated the neurotoxic effects of capsaicin (CAP) on pain sensitivity and on the expression of capsaicin receptor, the vanilloid receptor (VR1), in rats. High-dose application of CAP has been known to degenerate a large fraction of the sensory neurons. Although the neurotoxic effects of CAP are well documented, the effects of CAP on the vanilloid receptor (VR1) are not yet known. In this paper, we investigated the effects of high-dose application of CAP on the expression of VR1 in rats. Thermal and mechanical pain sensitivity was reduced when neonatal rats were treated with a high dose of CAP. This reduction of pain sensitivity was significantly decreased after initiating carrageenan-induced inflammation. The expression of VR1 in dorsal root ganglia (DRG) isolated from the CAP-treated rats was reduced compared to that from the vehicle-treated rats. Therefore, we can conclude that the neurotoxic effect of CAP is related to the decrease of VR1 expression.

• Journal of Preventive Medicine and Public Health
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• v.26 no.2 s.42
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• pp.210-221
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• 1993

In order to evaluate the confounding factors of neurobehavioral tests and the neurobehavioral effects in the workers exposed to organic solvents, NCTB was carried out on 100 workers. 46 workers had never been exposed to neurotoxic substances, and the others were being exposed to the solvents, mainly toluene. Simple reaction time, digit symbol, Santa Ana dexterity test and persuit aiming were different with age in non exposure group. Simple reaction time was carried out well in males, and digit symbol and persuit aiming were in females. There was no difference at educational level when the subject was educated over 12 years. Santa Ana dexterity and Benton visual test differed according to exposure level to toluene, however simple reaction time didn't. The acute neurotoxic effect was not excluded in this study. But, NCTB could be used to evaluate and prevent neurobehavioral changes in workers exposed to neurotoxic solvents in Korea.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.3
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• pp.553-556
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• 2002

To study the effects of Scorpio on oxygen free radical-mediated damage by xanthine oxidase/hypoxanthine (XO/HX) on cultured spinal sensory neurons, in vitro assays such as MTT assay were used in cultured spinal sensory neurons derived from mice. Spinal sensory neurons were cultured in media containing various concentrations of XO/HX for 6 hours, after which the neurotoxic effect of XO/HX was measured by in vitro assay. The protective effect of the herb extract, Scorpio water extract against XO/HX-induced neurotoxicity was also examined. The results are as follows : In MTT assay, XO/HX significantly decreased the cell viability of cultured mouse spinal sensory neurons according to exposure concentration and time in these cultures. The effect of Scorpio water extract on XO/HX-induced neurotoxicity showed a quantitative increase in neurdfilament. These results suggest that XO/HX has a neurotoxic effect on cultured spinal sensory neurons from mice and that the herb extract, Scorpio water extract, was very effective in protecting XO/HX-induced neurotoxicity.

• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.164-169
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• 2008

Methylmercury (MeHg) is known to have devastating effects on the mammalian nervous system. In order to characterize the mechanism of MeHg-induced neurotoxicity, we investigated the analysis of transcriptional profiles on human 8k cDNA microarray by treatment of $1.4{\mu}M$ MeHg at 3, 12, 24 and 48h in human neuroblastoma SH-SY5Y cell line. Some of the identified genes by MeHg treatment were significant at early time points (3h), while that of others was at late time points (48h). The early response genes that may represent those involved directly in the MeHg response included pantothenate kinase 3, a kinase (PRKA) anchor protein (yotiao) 9, neurotrophic tyrosine kinase, receptor, type 2 gene, associated with NMDA receptor activity regulation or perturbations of central nervous system homeostasis. Also, when SH-SY5Y cells were subjected to a longer exposure (48h), a relative increase was noted in a gene, glutamine-fructose-6-phosphate transaminase 1, reported that overexpression of this gene may lead to the increased resistance to MeHg. To confirm the alteration of these genes in cultured neurons, we then applied real time-RT PCR with SYBR green. Thus, this result suggests that a neurotoxic effect of the MeHg might be ascribed that MeHg alters neuronal receptor regulation or homeostasis of neuronal cells in the early phase. However, in the late phase, it protects cells from neurotoxic effects of MeHg.

• The Korea Journal of Herbology
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• v.28 no.2
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• pp.1-7
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• 2013

Objectives : Sesamin, a major lignan in sesame seeds, has been reported to have neuroprotective effects against in vitro ischemia and in vivo MCAo-reperfusion cerebral ischemia model, however, there is no reports in an in vivo global cerebral ischemia model. The purpose of the study was to investigate the neuroprotective effect of sesamin in global cerebral ischemia induced by four-vessel occlusion (4-VO) in rats through inhibition of microglial activation in this model. Methods : The neuroprotective effects were investigated using a 10 min of 4-VO ischemia rat model by measuring intact pyramidal neurons in the CA1 region of the hippocampus using Nissle staining. The antiinflammatory or reducing neurotoxicity effect was investigated using immunohistochemisty, RT-PCR and western blot analysis of inflammatory or neurotoxic mediators. Results : Intraperitoneal injection of sesamin at doses of 0.3, 1.0, 3.0, and 10.0 mg/kg at 0 min and 90 min after ischemia conferred 26.6%, 30.1%, 42.5%, and 30.5% neuroprotection, respectively, compared to the vehicle-treated control group. A 3.0 mg/kg dose of sesamin inhibited microglia activation and consequently, cyclooxygenase-2, inducible nitric oxide, and interleukine-$1{\beta}$ expressions at 48 h after reperfusion. Conclusions : Sesamin protects neuronal cell death through inhibition of microglial activation or the production of neurotoxic metabolites and proinflammatory mediators by microglia such as COX-2, iNOS and IL-$1{\beta}$ in global cerebral ischemia.

• Journal of Oriental Neuropsychiatry
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• v.11 no.1
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• pp.1-18
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• 2000

To study the effects of Ramulus et Uncus Uncariae (REUU) on oxygen free radical-mediated damage by hydrogen peroxide $(H_{2}O_{2})$ on cultured spinal sensory neurons, in vitro assays such as MTT assay, NR assay, neurofilament enzymeimmuno assay (EIA), sulforhodamine B (SRB) assay, assay for lactate dehydrogenase (LDH) activity and assay for lipid peroxidation were used in cultured spinal dorsal root ganglion neurons derived from mice, Spinal dorsal root ganglion neurons were cultured in media containing various concentrations of $H_{2}O_{2}$ for 5 hours, after which the neurotoxic effect of $H_{2}O_{2}$ was measured by in vitro assay. The protective effect of the herb extract, Ramulus et Uncus Uncariae (REUU) against H2O2-induced neurotoxicity was also examined. The results are as follows. 1. In NR assay and MTT assay, $H_{2}O_{2}$ significantly decreased the cell viability of cultured mouse spinal dorsal root ganglion neurons according to exposure concentration in these cultures. An additional time course study was done on these cultures. 2. Cultured spinal dorsal root ganglion neurons which were exposed to various concentrations of $H_{2}O_{2}$ showed a quantitative decrease of neuronal cells by EIA and of total protein by sulforhodamine B (SRB) assay, while they showed an increase of both lipid peroxidation and LDH activity. 3. The effect of Ramulus et Uncus Uncariae (REUU) on $H_{2}O_{2}$ induced neurotoxicity showed a quantitative increase in both neurofilament and total protein, but showed a decrease of lipid peroxidation and LDH activity. These results suggest that $H_{2}O_{2}$ has a neurotoxic effect on cultured spinal dorsal root ganglion neurons from mice and that the herb extract, Ramulus et Uncus Uncariae (REUU), was very effective in protecting $H_{2}O_{2}$ induced neurotoxicity by decreasing lipid peroxidation and LDH activity.

• Applied Microscopy
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• v.28 no.4
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• pp.591-601
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• 1998

The neurotoxic effects of radiation have been studied in NSC-34 hybrid cells derived from embryonic mouse spinal cord cells. NSC-34 cells irradiated at 25Gy were decreased the cell viability in a time and dose dependent manner. The decrease in cell viability induced by the irradiation was blocked by catalase. Antagonists of the N-methyl-D-aspartate (NMDA) receptor, including D-2-amino-5-phosphonovaleric acid (APV) and chlorokynurenic acid (CKA), similarly blocked radiational induced in cell viability. We performed morphological analysis of light and electron microscope. NSC-34 cells irradiated at 25Gy were decreased the cell density and increased lysosomes and vacuoles in the cytoplasm. Especially chromatin modification was observed. These results indicated that radiation was involved in the oxidant-initiated neurotoxicity and the compounds catalase, APV and CKA were shown to be neuroprotective against radiation.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.50 no.1
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• pp.85-91
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• 2017

Alzheimer's disease (AD) is a progressive neurodegenerative disorder of insidious onset that causes gradual loss of memory and cognitive function, and it is the most common form of dementia in the elderly. AD is characterized by neuritic plaques and neurofibrillary tangles in the brain, together with loss of neuronal cells. The major neuropathological hallmark of AD is the accumulation of extracellular neurotoxic ${\beta}-amyloid$ ($A{\beta}$) peptides, such as $A{\beta}1-42$, in the brain. In the present study, we investigated the effect of sargachromenol (SCM), sargaquinoic acid (SQA) and sargahydroquinoic acid (SHQA) isolated from Sargassum serratifoilum ethanol extract (SSE) on $A{\beta}$ production in vitro using APP751-transfected Chinese hamster ovary cells (CHO-751). CHO-751 cells were treated with various concentrations of SSE, SCM, SQA and SHQA, and the level of extracellular $A{\beta}1-42$ was evaluated by enzyme-linked immunosorbent assay. SSE and SHQA reduced the production of $A{\beta}1-42$ in CHO-751 cells. Therefore, SHQA isolated from S. serratifolium has potential as an inhibitor of neurotoxic $A{\beta}$ peptide production.