• 한국환경보건학회지
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• 제24권3호
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• pp.35-40
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• 1998

This study was conducted to examine the pathological changes of rat peripheral nervous system during exposure to tellurium known to be a demyelinating agent by using teasing nerve fiber method and quantitative light microscopic analysis by image analyzer. The pellet containing 1.2% of tellurium were fed for 3, 5, 7, 9, 13 days to male wistar rats (21 days old) and then neurologic symptom and the feature of nerve fiber myelination were studied. From this study, following results were obtained. In 3 days treated group, it showed various neurologic symptom and teased nerve fiber showed slight irregularity of the myeline sheath. In 5 days and 7 days treated groups, it showed the segmental demyetination in larger size fiber and widening of nodes of ranvier. In 9 days and 13 days treated groups, the remyelinated fibers were observed and it was generally small in size. We consequently suggest that teasing nerve fiber method and quantitative analysis of nerve fiber were useful pathologic screening method of neurotoxicity of the peripheral nervous system.

• 약학회지
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• 제31권2호
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• pp.82-91
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• 1987

The effect of neurotoxic compound 6-hydroxydopamine (6-OHDA) on the change in blood pressure and contractile response of Vas deference by centrally acting agents has been studied in normal and DOCA-salt induced hypertensive rats. The treatment of neonatal rats with 6-OHDA (2$\times$100mg, 250mg Kg$^{-1}$s.c) significantly inhibited the antihypertensive and relaxant effects of Vas deference of clonidine(100$\mu\textrm{g}$ Kg$^{-1}$iv.). The simultaneous administration of desipramine with clonidine into neonatal rats decreased the antihypertensive response of clonidine although treated did not affect the relaxative response of Vas deference. Furthermore, the antihypertensive and relaxant responses of clonidine were reduced by the neonatal rats with 6-OHDA regardless of the administration of desipramine. When neonatal rats were administered with 6-OHDA, the development of DOCA-salt hypertension was prevented. These results suggest that 6-OHDA, clonidine and desipramine hada significant effect on the development and the inhibition of central hypertension mediating the central adrenergic neuron due to their affinity to the central nervous system.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.246.2-247
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• 2003

It has been reported that 2-bromopropane might be a causative agent for reproductive toxicity and have immunotoxic effects. 1-Bromopropane known as an alternative to ozone depleting solvents, which has structural similarity to 2-bromopropane, has been reported to be neurotoxic to rats in long-term inhalation exposure. (omitted)

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2000년도 The 7th International Symposium
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• pp.84-95
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• 2000

Panax ginseng and the herbal medicinal mixtures containing ginseng have been widely used as a traditional medicinal prescriptions. In order to develop more efficient and protective prescriptions on seizures and subsequent memory deterioration, we investigated the biochemical and ethopharmacological effects of ginsenosides and fractions from the natural medicinal plant products related to control convulsions. In this studies we show results improving spatial teaming and memory deficits induced by kainic acid, a potent neurotoxic and neuroexcitatory analogue of the amino acid neurotransmitter glutamate.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.139-140
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• 2003

Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of Alzheimer's disease (AD), and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD. In the present study, we investigated the effect of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on inflammatory cell death induced by beta-amyloid, a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD.(omitted)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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• pp.64-67
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• 2003

Halogenated aromatic hydrocarbons (HAHs) including TCDD and PCBs are known to cause neurotoxic effects in both man and animals such as cognitive impairment and motor dysfunctions. While theses chemicals may lead to neurodevelopmental and neurobehavioral deficit, structural activity relationship and molecular targets for these chemicals are not elucidated.(omitted)

• Journal of Digestive Cancer Research
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• 제11권1호
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• pp.45-48
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• 2023

One of the most common side effects of chemotherapeutic agents is chemotherapy-induced peripheral neuropathy (CIPN). The occurrence of CIPN is increasing as the survival rate of patients with cancer improves and the cumulative dose or duration of neurotoxic drugs increases. Approximately 30-40% of patients receiving neurologically toxic drugs experience CIPN, which eventually increases the burden of medical expenses. However, preventive measures against CIPN have not yet been established. Clinical trials have tested various drugs for the management of neuropathic pain, but only duloxetine has shown any significant effect. Further studies should evaluate nonpharmaceutical treatments, such as exercise.

• 한국감성과학회:학술대회논문집
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• 한국감성과학회 2009년도 추계학술대회
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• pp.190-192
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• 2009

Kainic acid (KA), an agonist for kainate and AMPA receptors, is an excitatory neurotoxic substance. Vitamin E such as alpha-tocopherol and alpha-tocotrienol is a chain-breaking antioxidant, preventing the chain propagation step during lipid peroxidation. In the present study, we have investigated the neuroprotective effects of alphatocopherol and alpha-tocotrienol on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC). After 15h KA treatment, delayed neuronal death was detected in CA3 region. Alpha-tocopherol and alpha-tocotrienol increased cell survival and reduced the number of TUNEL-positive cells in CA3 region. These data suggest that alpha-tocopherol and alpha-tocotrienol treatment have protective effects on KA-induced cell death

• Clinical and Experimental Pediatrics
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• 제56권7호
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• pp.271-274
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• 2013

Brain insults, including neurotrauma, infection, and perinatal injuries such as hypoxic ischemic encephalopathy, generate inflammation in the brain. These inflammatory cascades induce a wide spectrum of cytokines, which can cause neuron degeneration, have neurotoxic effects on brain tissue, and lead to the development of seizures, even if they are subclinical and occur at birth. Cytokines are secreted by the glial cells of the central nervous system and they function as immune system mediators. Cytokines can be proinflammatory or anti-inflammatory. Interleukin (IL)-$1{\beta}$ and IL-8 are proinflammatory cytokines that activate additional cytokine cascades and increase seizure susceptibility and organ damage, whereas IL-1 receptor antagonist and IL-10 act as anti-inflammatory cytokines that have protective and anticonvulsant effects. Therefore, the immune system and its associated inflammatory reactions appear to play an important role in brain damage. Whether cytokine release is relevant for the processes of epileptogenesis and antiepileptogenesis, and whether epileptogenesis could be prevented by immunomodulatory treatment should be addressed in future clinical studies. Furthermore, early detection of brain damage and early intervention are essential for the prevention of disease progression and further neurological complications. Therefore, cytokines might be useful as biomarkers for earlier detection of brain damage in high-risk infants.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2001년도 International Symposium on Signal transduction in Toxicology
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• pp.149-149
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• 2001

Cytochrome P450 (CYP) 2D6 and CYP3A4 have been reported to be involved in the major metabolic pathways and formations of neurotoxic metabolites (HPP$\^$+/, RHPP$\^$+/) from haloperidol (HAL). However, no in vivo study has been addressed to the involvement of both CYP isoforms on the formation of toxic HAL metabolites.(omitted)