• YAKHAK HOEJI
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• v.44 no.6
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• pp.613-619
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• 2000

The author examined whether the methanol extracts of Opuntia ficus-indica fruit and Saururus chinensis have the inhibitory action on xanthine/xanthine oxidase (X/XO)-, $FeCl_2/ascorbic$ acid- and arachidonic acid-induced neurotoxicity in mouse cortical cell cultures. The methanol extracts ($10\;{\mu}g/ml{\sim}1\;mg/ml$) of Opuntia ficus-indica and Saururus chinensis were exhibited 53-89% and $48{\sim}100%$ inhibitory action on X/XO-induced neurotoxicity, respectively. At the range of same concentration, both extracts also attenuated the $FeCl_2/ascorbic$ acid-induced neurotoxicity by $35{\sim}100%$ and $15{\sim}98%$, respectively. In arachidonic acid neurotoxicity, the methanol extract (1 mg/ml) of Opuntia ficus-indica and Saururus chinensis reduced neuronal injury by 22% and 38%, respectively. These results suggest that Opuntia ficus-indica fruit and Saururus chinensis may contribute the neuroprotection in certain free radical-mediated neuronal injury.

• Molecules and Cells
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• v.38 no.8
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• pp.734-740
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• 2015

Recent studies report that a history of antidepressant use is strongly correlated with the occurrence of Parkinson' disease (PD). However, it remains unclear whether antidepressant use can be a causative factor for PD. In the present study, we examined whether tricyclic antidepressants amitriptyline and desipramine can induce dopaminergic cell damage, both in vitro and in vivo. We found that amitriptyline and desipramine induced mitochondria-mediated neurotoxicity and oxidative stress in SH-SY5Y cells. When injected into mice on a subchronic schedule, amitriptyline induced movement deficits in the pole test, which is known to detect nigrostriatal dysfunction. In addition, the number of tyrosine hydroxylase-positive neurons in the substantia nigra pars compacta was reduced in amitriptyline-injected mice. Our results suggest that amitriptyline and desipramine may induce PD-associated neurotoxicity.

• Journal of Korean Neurosurgical Society
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• v.65 no.2
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• pp.180-185
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• 2022

Objective : Drug-eluting stents and balloons are occasionally used to reduce restenosis in medically intractable intracranial atherosclerotic stenosis. The authors aimed to determine whether such drugs can cause neurotoxicity due to local effects in a rat model. Methods : Intra-arterial catheters were placed in the right common carotid artery of rats. Mannitol was injected to transiently open the brain-blood barrier (BBB), followed by high-dose drug (paclitaxel and rapamycin) injection. The optimal time interval of transient BBB opening for maximal drug penetration was determined to be 10 minutes. Paclitaxel and rapamycin were intra-arterially administered in various doses. All the rats were neurologically evaluated, and their brain tissues were histologically examined. Results : Neither neurological deficits nor histological abnormalities were observed in all the rats. Conclusion : Paclitaxel and rapamycin did not cause neurotoxicity in a rat model with transient BBB opening.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.2
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• pp.262-266
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• 2002

In order to elucidate the mechanism of cytotoxic effect of oxygen radicals on cultured mouse spinal motor neurons, the neurotoxicity induced by hydrogen peroxide(H₂O₂) was evaluated by MTT assay. The neuroprotective effect of Rhizoma Gastrodiae(RG) against H₂O₂-mediated neurotoxicity was also examined in these cultures by SRB assay. The results were as follows : The value of lethal concentration 50(LC50) of H₂O₂ was estimated at a concentration of 30 uM in these cultures. Cell viability of cultured mouse spinal motor neurons was remarkably decreased by H₂O₂-induced neurotoxicity in a dose- and time-dependent manner. RG was remarkably effective in blocking the neurotoxicity induced by H₂O₂ at a concentration of 120 μM as determined by SRB assay. From above the results, it is suggested that H₂O₂ induce neurotoxicity, and the selective herbal extracted RG was very effective in blocking H₂O₂-mediated neurotoxicity on cultured mouse spinal motor neurons.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.3
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• pp.177-183
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• 2000

We examined the neurotoxic effects of 3 glutathione (GSH) depletors, buthionine sulfoximine (BSO), diethyl maleate (DEM) and phorone, under the presence of trolox, cycloheximide (CHX), pyrrolidine dithiocarbamate (PDTC) or MK-801 in primary mouse cortical cell cultures. All three depletors induced neuronal death in dose and exposure time dependent manner, and decreased total cellular GSH contents. The patterns of the neuronal death and the GSH decrements were dependent on the individual agents. DEM $(200\;{\mu}M)$ induced rapid and irreversible decrement of the GSH. BSO (1 mM) also decreased the GSH irreversibly but the rate of decrement was more progressive than that of DEM. Phorone (1 mM) reduced the GSH content to 40% by 4 hr exposure, that is comparable to the decrement of BSO, but the GSH recovered and reached over the control value by 36 hr exposure. BSO showed a minimal neurotoxicity $(0{\sim}10%)$ at the end of 24 hr exposure, but marked neuronal cell death at the end of 48 hr exposure. The BSO (1 mM)-induced neurotoxicity was markedly inhibited by trolox or CHX and partially attenuated by MK-801. DEM induced dose-dependent cytotoxicity at the end of 24 hr exposure. Over the doses of $400\;{\mu}M,$ glial toxicity also appeared. DEM $(200\;{\mu}M)-induced$ neurotoxicity was markedly inhibited by trolox or PDTC. Phorone (1 mM) induced moderate neurotoxicity (40%) at the end of 48 hr exposure. Only CHX showed significant inhibitory effect on the phorone-induced neurotoxicity. These results suggest that the GSH depletors induce neuronal injury via different mechanisms and that GSH depletors should be carefully employed in the researches of neuronal oxidative injuries.

• Korean Journal of Clinical Laboratory Science
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• v.51 no.2
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• pp.235-244
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• 2019

This study examined the neurotoxicity of aluminum sulfate (AS), an environmental pollutant, and the protective effect of Phrymaleptostachya var. asiatica HARA (PLVAH) extract on the neurotoxicity induced by AS in the cultured C6 glioma cells. For this study, the cell viability and antioxidative effects, such as electron donating (ED) activity, lipid peroxidation (LP) activity, and superoxide anion-radical (SAR) scavenging activity, were analyzed. AS decreased the cell viability significantly in a dose-dependent manner and the $XTT_{50}$ value was measured at $120.0{\mu}M$ of AS. The neurotoxicity of AS was determined to be mid-toxic by Borenfreund and Puerner's toxic criteria. In addition, the catalase (CAT), antioxidant enzyme remarkably increased the cell viability injured by AS-induced neurotoxicity in these cultures. Regarding the protective effect of the PLVAH extract on AS-induced neurotoxicity, PLVAH extract significantly increased the ED ability, and the inhibitory ability of the LP and SAR scavenging ability. These findings suggest that oxidative stress is involved in the cytotoxicity of AS, and the PLVAH extract effectively protected against AS-induced neurotoxicity by its antioxidative effects. Natural resources, such as the PLVAH extract may be a putative therapeutic agent for the treatment of the toxicity induced by heavy metallic compounds, such as AS correlated with the oxidative stress.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.89-89
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• 2002

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.101-104
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• 2003

It has been suggested that oxidative stress of reactive oxygen species(ROS) may play a key role in the pathogenesis of neuronal complications. The aim of this study was to examine the cytotoxic effect of hydrogen peroxide(H₂O₂) in the cultured mouse cerebral neurons and the protective effect of Schisandrae Fructus(SF) on ROS-induced neurotoxicity. Cytotoxic effect of H₂O₂ and neuroprotective effect of SF were determined by MTT assay. H₂O₂ decreased cell viability in dose-and time-dependent mannner, and SF decreased H₂O₂-induced neurotoxicity in these cultures. From above the results, H₂O₂ has toxic effect, and herb extract, SF is very effective against H₂O₂-induced neurotoxicity in cultured cerebral neurons of mouse.

• Environmental Analysis Health and Toxicology
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• v.31
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• pp.18.1-18.8
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• 2016

Objectives This study aimed to evaluate the risk factors associated with depression and suicidal ideation in a rural population. Methods A survey was conducted with 543 farmers from Chungcheongnam-do Province using the Center for Epidemiologic Studies Depression Scale (CES-D) for depression, Lubben Social Network Scale (LSNS) for social support, Swedish Q16 for neurotoxicity symptoms and a survey tool for farmer's syndrome. Results After adjusting for socioeconomic factors using logistic regression analysis, poor self-rated health, low social support and neurotoxicity were positively associated with the risk of depression (odds ratio [OR], 15.96; 95% confidence interval [CI], 3.11 to 81.97; OR, 3.14; 95% CI, 1.26 to 7.82; and OR, 3.68; 95% CI, 1.08 to 12.57, respectively). The risk of suicidal ideation significantly increased with low social support, neurotoxicity and farmer's syndrome (OR, 2.28; 95% CI, 1.18 to 4.40; OR, 6.17; 95% CI, 2.85 to 13.34; and OR, 3.70; 95% CI, 1.51 to 9.07, respectively). Conclusions Given the overall results of this study, there is a need to establish programs which can improve the health and social relationships of farmers. Also, when farmers have neurological symptoms from pesticide exposure and characteristic symptoms of farmer's syndrome, a monitoring system for depression and suicide must be made available.

• Journal of the Korean Institute of Oriental Medical Informatics
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• v.19 no.2
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• pp.1-20
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• 2013

This research observed the interrelations between the active components found specifically in red ginseng and fermented red ginseng from among the variety of ginseng variations and the protective effect and anti-oxidant effect exercised on brain cells in the animal model for MPTP-induced neurotoxic Parkinson's Disease and obtained the following conclusions. The results above comprehensively demonstrated that the fermented red ginseng extract exercised greater protective effects against oxidant brain damage by MPTP when compared to the group administered with the red ginseng extract. This was induced an increase in TH protein expression, and further raised the efficiency of the anti-oxidant enzyme defensive system against neurotoxicity, thereby restraining the lipid peroxidation caused by the active oxygen generated during the course of MPTP metabolism and enhancing the body's defensive capacities in response to tissue damage, thereby demonstrating a protective effect against MPTP induced neurotoxicity.