• Journal of Preventive Medicine and Public Health
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• v.41 no.6
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• pp.397-406
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• 2008

This paper reviews the published literature that is concerned with color vision impairment from industrial and environmental exposure to neurotoxic substances, and we evaluated whether testing for color vision impairment could be an affordable procedure for assessing these neurotoxic effects. In general, most cases of congenital color vision impairment are red-green, and blue-yellow impairment is extremely rare. However, most of the acquired color vision impairment that is related to age, alcohol or environmental factors is blue-yellow impairment. Therefore, many studies have been performed to identify this relationship between exposure to neurotoxic substances, such as organic solvents and heavy metals, and the prevalence of blue-yellow color vision impairment. The test for color vision impairment is known to be very sensitive to the early signs of nervous system dysfunction and this can be useful for making the early diagnosis of neurotoxic effects from exposure to very low concentrations of toxic substances.

• 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.

• Toxicological Research
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• v.28 no.2
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• pp.107-112
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• 2012

Polychlorinated biphenyls (PCBs) are persistent and bioaccumulative environmental pollutants. Recently, it is suggested that neurotoxic effects such as motor dysfunction and impairment in memory and learning have been associated with PCB exposure. However, structure relationship of PCB congeners with neurotoxic effects remains unknown. Since PKC signaling pathway is implicated in the modulation of motor behavior as well as learning and memory and the role of PKC are subspecies-specific, we attempted to study the effects of structurally distinct PCBs on the total PKC activity as well as subspecies of PKC in cerebellar granule cell culture model. Cells were exposed to 0, 25 and 50 ${\mu}M$ of PCB-126, PCB-169, PCB-114, PCB-157, PCB-52 and PCB-4 for 15 min. Cells were subsequently analyzed by [$^3H$] phorbol ester binding assay or immunoblotted against PKC-${\alpha}$ and -${\varepsilon}$ monoclonal antibodies. While non-dioxin-like-PCB (PCB-52 and PCB-4) induced a translocation of PKC-${\alpha}$ and -${\varepsilon}$ from cytosol to membrane fraction, dioxin-like PCBs (PCB-126, -169, -114, -157) had no effects. [$^3H$] Phorbol ester binding assay also revealed structure-dependent increase similar to translocation of PKC isozymes. While PCB-4 induced translocation of PKC-${\alpha}$ and -${\varepsilon}$ was inhibited by ROS inhibitor, the pattern of translocation was not affected in presence of AhR inhibitor. It is suggested that PCB-4-induced PKC activity may not be mediated via AhR-dependent pathway. Taken together, our findings suggest that chlorination of ortho-position in PCB may be a critical structural moiety associated with neurotoxic effects, which may be preferentially mediated via non-AhR-dependent pathway. Therefore, the present study may contribute to understanding the neurotoxic mechanism of PCBs as well as providing a basis for establishing a better neurotoxic assessment.

• Toxicological Research
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• v.20 no.3
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• pp.241-250
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• 2004

We previously found that bisphenol A (BPA) caused neurotoxic behavioral alteration. Since disturbance of calcium homeostasis is an implicated contributor in the neurotoxic mechanism of environmental toxicants, we investigated whether BPA alters calcium homeostasis. Unlike other neurotoxic agents which cause increase of intracellular calcium level, BPA decreased $[Ca^{2+}]_i$ dose-dependently in PC12 cells and cortical neuronal cells regardless of the calcium existence in buffer. BPA at greater concentrations than 100 $\mu\textrm{M}$ reduced cell viability significantly in both types of cells. BPA also suppressed L-glutamate (L-type channel activator, 30 mM) and trifluoperazine (calmodulin antagonist, 30 $\mu\textrm{M}$)-induced increase of $[Ca^{2+}]_i$. BPA further lowered caffeine (RYR activator, 100 $\mu\textrm{M}$)-decreased $[Ca^{2+}]_i$, but did not alter dantrolene (RYR inhibitor, 100 $\mu\textrm{M}$), heparin (IP3 inhibitor, 200 units/ml) and xestospongin C (IP3 inhibitor, 5 $\mu\textrm{M}$)-decreased $[Ca^{2+}]_i$. Cell viability was not directly related to intracellular calcium change by bisphenol A that alternation of intracellular calcium may not be a direct causal factor of BPA-induced neuronal cell death.

• Safety and Health at Work
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• v.3 no.4
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• pp.257-267
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• 2012

Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.

• Journal of Dental Anesthesia and Pain Medicine
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• v.20 no.2
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• pp.63-72
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• 2020

Dental local anesthesia is performed daily on a global scale. Adverse effects are rare, but the topic of neurotoxicity of local anesthetics deserves to be explored, as publications can be controversial and confusing. Therefore, a need was felt to address and question the evidence for potential neurotoxicity of dental local anesthetics. This review aimed to assess the studies published on the neurotoxicity of dental local anesthetics. A Pubmed^Ⓡ search was conducted between January 2019 and August 2019. This revealed 2802 hits on the topic of neurotoxicity or cytotoxicity of the following anesthetics: lidocaine, prilocaine, mepivacaine, articaine, ropivacaine, and bupivacaine. Only 23 papers were deemed eligible for this review: 17 in vitro studies, 3 reviews and 3 audits of national inquiries. The heterogeneous literature on this topic showed that all dental local anesthetics are potentially neurotoxic in a concentration and/or exposure time fashion. There seems no consensus about what cell lines are to be used to investigate the neurotoxicity of local anesthetics, which makes the comparison between studies difficult and ambiguous. However, the bottom line is that all dental local anesthetics have a neurotoxic potential, but that there is no unanimity in the publications about which local anesthetic is the least or the most neurotoxic.

• 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.

• ALGAE
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• v.30 no.1
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• pp.49-58
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• 2015

In September 2007, reports of respiratory irritation and fish kills were received by the Florida Fish and Wildlife Conservation Commission (FWC) from the Jacksonville, Florida area. Water samples collected in this area indicated a bloom of Karenia brevis, the dinoflagellate that produces brevetoxin, which can cause neurotoxic shellfish poisoning. For the next four months, K. brevis was found along approximately 400 km of coastal and Intracoastal waterways from Jacksonville to Jupiter Inlet. This event represents the longest and most extensive red tide the east coast of Florida has experienced and the first time Karenia species other than K. brevis have been reported in this area. This extensive red tide influenced commercial and recreational shellfish harvesting activities along Florida's east coast. Fourteen shellfish harvesting areas (SHAs) were monitored weekly during this event and 10 SHAs were closed for an average of 53 days due to this red tide. The length of SHA closure was dependent on the shellfish species present. Interagency cooperation in monitoring this K. brevis bloom was successful in mitigating any human health impacts. Kernel density estimation was used to create geographic extent maps to help extrapolate discreet sample data points into $5km^2$ radius values for better visualization of the bloom.

• Molecular & Cellular Toxicology
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• v.5 no.3
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• pp.265-271
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• 2009

Concentrations of industrial, agricultural and natural chemicals have been increasing in secondary effluents without their combined sub-lethal effects having been elucidated. In this study, two assays (the comet and acetylcholinesterase assays) were combined to evaluate the genotoxic and neurotoxic effects of effluent from the Noksan wastewater treatment plant (WWTP) on two local marine fish species (flounder and sea eel). The fish were exposed to WWTP secondary effluent that had been diluted with filtered seawater to final concentrations of 1%, 10% and 50%. Analysis of fish samples collected 3 and 5 days after exposure showed that DNA damage occurred in flounder exposed to 50% effluent and in sea eels exposed to 10% or 50% effluent. Furthermore, it was found that acetylcholinesterase (EC:3.1.1.7, AChE) activity decreased in both species when exposed to 10% effluent, indicating the presence of large amounts of genotoxic and neurotoxic chemicals in the effluent. Our results indicate that the comet and AChE assays are promising tools for biomonitoring of secondary effluents.

• Journal of Marine Bioscience and Biotechnology
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• v.8 no.1
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• pp.10-17
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• 2016

A wide-spread contamination of persistent organic pollutants (POPs) such as dioxins, PCBs, PBDEs in the aquatic ecosystem has generated a great concern over the potential risk for these substances to impact marine biotas and food web. Since a major exposure route of these substances to the humans is through the consumption of food including fish and marine byproducts, the consumption of contaminated products has been a great public health concern. Exposure to POPs has been associated with a wide spectrum of adverse effects including reproductive, developmental, immunologic, carcinogenic, and neurotoxic effects. This review covers the background information of key POPs substances and the recent development of toxicity studies including the mode of action. Because neurotoxic effects of some POPs have been observed in humans at low concentrations, polychlorinated biphenyl (PCB), a representative chemical of POPs, is focused to discuss the possible mode(s) of action for the neurotoxic effects. This review provides the updates of toxicity studies on POPs and paves ways to discuss a possible implication of contaminated marine biota over the human health among the marine biotechnology researchers.