• 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.

• 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.

• 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 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.

• 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.

• Biomolecules & Therapeutics
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• v.29 no.4
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• pp.399-409
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• 2021

1,2-Diacetylbenzene (DAB) is a metabolite of 1,2-diethylbenzene, which is commonly used in the manufacture of plastics and gasoline. We examined the neurotoxic effects of DAB in young and old rats, particularly its effects on hippocampus. Previously, we reported DAB impairs hippocampal neurogenesis but that the underlying mechanism remained unclear. In this study, we evaluate the toxicities exhibited by DAB in the hippocampi of 6-month-old (young) and 20-month-old (old) male SD rats by treating animals intraperitoneally with DAB at 3 mg/kg/day for 1 week. Hippocampal areas were dissected from brains and RNA was extracted and subjected to RNA-seq analysis. RNA results showed animals exhibited age-dependent sensitivity to the neurotoxic effects of DAB. We observed that inflammatory pathways were up-regulated in old rats but that metabolism- and detoxification-related pathways were up-regulated in young rats. This result in old rats, especially upregulation of the TREM1 signaling pathway (an inflammatory response involved in Alzheimer's disease (AD)) was confirmed by RT-PCR. Our study results provide a better understanding of age-dependent responses to DAB and new insight into the association between DAB and AD.

• 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.

• 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.

• 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.

• Journal of Microbiology and Biotechnology
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• v.27 no.4
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• pp.725-730
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• 2017

A heteronemertean, Yininemertes pratensis, was collected in Han River Estuary, South Korea. This estuarine nemertean has been known by the local fishermen for harmful effects to the glass eels, juveniles of Japanese eel Anguilla japonica, migrating to fresh water. The present study confirmed the neurotoxic effects of this heteronemertean ribbon worm at the cellular level. Derivative types of neurotoxic tetrodotoxin (TTX), 5,11-dideoxy TTX (m/z 288) and 11-norTTX-6(S)-01 (m/z 305.97), were identified through HPLC and MALDI-TOF MS. However, significant neurotoxicity was confirmed in the fraction containing an undefined molecule corresponding to the 291.1 (m/z) peak, when tested in rat primary astrocytes and dorsal ganglion cells. This study is the first to report neurotoxins of the estuarine nemertean, fairly abundant in the Han River estuary, and suggests the long-term monitoring of population dynamics and surveillance of the toxicity in this river estuary.