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Article ; Online: [Neurotoxicity Mechanism of Environmental Chemicals and Its Evaluation System].

Kotake, Yaichiro

Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan

2018 Volume 138, Issue 10, Page(s) 1227–1233

Abstract: It is pivotal to assess the toxicity and safety of chemicals, including medicines, in the research field of environmental health science. Here we introduce neurotoxic mechanisms in mammals of environmental organotin and Parkinson's disease-related ... ...

Abstract	It is pivotal to assess the toxicity and safety of chemicals, including medicines, in the research field of environmental health science. Here we introduce neurotoxic mechanisms in mammals of environmental organotin and Parkinson's disease-related chemicals. We clarified that low concentrations of tributyltin decrease α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptor subunit GluA2 (GluR2) expression, leading to the vulnerability of cultured neurons. That is, tributyltin reduces GluA2 prior to neuronal death. This GluA2 decrease can be used as a sensitive evaluation index of neurotoxicity, since low levels of certain chemicals, for example some agrochemicals, decrease GluA2 expression. We also elucidated the mechanisms of abnormal protein metabolism induced by low levels of two Parkinson's disease-related chemicals: 1-methyl-4-phenylpyridinium ion (MPP
MeSH term(s)	1-Methyl-4-phenylpyridinium/toxicity ; Animals ; Cell Death/drug effects ; Environmental Exposure/adverse effects ; Environmental Health ; Environmental Pollutants/toxicity ; Gene Expression/drug effects ; Hazardous Substances/toxicity ; Humans ; Neurons/pathology ; Parkinson Disease, Secondary/chemically induced ; Receptors, AMPA/genetics ; Receptors, AMPA/metabolism ; Tetrahydroisoquinolines/toxicity ; Trialkyltin Compounds/toxicity
Chemical Substances	Environmental Pollutants ; Hazardous Substances ; Receptors, AMPA ; Tetrahydroisoquinolines ; Trialkyltin Compounds ; glutamate receptor ionotropic, AMPA 2 ; tributyltin (4XDX163P3D) ; 1,2,3,4-tetrahydroisoquinoline (56W89FBX3E) ; 1-Methyl-4-phenylpyridinium (R865A5OY8J)
Language	Japanese
Publishing date	2018-09-27
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	200514-1
ISSN	1347-5231 ; 0031-6903 ; 0372-7750 ; 0919-2085 ; 0919-2131
ISSN (online)	1347-5231
ISSN	0031-6903 ; 0372-7750 ; 0919-2085 ; 0919-2131
DOI	10.1248/yakushi.18-00014
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Article ; Online: Tributyltin activates the Keap1-Nrf2 pathway via a macroautophagy-independent reduction in Keap1.

Hatano, Misaki / Hatamiya, Shunichi / Miyara, Masatsugu / Kotake, Yaichiro

The Journal of toxicological sciences

2023 Volume 48, Issue 3, Page(s) 161–168

Abstract: Tributyltin (TBT) is an environmental chemical, which was used as an antifouling agent for ships. Although its use has been banned, it is still persistently present in ocean sediments. Although TBT reportedly causes various toxicity in mammals, few ... ...

Abstract	Tributyltin (TBT) is an environmental chemical, which was used as an antifouling agent for ships. Although its use has been banned, it is still persistently present in ocean sediments. Although TBT reportedly causes various toxicity in mammals, few studies on the mechanisms of biological response against TBT toxicity exist. The well-established Keap1-Nrf2 pathway is activated as a cytoprotective mechanism under stressful conditions. The relationship between TBT and the Keap1-Nrf2 pathway remains unclear. In the present study, we evaluated the effect of TBT on the Keap1-Nrf2 pathway. TBT reduced Keap1 protein expression in Neuro2a cells, a mouse neuroblastoma cell line, after 6 hr without altering mRNA expression levels. TBT also promoted the nuclear translocation of Nrf2, a transcription factor for antioxidant proteins, after 12 hr and augmented the expression of heme oxygenase 1, a downstream protein of Nrf2. Furthermore, TBT decreased Keap1 levels in mouse embryonic fibroblast (MEF) cells, with the knockout of Atg5, which is essential for macroautophagy, as well as in wild-type MEF cells. These results suggest that TBT activates the Keap1-Nrf2 pathway via the reduction in the Keap1 protein level in a macroautophagy-independent manner. The Keap1-Nrf2 pathway is activated by conformational changes in Keap1 induced by reactive oxygen species or electrophiles. Furthermore, any unutilized Keap1 protein is degraded by macroautophagy. Understanding the novel mechanism governing the macroautophagy-independent reduction in Keap1 by TBT may provide insights into the unresolved biological response mechanism against TBT toxicity and the activation mechanism of the Keap1-Nrf2 pathway.
MeSH term(s)	Animals ; Mice ; Fibroblasts ; Kelch-Like ECH-Associated Protein 1 ; Macroautophagy ; NF-E2-Related Factor 2 ; Trialkyltin Compounds/toxicity
Chemical Substances	Keap1 protein, mouse ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; tributyltin (4XDX163P3D) ; Trialkyltin Compounds
Language	English
Publishing date	2023-02-28
Publishing country	Japan
Document type	Journal Article
ZDB-ID	770623-6
ISSN	1880-3989 ; 0388-1350
ISSN (online)	1880-3989
ISSN	0388-1350
DOI	10.2131/jts.48.161
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Article ; Online: Photodegradation profiling of nitrendipine: evaluation of active pharmaceutical ingredient, tablets and its altered forms.

Kawabata, Kohei / Muraoka, Haruka / Miyara, Masatsugu / Kotake, Yaichiro / Nishi, Hiroyuki

Analytical sciences : the international journal of the Japan Society for Analytical Chemistry

2023 Volume 39, Issue 11, Page(s) 1791–1803

Abstract: Nitrendipine (NTR) is a dihydropyridine drug, which is well-known as a photodegradable pharmaceutical. However, the photochemical reaction of NTR has not been evaluated in detail from now. In this study, we perform the photodegradation profiling of NTR ... ...

Abstract	Nitrendipine (NTR) is a dihydropyridine drug, which is well-known as a photodegradable pharmaceutical. However, the photochemical reaction of NTR has not been evaluated in detail from now. In this study, we perform the photodegradation profiling of NTR for the elucidation of its photochemical behavior. NTR amounts during ultraviolet light (UV) irradiation were monitored using high performance liquid chromatography (HPLC). NTR was photodegraded almost completely within 24 h along with the generation of some photoproducts. Structural determination of two NTR photoproducts were carried out by means of electrospray ionization liquid chromatography tandem mass spectrometry (LC-ESI-MS/MS). Obtained results from this study clarified one novel NTR photoproduct, a nitroso pyridine analogue, in addition to a pyridine analogue. Furthermore, photodegradation pathway of NTR was speculated based on chemical structures of NTR photoproducts to clarify its photochemical behavior. It was proposed that a singlet oxygen molecule might withdraw two hydrogen radicals resulting in the form of a pyridine analogue, and the following reduction of its nitro group might produce a nitroso pyridine analogue. Finally, we evaluated the photostability of NTR tablets and its altered forms, indicating that the change of the dosage form led to a decrease of the photostability of NTR tablets. The obtained results will be helpful for the additional research to evaluate the effect of NTR photodegradation on its own biological activities.
Language	English
Publishing date	2023-08-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1483376-1
ISSN	1348-2246 ; 1348-2246
ISSN (online)	1348-2246
ISSN	1348-2246
DOI	10.1007/s44211-023-00400-x
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Article ; Online: Tributyltin inhibits autophagy by decreasing lysosomal acidity in SH-SY5Y cells.

Hatamiya, Shunichi / Miyara, Masatsugu / Kotake, Yaichiro

Biochemical and biophysical research communications

2022 Volume 592, Page(s) 31–37

Abstract: Tributyltin (TBT) is an environmental pollutant that remains in marine sediments and is toxic to mammals. For example, TBT elicits neurotoxic and immunosuppressive effects on rats. However, it is not entirely understood how TBT causes toxicity. Autophagy ...

Abstract	Tributyltin (TBT) is an environmental pollutant that remains in marine sediments and is toxic to mammals. For example, TBT elicits neurotoxic and immunosuppressive effects on rats. However, it is not entirely understood how TBT causes toxicity. Autophagy plays a pivotal role in protein quality control and eliminates aggregated proteins and damaged organelles. We previously reported that TBT dephosphorylates mammalian target of rapamycin (mTOR), which may be involved in enhancement of autophagosome synthesis, in primary cultures of cortical neurons. Autophagosomes can accumulate due to enhancement of autophagosome synthesis or inhibition of autophagic degradation, and we did not clarify whether TBT alters autophagic flux. Here, we investigated the mechanism by which TBT causes accumulation of autophagosomes in SH-SY5Y cells. TBT inhibited autophagy without affecting autophagosome-lysosome fusion before it caused cell death. TBT dramatically decreased the acidity of lysosomes without affecting lysosomal membrane integrity. TBT decreased the mature protein level of cathepsin B, and this may be related to the decrease in lysosomal acidity. These results suggest that TBT inhibits autophagic degradation by decreasing lysosomal acidity. Autophagy impairment may be involved in the mechanism underlying neuronal death and/or T-cell-dependent thymus atrophy induced by TBT.
MeSH term(s)	Autophagosomes/drug effects ; Autophagosomes/metabolism ; Autophagy/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Humans ; Hydrolysis ; Intracellular Membranes/drug effects ; Intracellular Membranes/metabolism ; Lysosomes/drug effects ; Lysosomes/metabolism ; Microtubule-Associated Proteins/metabolism ; Sequestosome-1 Protein/metabolism ; Trialkyltin Compounds/pharmacology
Chemical Substances	MAP1LC3A protein, human ; Microtubule-Associated Proteins ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Trialkyltin Compounds ; tributyltin (4XDX163P3D)
Language	English
Publishing date	2022-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.12.118
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Article: Tributyltin inhibits autophagy by decreasing lysosomal acidity in SH-SY5Y cells

Hatamiya, Shunichi / Miyara, Masatsugu / Kotake, Yaichiro

Biochemical and biophysical research communications. 2022 Feb. 12, v. 592

2022

Abstract	Tributyltin (TBT) is an environmental pollutant that remains in marine sediments and is toxic to mammals. For example, TBT elicits neurotoxic and immunosuppressive effects on rats. However, it is not entirely understood how TBT causes toxicity. Autophagy plays a pivotal role in protein quality control and eliminates aggregated proteins and damaged organelles. We previously reported that TBT dephosphorylates mammalian target of rapamycin (mTOR), which may be involved in enhancement of autophagosome synthesis, in primary cultures of cortical neurons. Autophagosomes can accumulate due to enhancement of autophagosome synthesis or inhibition of autophagic degradation, and we did not clarify whether TBT alters autophagic flux. Here, we investigated the mechanism by which TBT causes accumulation of autophagosomes in SH-SY5Y cells. TBT inhibited autophagy without affecting autophagosome–lysosome fusion before it caused cell death. TBT dramatically decreased the acidity of lysosomes without affecting lysosomal membrane integrity. TBT decreased the mature protein level of cathepsin B, and this may be related to the decrease in lysosomal acidity. These results suggest that TBT inhibits autophagic degradation by decreasing lysosomal acidity. Autophagy impairment may be involved in the mechanism underlying neuronal death and/or T-cell-dependent thymus atrophy induced by TBT.
Keywords	acidity ; atrophy ; autophagosomes ; autophagy ; cathepsin B ; death ; immunosuppression ; lysosomes ; neurons ; neurotoxicity ; pollutants ; protein content ; protein value ; quality control ; rapamycin ; research ; tributyltin
Language	English
Dates of publication	2022-0212
Size	p. 31-37.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.12.118
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Article ; Online: Trehalose decreases mRNA and protein expressions of c-Jun and JunB in human cervical cancer HeLa cells.

Umeda-Miyara, Kanae / Miyara, Masatsugu / Sanoh, Seigo / Kotake, Yaichiro

Journal of biochemistry

2022 Volume 172, Issue 3, Page(s) 177–187

Abstract: Increasing evidence suggests that trehalose, a non-reducing disaccharide, ameliorates disease phenotypes by activating autophagy in animal models of various human diseases, including neurodegenerative diseases. Multiple in vitro studies suggest that ... ...

Abstract	Increasing evidence suggests that trehalose, a non-reducing disaccharide, ameliorates disease phenotypes by activating autophagy in animal models of various human diseases, including neurodegenerative diseases. Multiple in vitro studies suggest that activation of transcription factor EB, a master regulator of lysosomal biogenesis and autophagy genes, is a major contributor to trehalose-induced autophagy at later stages of exposure. However, underlying causes of trehalose-induced autophagy possibly occur at the early stage of the exposure period. In this study, we investigated the effects of short-term exposure of HeLa cells to trehalose on several signal transduction pathways to elucidate the initial events involved in its beneficial effects. Phospho-protein array analysis revealed that trehalose decreases levels of phosphorylated c-Jun, a component of the transcription factor activator protein-1, after 6 h. Trehalose also rapidly reduced mRNA expression levels of c-Jun and JunB, a member of the Jun family, within 1 h, resulting in a subsequent decrease in their protein levels. Future studies, exploring the interplay between decreased c-Jun and JunB protein levels and beneficial effects of trehalose, may provide novel insights into the mechanisms of trehalose action.
MeSH term(s)	Autophagy ; Female ; HeLa Cells ; Humans ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/metabolism ; RNA, Messenger/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Trehalose/pharmacology ; Uterine Cervical Neoplasms
Chemical Substances	JunB protein, human ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; Transcription Factors ; Trehalose (B8WCK70T7I)
Language	English
Publishing date	2022-06-24
Publishing country	England
Document type	Journal Article
ZDB-ID	218073-x
ISSN	1756-2651 ; 0021-924X
ISSN (online)	1756-2651
ISSN	0021-924X
DOI	10.1093/jb/mvac051
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Article ; Online: Improved Predictability of Hepatic Clearance with Optimal pH for Acyl-Glucuronidation in Liver Microsomes.

Mizutare, Tohru / Sanoh, Seigo / Kanazu, Takushi / Ohta, Shigeru / Kotake, Yaichiro

Journal of pharmaceutical sciences

2022 Volume 111, Issue 11, Page(s) 3165–3173

Abstract: The purpose of this study was to investigate the optimal pH for acyl-glucuronidation formation with carboxylic acid-containing compounds in human and rat liver microsomes to improve the predictability of their hepatic clearance. The optimal pH for acyl- ... ...

Abstract	The purpose of this study was to investigate the optimal pH for acyl-glucuronidation formation with carboxylic acid-containing compounds in human and rat liver microsomes to improve the predictability of their hepatic clearance. The optimal pH for acyl-glucuronidation of all 17 compounds was around pH 6.0 in human and rat liver microsomes. Correlation analysis was done with the predicted in vitro intrinsic clearance (CL
MeSH term(s)	Animals ; Carboxylic Acids ; Glucuronosyltransferase ; Hepatocytes ; Humans ; Hydrogen-Ion Concentration ; Liver ; Microsomes ; Microsomes, Liver ; Rats
Chemical Substances	Carboxylic Acids ; Glucuronosyltransferase (EC 2.4.1.17)
Language	English
Publishing date	2022-08-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	3151-3
ISSN	1520-6017 ; 0022-3549
ISSN (online)	1520-6017
ISSN	0022-3549
DOI	10.1016/j.xphs.2022.08.015
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Article ; Online: Evaluation of photostability of azelnidipine tablets and structure determination of its photoproducts.

Kawabata, Kohei / Sakaue, Momoko / Akimoto, Shiori / Miyara, Masatsugu / Kotake, Yaichiro / Nishi, Hiroyuki

Journal of pharmaceutical and biomedical analysis

2023 Volume 233, Page(s) 115471

Abstract: Photo-exposure has a crucial effect on the natures of photosensitive pharmaceuticals in addition to their contents in medicines through the photodegradation. Generated photoproducts might be more bioactive and contribute to the expression of adverse side ...

Abstract	Photo-exposure has a crucial effect on the natures of photosensitive pharmaceuticals in addition to their contents in medicines through the photodegradation. Generated photoproducts might be more bioactive and contribute to the expression of adverse side effects. This study aimed to clarify the photochemical behavior of medicines of azelnidipine, which is a member of dihydropyridine antihypertensive drugs, by the evaluation of its photostability and the determination of chemical structures of generated photoproducts. Calblock® tablets and its altered forms (powders and suspensions) were UV-irradiated by a black light. Residual amounts of active pharmaceutical ingredients (APIs) were monitored by high-performance liquid chromatography. The chemical structures of two photoproducts were determined by electrospray ionization tandem mass spectrometry. API of Calblock® tablets was photodegraded with the generation of several photoproducts. Its photodegradability was more significant when Calblock® tablets were crushed or suspended. Structural determination revealed that two photoproducts were benzophenone and a pyridine derivative. It was speculated that these photoproducts were generated by the elimination of diphenyl methylene radical and additional chemical reaction including oxidation and hydrolysis. Azelnidipine was photosensitive and its photodegradation in Calblock® tablets was promoted by the change of the dosage form. This difference might be derived from the light emission efficiency. This study suggests that API contents of Calblock® tablets might decrease when tablets or its altered forms are exposed to sunlight irradiation with the generation of benzophenone, which is a toxicological potent.
MeSH term(s)	Chromatography, High Pressure Liquid/methods ; Spectrometry, Mass, Electrospray Ionization/methods ; Dihydropyridines ; Photolysis ; Tablets
Chemical Substances	azelnidipine (PV23P19YUG) ; Dihydropyridines ; Tablets
Language	English
Publishing date	2023-05-24
Publishing country	England
Document type	Journal Article
ZDB-ID	604917-5
ISSN	1873-264X ; 0731-7085
ISSN (online)	1873-264X
ISSN	0731-7085
DOI	10.1016/j.jpba.2023.115471
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Article ; Online: Establishment of hyperoxic cell culture system for predicting drug-induced liver injury: reducing accumulated lipids in hepatocytes derived from chimeric mice with humanized liver.

Ohtsuki, Yuya / Sanoh, Seigo / Yamao, Mikaru / Kojima, Yuha / Kotake, Yaichiro / Tateno, Chise

The Journal of toxicological sciences

2023 Volume 48, Issue 2, Page(s) 99–108

Abstract: Drug-induced liver injury (DILI) is a major adverse reaction. Species-specific differences between humans and laboratory animals make it difficult to establish evaluation models that can accurately predict DILI in the preclinical phase. Chimeric mice ... ...

Abstract	Drug-induced liver injury (DILI) is a major adverse reaction. Species-specific differences between humans and laboratory animals make it difficult to establish evaluation models that can accurately predict DILI in the preclinical phase. Chimeric mice with humanized liver are potential predictive models for understanding DILI. Chimeric mice generated by transplanting human hepatocytes into urokinase-type plasminogen activator/severe combined immunodeficient mice are known to develop fatty liver and show lipid accumulation in isolated hepatocytes. It is speculated that the lipids accumulated in hepatocytes may interfere with DILI assessment. It is known that normal 20% oxygen culture conditions do not meet oxygen demand because oxygen consumption rate is higher than the oxygen supply rate. Therefore, we predicted that hyperoxic cultures could induce hepatocyte function and reduce accumulated lipids. A culture of chimeric mouse hepatocytes in 40% oxygen showed reduced intracellular lipid and triglyceride levels compared to those cultured in 20% oxygen on days 7 and 10. In addition, fatty acid β-oxidation (FAO) activity increased from day 7 under 40% oxygen conditions. On the other hand, FAO activity increased on day 10 under 20% conditions. Microarray and Ingenuity Pathway Analysis showed that lipid metabolism-related pathways were downregulated under 40% oxygen conditions for 7 days, suggesting the involvement of several mechanisms in decreasing lipid levels and increasing FAO. Furthermore, some pathways related to cellular function and maintenance were upregulated under 40% oxygen conditions for 7 days. In conclusion, chimeric mouse hepatocytes cultured under hyperoxic conditions may be useful for predicting DILI.
MeSH term(s)	Humans ; Mice ; Animals ; Liver/metabolism ; Hepatocytes/metabolism ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Oxygen/metabolism ; Cell Culture Techniques ; Lipids
Chemical Substances	Oxygen (S88TT14065) ; Lipids
Language	English
Publishing date	2023-02-01
Publishing country	Japan
Document type	Journal Article
ZDB-ID	770623-6
ISSN	1880-3989 ; 0388-1350
ISSN (online)	1880-3989
ISSN	0388-1350
DOI	10.2131/jts.48.99
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Article ; Online: Molecular mechanisms of environmental organotin toxicity in mammals.

Kotake, Yaichiro

Biological & pharmaceutical bulletin

2012 Volume 35, Issue 11, Page(s) 1876–1880

Abstract: Organotins such as tributyltin are suspected of having multiple toxic effects in mammals, in addition to their endocrine-disrupting function. Endogenous organotin concentrations in human blood range from a few to a few hundred nM. In this review, we ... ...

Abstract	Organotins such as tributyltin are suspected of having multiple toxic effects in mammals, in addition to their endocrine-disrupting function. Endogenous organotin concentrations in human blood range from a few to a few hundred nM. In this review, we summarize recent findings on the mechanisms of toxicity of environmental organotins such as tributyltin (TBT) and triphenyltin (TPT) in mammals. TBT and TPT are potent inhibitors of mitochondrial ATP synthase, and a recent study suggests that TBT binds directly to ATP synthase. Organotins disturb steroid biosynthesis and degradation. TBT and TPT are dual agonists of retinoid X receptor (RXR) and peroxisome proliferator-activated receptor γ (PPARγ); they also induce the differentiation of adipocytes in vitro and in vivo, probably through PPARγ activation, suggesting that they may work as obesogens. Environmental organotins are also neurotoxic; they induce behavioral abnormality and are toxic to the developing central nervous system. In vitro studies have shown that organotins induce intracellular Ca(2+) elevation and glutamate excitotoxicity. Recently, it was reported that endogenous levels of TBT decrease expression of 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic acid (AMPA) receptor subunit GluR2, leading to neuronal vulnerability. Most of the experimental studies have employed organotins at concentrations of µM order, and it remains important to clarify the molecular mechanisms of events induced by endogenous levels of environmental organotins.
MeSH term(s)	Animals ; Environmental Pollutants/toxicity ; Homeostasis/drug effects ; Humans ; Mitochondrial Proton-Translocating ATPases/antagonists & inhibitors ; Obesity/chemically induced ; Organotin Compounds/toxicity ; Receptors, Cytoplasmic and Nuclear/agonists
Chemical Substances	Environmental Pollutants ; Organotin Compounds ; Receptors, Cytoplasmic and Nuclear ; Mitochondrial Proton-Translocating ATPases (EC 3.6.3.-)
Language	English
Publishing date	2012-10-30
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1150271-x
ISSN	1347-5215 ; 0918-6158
ISSN (online)	1347-5215
ISSN	0918-6158
DOI	10.1248/bpb.b212017
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