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Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones
Hyperthermia is one of the severe acute adverse effects that can be caused by the ingestion of recreational drugs, such as methcathinones. The effect of hyperthermia on neurotoxicity is currently not known. The primary aim of our study was therefore to investigate the effects of hyperthermia (40.5 °...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7227000/ https://www.ncbi.nlm.nih.gov/pubmed/32295288 http://dx.doi.org/10.3390/cells9040965 |
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author | Zhou, Xun Bouitbir, Jamal Liechti, Matthias E. Krähenbühl, Stephan Mancuso, Riccardo V. |
author_facet | Zhou, Xun Bouitbir, Jamal Liechti, Matthias E. Krähenbühl, Stephan Mancuso, Riccardo V. |
author_sort | Zhou, Xun |
collection | PubMed |
description | Hyperthermia is one of the severe acute adverse effects that can be caused by the ingestion of recreational drugs, such as methcathinones. The effect of hyperthermia on neurotoxicity is currently not known. The primary aim of our study was therefore to investigate the effects of hyperthermia (40.5 °C) on the neurotoxicity of methcathinone (MC), 4-chloromethcathinone (4-CMC), and 4-methylmethcathinone (4-MMC) in SH-SY5Y cells. We found that 4-CMC and 4-MMC were cytotoxic (decrease in cellular ATP and plasma membrane damage) under both hyper- (40.5 °C) and normothermic conditions (37 °C), whereby cells were more sensitive to the toxicants at 40.5 °C. 4-CMC and 4-MMC impaired the function of the mitochondrial electron transport chain and increased mitochondrial formation of reactive oxygen species (ROS) in SH-SY5Y cells, which were accentuated under hyperthermic conditions. Hyperthermia was associated with a rapid expression of the 70 kilodalton heat shock protein (Hsp70), which partially prevented cell death after 6 h of exposure to the toxicants. After 24 h of exposure, autophagy was stimulated by the toxicants and by hyperthermia but could only partially prevent cell death. In conclusion, hyperthermic conditions increased the neurotoxic properties of methcathinones despite the stimulation of protective mechanisms. These findings may be important for the understanding of the mechanisms and clinical consequences of the neurotoxicity associated with these compounds. |
format | Online Article Text |
id | pubmed-7227000 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-72270002020-05-18 Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones Zhou, Xun Bouitbir, Jamal Liechti, Matthias E. Krähenbühl, Stephan Mancuso, Riccardo V. Cells Article Hyperthermia is one of the severe acute adverse effects that can be caused by the ingestion of recreational drugs, such as methcathinones. The effect of hyperthermia on neurotoxicity is currently not known. The primary aim of our study was therefore to investigate the effects of hyperthermia (40.5 °C) on the neurotoxicity of methcathinone (MC), 4-chloromethcathinone (4-CMC), and 4-methylmethcathinone (4-MMC) in SH-SY5Y cells. We found that 4-CMC and 4-MMC were cytotoxic (decrease in cellular ATP and plasma membrane damage) under both hyper- (40.5 °C) and normothermic conditions (37 °C), whereby cells were more sensitive to the toxicants at 40.5 °C. 4-CMC and 4-MMC impaired the function of the mitochondrial electron transport chain and increased mitochondrial formation of reactive oxygen species (ROS) in SH-SY5Y cells, which were accentuated under hyperthermic conditions. Hyperthermia was associated with a rapid expression of the 70 kilodalton heat shock protein (Hsp70), which partially prevented cell death after 6 h of exposure to the toxicants. After 24 h of exposure, autophagy was stimulated by the toxicants and by hyperthermia but could only partially prevent cell death. In conclusion, hyperthermic conditions increased the neurotoxic properties of methcathinones despite the stimulation of protective mechanisms. These findings may be important for the understanding of the mechanisms and clinical consequences of the neurotoxicity associated with these compounds. MDPI 2020-04-14 /pmc/articles/PMC7227000/ /pubmed/32295288 http://dx.doi.org/10.3390/cells9040965 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Zhou, Xun Bouitbir, Jamal Liechti, Matthias E. Krähenbühl, Stephan Mancuso, Riccardo V. Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones |
title | Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones |
title_full | Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones |
title_fullStr | Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones |
title_full_unstemmed | Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones |
title_short | Hyperthermia Increases Neurotoxicity Associated with Novel Methcathinones |
title_sort | hyperthermia increases neurotoxicity associated with novel methcathinones |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7227000/ https://www.ncbi.nlm.nih.gov/pubmed/32295288 http://dx.doi.org/10.3390/cells9040965 |
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