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Biomedicines
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The Neurotoxicity of Biomedicines
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The Neurotoxicity of Biomedicines

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 4280

Special Issue Editor

Dr. Wayne Carter

E-Mail Website1 Website2
Guest Editor
Clinical Toxicology, School of Medicine, The University of Nottingham, Nottingham NG7 2RD, UK
Interests: biomedicines; neurotoxicity; neurodegeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurotoxicity arises when excessive exposure to natural or synthetic substances detrimentally affects the functioning of the peripheral and/or central nervous system. Biomedicines or ethnomedicines may be neurotoxic via a number of molecular mechanisms, for example, via the induction of redox stress, and they may trigger or contribute to neurodegeneration and neuronal death. In this Special Issue titled “The Neurotoxicity of Biomedicines”, we are requesting manuscripts or review articles that cover agents that initiate or propagate neurotoxicity.  This includes the neurotoxicity of biomedicines and ethnomedicines as pure or partially pure extracts or fractions as well as the neurotoxicity of synthetic medicines. The evaluation of neurotoxicity will consider agent application to cell lines, administration to animals, or the neurotoxicity of an agent evidenced from human studies.  The collation of novel research studies and review articles covering neurotoxicity will produce a useful resource of cutting-edge research in this field to help evaluate the next generation of biomedicines.

Dr. Wayne Carter
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ethnomedicines
  • ethnopharmacology
  • neurotoxicity
  • neurodegeneration
  • redox stress

Published Papers (3 papers)

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Research

27 pages, 5869 KiB  
Article
An In Silico and In Vitro Assessment of the Neurotoxicity of Mefloquine
by Basma M. El Sharazly, Abrar Ahmed, Hany M. Elsheikha and Wayne G. Carter
Biomedicines 2024, 12(3), 505; https://doi.org/10.3390/biomedicines12030505 - 23 Feb 2024
Viewed by 662
Abstract
Mefloquine (MQ) is a quinoline-based anti-malarial drug used for chemoprophylaxis or as a treatment in combination with artesunate. Although MQ has clear anti-Plasmodium falciparum properties, it can induce neurotoxicity and undesired neuropsychiatric side effects in humans. Hence, this study aimed to characterize the [...] Read more.
Mefloquine (MQ) is a quinoline-based anti-malarial drug used for chemoprophylaxis or as a treatment in combination with artesunate. Although MQ has clear anti-Plasmodium falciparum properties, it can induce neurotoxicity and undesired neuropsychiatric side effects in humans. Hence, this study aimed to characterize the neurotoxicity of MQ using human neuroblastoma SH-SY5Y cells. The effects of MQ on neuronal toxicity and cell viability were investigated over a concentration range of 1–100 µM using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. The influence of MQ on cellular bioenergetics was examined by measuring cellular ATP levels and from the induction of reactive oxygen species (ROS). An in silico approach was used to assess the potential neurotoxicity of MQ mediated via binding to the active sites of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) and then experimentally validated via in vitro enzymatic assays. MQ was cytotoxic to neuronal cells in a concentration and exposure duration dependent manner and induced a significant reduction in viability at concentrations of ≥25 µM after a 24 h exposure. MQ adversely impacted cellular bioenergetics and significantly depleted ATP production at concentrations of ≥1 µM after 24 h. MQ-induced cellular ROS production, which was correlated with the induction of apoptosis, as revealed by flow cytometry. In silico studies suggested that MQ was a dual cholinesterase inhibitor and one with remarkably potent binding to BuChE. Modelling data were supported by in vitro studies which showed that MQ inhibited both human AChE and BuChE enzymes. In summary, MQ is an antimalarial drug that may induce neurotoxicity by impacting cellular bioenergetics and perturbing the activity of cholinesterases at exposure concentrations relevant to human dosage. Full article
(This article belongs to the Special Issue The Neurotoxicity of Biomedicines)
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21 pages, 13559 KiB  
Article
Dexmedetomidine Pre-Treatment of Neonatal Rats Prevents Sevoflurane-Induced Deficits in Learning and Memory in the Adult Animals
by Nerea Jimenez-Tellez, Marcus Pehar, Fahad Iqbal, Alberto Casas-Ortiz, Tiffany Rice and Naweed I. Syed
Biomedicines 2023, 11(2), 391; https://doi.org/10.3390/biomedicines11020391 - 28 Jan 2023
Cited by 1 | Viewed by 1352
Abstract
Anesthetics have been shown to cause cytotoxicity, cell death, affect neuronal growth and connectivity in animal models; however, their effects on learning and memory remain to be fully defined. Here, we examined the effects of the inhalation anesthetic sevoflurane (SEV)—both in vivo by [...] Read more.
Anesthetics have been shown to cause cytotoxicity, cell death, affect neuronal growth and connectivity in animal models; however, their effects on learning and memory remain to be fully defined. Here, we examined the effects of the inhalation anesthetic sevoflurane (SEV)—both in vivo by examining learning and memory in freely behaving animals, and in vitro using cultured neurons to assess its impact on viability, mitochondrial structure, and function. We demonstrate here that neonatal exposure to sub-clinically used concentrations of SEV results in significant, albeit subtle and previously unreported, learning and memory deficits in adult animals. These deficits involve neuronal cell death, as observed in cell culture, and are likely mediated through perturbed mitochondrial structure and function. Parenthetically, both behavioural deficits and cell death were prevented when the animals and cultured neurons were pre-treated with the anesthetic adjuvant Dexmedetomidine (DEX). Taken together, our data provide direct evidence for sevoflurane-induced cytotoxic effects at the neuronal level while perturbing learning and memory at the behavioural level. In addition, our data underscore the importance of adjuvant agents such as DEX that could potentially counter the harmful effects of commonly used anesthetic agents for better clinical outcomes. Full article
(This article belongs to the Special Issue The Neurotoxicity of Biomedicines)
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23 pages, 6570 KiB  
Article
Systemic Rotenone Administration Causes Extra-Nigral Alterations in C57BL/6 Mice
by Sarah Thomas Broome and Alessandro Castorina
Biomedicines 2022, 10(12), 3174; https://doi.org/10.3390/biomedicines10123174 - 07 Dec 2022
Cited by 2 | Viewed by 1610
Abstract
Systemic administration of rotenone replicates several pathogenic and behavioural features of Parkinson’s disease (PD), some of which cannot be explained by deficits of the nigrostriatal pathway. In this study, we provide a comprehensive analysis of several neurochemical alterations triggered by systemic rotenone administration [...] Read more.
Systemic administration of rotenone replicates several pathogenic and behavioural features of Parkinson’s disease (PD), some of which cannot be explained by deficits of the nigrostriatal pathway. In this study, we provide a comprehensive analysis of several neurochemical alterations triggered by systemic rotenone administration in the CNS of C57BL/6 mice. Mice injected with either 1, 3 or 10 mg/kg rotenone daily via intraperitoneal route for 21 days were assessed weekly for changes in locomotor and exploratory behaviour. Rotenone treatment caused significant locomotor and exploratory impairment at dosages of 3 or 10 mg/kg. Molecular analyses showed reductions of both TH and DAT expression in the midbrain, striatum and spinal cord, accompanied by altered expression of dopamine receptors and brain-derived neurotrophic factor (BDNF). Rotenone also triggered midbrain-restricted inflammatory responses with heightened expression of glial markers, which was not seen in extra-nigral regions. However, widespread alterations of mitochondrial function and increased signatures of oxidative stress were identified in both nigral and extra-nigral regions, along with disruptions of neuroprotective peptides, such as pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal peptide (VIP) and activity-dependent neuroprotective protein (ADNP). Altogether, this study shows that systemic rotenone intoxication, similarly to PD, causes a series of neurochemical alterations that extend at multiple CNS levels, reinforcing the suitability of this pre-clinical model for the study extra-nigral defects of PD. Full article
(This article belongs to the Special Issue The Neurotoxicity of Biomedicines)
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