Drug-Induced Neurotoxicity

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 1149

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Guest Editor
College of Veterinary Medicine, Chungbuk National University, Cheongju 28644, Republic of Korea
Interests: reproductive toxicology; endocrine disruptors; animal alternative tests; guidelines of toxicology; calcium metabolism; steroid receptors; stem cells in pharmacological and toxicological test
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Special Issue Information

Dear Colleagues,

Drug-induced neurotoxicity implies damage or dysfunction in the nervous system caused by certain drugs or chemicals. This neurotoxicity can occur due to direct toxicity to nerve cells, interference with the normal function of neurotransmitters or the disruption of neuronal signaling pathways. The symptoms of these exposures could include mild or severe cognitive impairment, memory loss, behavior, or mood changes. Drug-induced neurotoxicity is a critical issue in pharmacology and neurology. It has been increasingly important due to the increased use of prescription drugs. Searching for pathways and mechanisms that induce neurotoxicity is challenging; however, numerous advances have been made to elucidate such diseases.

This Special Issue of Pharmaceuticals will provide new insights into the correlations between drugs and neurotoxicity and its related disease, expanding our understanding of how drugs induce adverse effects.

The aims of this Special Issue are as follows:

  1. The risk assessment of drugs on neurotoxicity;
  2. The mechanism and pathway of drugs on neurotoxicity;
  3. The association between drug and neurotoxicity;
  4. The toxicity testing and biomonitoring of drugs on neurotoxicity.

Dr. Eui-Bae Jeung
Guest Editor

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Keywords

  • neurotoxicity
  • neurology
  • nerve dysfunction
  • drug induced neurotoxicity
  • behavior test

Published Papers (1 paper)

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Research

19 pages, 6336 KiB  
Article
The Influence of Nucleoside Reverse Transcriptase Inhibitors on Mitochondrial Activity, Lipid Content, and Fatty-Acid-Binding Protein Levels in Microglial HMC3 Cells
by Katarzyna Lipke, Adriana Kubis-Kubiak and Agnieszka Piwowar
Pharmaceuticals 2023, 16(12), 1661; https://doi.org/10.3390/ph16121661 - 29 Nov 2023
Cited by 1 | Viewed by 747
Abstract
Despite the availability of a wide range of preventive measures and comprehensive treatment options following infection, the development of acquired immunodeficiency syndrome (AIDS) remains a persistent challenge. Nucleoside reverse transcriptase inhibitors (NRTIs) represent the most commonly utilized therapeutic approach, despite being on the [...] Read more.
Despite the availability of a wide range of preventive measures and comprehensive treatment options following infection, the development of acquired immunodeficiency syndrome (AIDS) remains a persistent challenge. Nucleoside reverse transcriptase inhibitors (NRTIs) represent the most commonly utilized therapeutic approach, despite being on the pharmaceutical market for nearly four decades. During this time, a spectrum of side effects ranging from mild discomfort and hypersensitivity reactions to the more prevalent nephrotoxicity and hepatotoxicity has been documented. In light of these considerations, our study aimed to investigate the impacts of two NRTIs, lamivudine and zidovudine, on lipid metabolism in HMC3 microglial cells. Our findings revealed statistically significant reductions in the ATP levels (nearly 8%) and increased mitochondrial superoxide levels (around 10%) after 24 h of treatment with the maximum therapeutic concentration of zidovudine compared to the untreated microglial cells. Furthermore, the concentrations of fatty-acid-binding proteins 4 and 5 were significantly lower (approximately 40%) in the microglial cells that were exposed to NRTIs than in the untreated cells. Notably, the total lipid concentration within the microglial cells markedly increased following NRTI administration with a 13% rise after treatment with 10 µM lamivudine and a remarkable 70% surge following the administration of 6 µM zidovudine. These results suggest that the prolonged administration of NRTIs may potentially lead to lipid accumulation, posing a significant risk to the delicate homeostasis of the neuronal system and potentially triggering a pro-inflammatory response in microglial cells. Full article
(This article belongs to the Special Issue Drug-Induced Neurotoxicity)
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