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Drug Toxicity in Disease Therapy
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Drug Toxicity in Disease Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 4443

Special Issue Editor

Dr. Lauro M. Souza

E-Mail Website
Guest Editor
Instituto de Pesquisa Pelé Pequeno Príncipe, Curitiba 80250-060, Brazil
Interests: liquid chromatography; gas chromatography; analytical chemistry; drug identification

Special Issue Information

Dear Colleagues,

Drug toxicity covers a series of adverse and harmful side effects that patients can develop throughout the usage of different medications. These medication toxicities are considered one of the most important limiting factors for the efficacy of different therapies using different drugs widely employed in medicine. Usually, harmful side effects are observed after a drug accumulation in the bloodstream, over time, till medications reach higher concentrations than their therapeutic range. In such conditions, the patients are more prompt to develop intoxications, nevertheless, even at regular bloodstream concentrations, many patients undergo from moderate side effects to acute intoxications. These mechanisms of intoxication are not even well known at all and could be related to the patient metabolism or drug-drug interactions that result in toxic reactions, being an important research field in order to understand how these reactions occur and how to overcome them, in order to warranty the safety and of the patients and therapy efficacy.

In this Special Issue, we hope to discuss all aspects of the toxic effects of different drugs and their complications to patient health, and how to prevent these complications as well. Drug control and management through personalized medicine, such as therapeutic drug monitoring, employed as a tool to minimize drug toxicity are also welcome.

Dr. Lauro M. Souza
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • drug toxicity
  • toxic drug interactions
  • drug management
  • therapeutic drug monitoring

Published Papers (3 papers)

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Research

9 pages, 1100 KiB  
Article
Gas Chromatography–Mass Spectrometry Detection of Thymoquinone in Oil and Serum for Clinical Pharmacokinetic Studies
by A. Tekbaş, S. Bremer-Streck, D. K. Wissenbach, F. T. Peters, M. von Lilienfeld-Toal, Z. Soonawalla, F. Rauchfuß, U. Settmacher and U. Dahmen
Int. J. Mol. Sci. 2023, 24(22), 16431; https://doi.org/10.3390/ijms242216431 - 17 Nov 2023
Viewed by 698
Abstract
Thymoquinone (TQ) is the primary component of Nigella sativa L. (NS) oil, which is renowned for its potent hepatoprotective effects attributed to its antioxidant, anti-fibrotic, anti-inflammatory, anti-carcinogenic, and both anti- and pro-apoptotic properties. The aim of this work was to establish a method [...] Read more.
Thymoquinone (TQ) is the primary component of Nigella sativa L. (NS) oil, which is renowned for its potent hepatoprotective effects attributed to its antioxidant, anti-fibrotic, anti-inflammatory, anti-carcinogenic, and both anti- and pro-apoptotic properties. The aim of this work was to establish a method of measuring TQ in serum in order to investigate the pharmacokinetics of TQ prior to a targeted therapeutic application. In the first step, a gas chromatography–mass spectrometry method for the detection and quantification of TQ in an oily matrix was established and validated according to European Medicines Agency (EMA) criteria. For the assessment of the clinical application, TQ concentrations in 19 oil preparations were determined. Second, two serum samples were spiked with TQ to determine the TQ concentration after deproteinization using toluene. Third, one healthy volunteer ingested 1 g and another one 3 g of a highly concentrated NS oil 30 and 60 min prior to blood sampling for the determination of serum TQ level. After the successful establishment and validation of the measurement method, the highest concentration of TQ (36.56 g/L) was found for a bottled NS oil product (No. 1). Since a capsule is more suitable for oral administration, the product with the third highest TQ concentration (No. 3: 24.39 g/L) was used for all further tests. In the serum samples spiked with TQ, the TQ concentration was reliably detectable in a range between 5 and 10 µg/mL. After oral intake of NS oil (No. 3), however, TQ and/or its derivatives were not detectable in human serum. This discrepancy in detecting TQ after spiking serum or following oral ingestion may be attributed to the instability of TQ in biomatrices as well as its strong protein binding properties. A pharmacokinetics study was therefore not viable. Studies on isotopically labeled TQ in an animal model are necessary to study the pharmacokinetics of TQ using alternative modalities. Full article
(This article belongs to the Special Issue Drug Toxicity in Disease Therapy)
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12 pages, 2295 KiB  
Article
Assessment of Neurotoxic Effects of Oxycodone and Naloxone in SH-SY5Y Cell Line
by Luíza Siqueira Lima, Nayara de Souza da Costa, Maria Eduarda Andrade Galiciolli, Meire Ellen Pereira, William Almeida, Marta Margarete Cestari, Pablo Andrei Nogara, Ana Carolina Irioda and Cláudia Sirlene Oliveira
Int. J. Mol. Sci. 2023, 24(2), 1424; https://doi.org/10.3390/ijms24021424 - 11 Jan 2023
Viewed by 1622
Abstract
Opioid drugs have analgesic properties used to treat chronic and post-surgical pain due to descending pain modulation. The use of opioids is often associated with adverse effects or clinical issues. This study aimed to evaluate the toxicity of opioids by exposing the neuroblastoma [...] Read more.
Opioid drugs have analgesic properties used to treat chronic and post-surgical pain due to descending pain modulation. The use of opioids is often associated with adverse effects or clinical issues. This study aimed to evaluate the toxicity of opioids by exposing the neuroblastoma cell line (SH-SY5Y) to 0, 1, 10, and 100 µM oxycodone and naloxone for 24 h. Analyses were carried out to evaluate cell cytotoxicity, identification of cell death, DNA damage, superoxide dismutase (SOD), glutathione S-transferase (GST), and acetylcholinesterase (AChE) activities, in addition to molecular docking. Oxycodone and naloxone exposure did not alter the SH-SY5Y cell viability. The exposure to 100 µM oxycodone and naloxone significantly increased the cells’ DNA damage score compared to the control group. Naloxone exposure significantly inhibited AChE, GST, and SOD activities, while oxycodone did not alter these enzymes’ activities. Molecular docking showed that naloxone and oxycodone interact with different amino acids in the studied enzymes, which may explain the differences in enzymatic inhibition. Naloxone altered the antioxidant defenses of SH-SY5Y cells, which may have caused DNA damage 24 h after the exposure. On the other hand, more studies are necessary to explain how oxycodone causes DNA damage. Full article
(This article belongs to the Special Issue Drug Toxicity in Disease Therapy)
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14 pages, 1973 KiB  
Article
Hepatocyte-Specific Deficiency of DAX-1 Protects Mice from Acetaminophen-Induced Hepatotoxicity by Activating NRF2 Signaling
by Young-Joo Suh, Hyo-Jeong Yun, Yu-Bin Kim, Eun-Jung Kang, Jung Hyeon Choi, Young-Keun Choi, In-Bok Lee, Dong-Hee Choi, Yun Jeong Seo, Jung-Ran Noh, Jong-Soo Lee, Yong-Hoon Kim and Chul-Ho Lee
Int. J. Mol. Sci. 2022, 23(19), 11786; https://doi.org/10.3390/ijms231911786 - 04 Oct 2022
Cited by 2 | Viewed by 1655
Abstract
Acetaminophen (APAP) is a widely used analgesic and antipyretic drug, but its overdose can cause acute liver failure. The dosage-sensitive sex reversal adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX-1, NR0B1), is an orphan nuclear receptor that acts as [...] Read more.
Acetaminophen (APAP) is a widely used analgesic and antipyretic drug, but its overdose can cause acute liver failure. The dosage-sensitive sex reversal adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX-1, NR0B1), is an orphan nuclear receptor that acts as a transcriptional co-repressor of various genes. In this study, we identified the role of DAX-1 in APAP-induced liver injury using hepatocyte-specific Dax-1 knockout (Dax-1 LKO) mice. Mouse primary hepatocytes were used as a comparative in vitro study. APAP overdose led to decreased plasma alanine aminotransferase and aspartate aminotransferase levels in Dax-1 LKO mice compared to C57BL/6J (WT) controls, accompanied by reduced liver necrosis. The expression of the genes encoding the enzymes catalyzing glutathione (GSH) synthesis and metabolism and antioxidant enzymes was increased in the livers of APAP-treated Dax-1 LKO mice. The rapid recovery of GSH levels in the mitochondrial fraction of APAP-treated Dax-1 LKO mice led to reduced reactive oxygen species levels, resulting in the inhibition of the prolonged JNK activation. The hepatocyte-specific DAX-1 deficiency increased the protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) compared with WT controls after APAP administration. These results indicate that DAX-1 deficiency in hepatocytes protects against APAP-induced liver injury by Nrf2-regulated antioxidant defense. Full article
(This article belongs to the Special Issue Drug Toxicity in Disease Therapy)
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