Drug and Pesticides-Induced Oxidative Stress and Apoptosis

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Drugs Toxicity".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1268

Special Issue Editor


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Guest Editor
Faculty of Veterinary, Universidad Complutense de Madrid, 28040 Madrid, Spain
Interests: in vitro and in vivo studies; agrochemicals; medicinal plant extracts; cytotoxicity; toxicology

Special Issue Information

Dear Colleagues,

Drugs and pesticides are often used to improve the quality of human life directly (drugs) or indirectly (pesticides, food safety security), promoting better conditions for human health. However, excessive use or abuse of these compounds leads to various forms of resistance in target organisms, such as pathogenic microorganisms, insect vectors, etc. In addition to these effects, we can identify cytotoxicity in non-target organisms, as has been reported in humans. It has been reported that these cytotoxic effects may start with a high rate of oxidative stress, mainly with the production of mitochondrial reactive oxygen species (ROS) that trigger the generation of intracellular molecules such as malondialdehyde as a product of lipid peroxidation by ROS, activation of the inflammasome complex or activation of cell death pathways related to the BCL-2 family or the increased activity of caspase enzymes that will lead the cell to its imminent death. This possible concomitant effect between drugs and pesticides is always evaluated separately in vitro or in vivo, hence the importance of further investigating the mechanisms underlying the toxic effects of drugs and pesticides.

Dr. José Luis Rodríguez Gutiérrez
Guest Editor

Manuscript Submission Information

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Keywords

  • drugs
  • pesticides
  • cell death
  • oxidative stress
  • inflammasome complex
  • in vitro
  • in vivo
  • DNA damage
  • molecular biology

Published Papers (1 paper)

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Research

22 pages, 18013 KiB  
Article
Role of IRE1α/XBP1/CHOP/NLRP3 Signalling Pathway in Neonicotinoid Imidacloprid-Induced Pancreatic Dysfunction in Rats and Antagonism of Lycopene: In Vivo and Molecular Docking Simulation Approaches
by Walaa Bayoumie El Gazzar, Heba Bayoumi, Heba S. Youssef, Tayseer A. Ibrahim, Reham M. Abdelfatah, Noha M. Gamil, Mervat K. Iskandar, Amal M. Abdel-Kareim, Shaymaa M. Abdelrahman, Mohammed A. Gebba, Mona Atya Mohamed, Maha M. Mokhtar, Tayseir G. Kharboush, Nervana M. Bayoumy, Hatun A. Alomar and Amina A. Farag
Toxics 2024, 12(7), 445; https://doi.org/10.3390/toxics12070445 - 21 Jun 2024
Viewed by 967
Abstract
Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse effects on the pancreas following oral consumption of imidacloprid neonicotinoids (45 mg/kg daily for 30 days) and the potential [...] Read more.
Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse effects on the pancreas following oral consumption of imidacloprid neonicotinoids (45 mg/kg daily for 30 days) and the potential protective effects of lycopene (LYC) administration (10 mg/kg/day for 30 days) with IMI exposure in male Sprague–Dawley rats. The apoptotic, pyroptotic, inflammatory, oxidative stress, and endoplasmic reticulum stress biomarkers were evaluated, along with the histopathological alterations. Upon IMI administration, noticeable changes were observed in pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress biomarkers, inflammatory, pyroptotic, and apoptotic biomarkers were also observed following IMI administration. LYC effectively reversed these alterations by reducing oxidative stress markers (e.g., MDA) and enhancing antioxidant enzymes (SOD, CAT). It downregulated ER stress markers (IRE1α, XBP1, CHOP), decreased pro-inflammatory cytokines (TNF-α, IL-1β), and suppressed pyroptotic (NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the histopathological and ultrastructure alterations brought on by IMI toxicity. Full article
(This article belongs to the Special Issue Drug and Pesticides-Induced Oxidative Stress and Apoptosis)
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