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: 10 July 2025 | Viewed by 7991

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

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Keywords

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

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Published Papers (3 papers)

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Research

19 pages, 9795 KiB  
Article
Integrated Biomarker Response Emphasizing Neuronal Oxidative Stress and Genotoxicity Induced by Oxamyl in Sprague Dawley Rats: Ameliorative Effect of Ginseng as a Neuroprotective Agent
by Salwa M. Abdallah, Reham E. Muhammed, Reda E. Mohamed, Wagdy K. B. Khalil, Dalia A. Taha, Mohamed B. Shalaby, Islam Elgohary, Amr A. Abdallah, Hosam M. Habib and Ahmed F. El-Yazbi
Toxics 2024, 12(9), 655; https://doi.org/10.3390/toxics12090655 - 7 Sep 2024
Cited by 1 | Viewed by 1276
Abstract
Climate change has led to increased and varying pest infestation patterns, triggering a rise in pesticide usage and exposure. The effects of oxamyl, a widely used nematicide in Egypt, encompasses typical signs of carbamate intoxication; nevertheless, long-term effects of oxamyl exposure, particularly on [...] Read more.
Climate change has led to increased and varying pest infestation patterns, triggering a rise in pesticide usage and exposure. The effects of oxamyl, a widely used nematicide in Egypt, encompasses typical signs of carbamate intoxication; nevertheless, long-term effects of oxamyl exposure, particularly on the nervous system, require further elucidation. This study systematically investigated the mechanism and manifestations of repeated subacute exposure to sublethal doses of oxamyl in male SD rats. Data showed a dose-dependent genotoxic effect, manifested as increased bone marrow micronuclei and decreased brain expression of key genes involved in neurogenesis and neuronal development. Coincidently, brain histopathology showed dose-dependent neurodegeneration in various regions, associated with a significant increase in GFAP immunoreactivity, indicative of neuroinflammation. Biochemical examination revealed a typical pattern of cholinesterase inhibition by carbamates in serum and brain tissue, as well as increased oxidative stress markers in the brain such as SOD activity reduction, alongside an increase in NO and MDA. The ability of Ginseng at a 100 mg/Kg dose to ameliorate the effects of oxamyl exposure was investigated. Ginseng use, either as a protective or therapeutic regimen, attenuated the observed genotoxic, neuroinflammatory, and biochemical alterations. Our results indicate that repeated exposure to oxamyl triggers an integrative neurotoxic response, driven by genotoxicity, oxidative stress, and neuroinflammation, that could trigger an increase in neurological and cognitive disorders. These findings emphasize the urgent need for confirmatory translational studies in human subjects to assess these changes and inform policy decisions regarding safe levels of usage and appropriate agricultural and public health practices. Full article
(This article belongs to the Special Issue Drug and Pesticides-Induced Oxidative Stress and Apoptosis)
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17 pages, 3561 KiB  
Article
The Fungicide Ipconazole Can Activate Mediators of Cellular Damage in Rat Brain Regions
by Carlos Villaorduña, Luis Barrios-Arpi, Boris Lira-Mejía, Mariella Ramos-Gonzalez, Olger Ramos-Coaguila, Luis Inostroza-Ruiz, Alejandro Romero and José-Luis Rodríguez
Toxics 2024, 12(9), 638; https://doi.org/10.3390/toxics12090638 - 31 Aug 2024
Viewed by 1205
Abstract
This study aimed to investigate the toxicity of the fungicide ipconazole on oxidative status, cell death and inflammasome complex activation in the hypothalamus, cerebral cortex, striatum and hippocampus of rats. Female albino rats were randomly divided into a control group and four groups [...] Read more.
This study aimed to investigate the toxicity of the fungicide ipconazole on oxidative status, cell death and inflammasome complex activation in the hypothalamus, cerebral cortex, striatum and hippocampus of rats. Female albino rats were randomly divided into a control group and four groups treated with ipconazole at doses of 1, 5, 10 and 20 mg/kg b.w., administered for six days. Ipconazole significantly increased MDA and ROS levels in all brain regions studied, while reducing catalase enzyme activity. The molecular expression of cell death-related genes (AKT1, APAF1, BNIP3, CASP3 and BAX) and the inflammasome complex (CASP1, IL1β, IL6, NLRP3, NFĸB and TNFα) was also assessed, showing increased expression in at least one brain region. The findings demonstrate that ipconazole induces central nervous system toxicity in mammals, highlighting its potential role as a risk factor in the development of neurodegenerative disorders in individuals exposed to this contaminant. Full article
(This article belongs to the Special Issue Drug and Pesticides-Induced Oxidative Stress and Apoptosis)
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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 4908
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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