Toxicology Reports最新文献

{"title":"Rising incidence of recreational ketamine use: Clinical cases and management in emergency settings","authors":"Sabrina Marongiu ,&nbsp;Maarten van Eijk ,&nbsp;Femke M.J. Gresnigt ,&nbsp;Esther A. Croes ,&nbsp;Eric J.F. Franssen","doi":"10.1016/j.toxrep.2025.101940","DOIUrl":"10.1016/j.toxrep.2025.101940","url":null,"abstract":"<div><div>The recreational use of ketamine has risen significantly in the Netherlands, particularly among young adults in nightlife settings. This trend has been accompanied by an increase in first aid incidents involving ketamine, often in combination with other substances such as alcohol or MDMA, leading to heightened toxicity. Acute intoxication with ketamine manifests through symptoms like agitation, hallucinations, nausea, tachycardia, and hypertension, while frequent use is associated with long-term complications, including ketamine-induced uropathy. Although ketamine is not currently included in standard toxicological screenings, its detection can aid in diagnosing mixed intoxications, excluding alternative causes, and facilitating referral to follow-up care. Routine inclusion of ketamine in toxicological screening could improve diagnostic precision and better address the health risks associated with its growing prevalence.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101940"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143349534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective effect of coadministration of coenzyme Q10 and vitamin E on myopathy induced by simvastatin in rats","authors":"Omar Ammar Hashim ,&nbsp;Intesar Tarik Numan ,&nbsp;Nadia Hameed Mohammed","doi":"10.1016/j.toxrep.2025.101942","DOIUrl":"10.1016/j.toxrep.2025.101942","url":null,"abstract":"<div><div>The use of Simvastatin has been reported to induced muscle myopathy, with no effective preventive measures. The study objective is to study the protective effect of CoQ10, vitamin E, and their combination to prevent simvastatin-induced skeletal muscle myopathy in rat models and explore possible mechanisms by measuring muscle biomarkers and histopathological changes. All rats (n = 49) received 80 mg/kg/day of simvastatin to induce myopathy for 30 days, the study includes 7 groups (n = 7): negative control, CMC and cotton seed oils vehicles, simvastatin induction, CoQ10, vitamin E and combination of vitamin E and CoQ10 groups; rats in the intervention groups received either 100 mg/kg CoQ10 or 40 mg/kg vitamin E or their combination once daily orally for 30 days. At the end of the experiment, rats were euthanized by cervical dislocation, and blood and the collected tissue samples were collected to measure creatinine kinase (CKM), malondialdehyde (MDA), total antioxidant capacity (TAOC), inducible nitric oxide synthase-2 (iNOS2), and aldolase. In addition, gastrocnemius muscle histopathology was examined. Treatment with CoQ10, vitamin E, or their combination significantly reduced the levels of CKM, aldolase, iNO2, and MDA and increased TAOC compared to the simvastatin induction group. The combination group showed a superior protective effect than either drug alone. Treatment with vitamin E and CoQ10 showed mild vacuolation and cytoplasm with focal splitting and fragmentation of muscle fibers, scattered central nuclei, and eosinophilic cytoplasm. In conclusion, CoQ10 and vitamin E combined showed a superior protective effect against simvastatin-induced myopathy through antioxidant and antiapoptotic pathways.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101942"},"PeriodicalIF":0.0,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143351136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IONPs-induced neurotoxicity via cascade of neuro-oxidative stress, parthanatos-mediated cell death, neuro-inflammation and neurodegenerative changes: Ameliorating effect of rosemary methanolic extract","authors":"Arwa A. Elsheikh ,&nbsp;Noha Ali Abd-Almotaleb ,&nbsp;Mona Mostafa Ahmed ,&nbsp;Eman El-Sayed Khayal","doi":"10.1016/j.toxrep.2025.101935","DOIUrl":"10.1016/j.toxrep.2025.101935","url":null,"abstract":"<div><div>Iron oxide nanoparticles (IONPs) are widely used in various fields, particularly in medicine, where they can be directly injected for diagnostic and therapeutic purposes, although they may induce certain types of toxicity. Therefore, the present work aimed to estimate the potential protective role of the oral extract of rosemary (RO)against the toxic effects of injected IONPs on the brain tissues of adult male rats, and to explore the potential underlying mechanisms involved in reversing such toxicity. Thirty adult male albino rats were allocated into five groups: the control, the vehicle (intravenous saline injection once/week), the RO extract group (orally gavaged100mg/kg/day), IONPs (intravenously injected 30 mg/kg once/week), and the combined RO+IONPs (orally gavaged RO extract 1 hrh before intravenous injection of IONPs). IONPs induced neurotoxicity via triggering a cascade of neuro-oxidative stress, neuro-inflammation, and parthanatos-mediated neuronal cell death by increasing MDA, NO, TNF-α levels, PARP-1, AIF, and NF-κB mRNA expression alongside reducing GSH levels. These incidents contributed to neurodegenerative changes, reflected in increased mRNA expression of α-S, β-APP, and TDP-43. Additionally, IONPs induced structural degenerative changes and elevated iron levels in brain tissues reduced occludin expression, and disrupted the BBB. Furthermore, the concurrent oral RO extract alleviated these conditions and repaired BBB by increasing the occludin expression and ameliorating structural changes in brain tissues. Consequently, the current data provide evidence that RO supplementation during IONP administration holds promise to minimize potential health risks, which should be corroborated by translational studies.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101935"},"PeriodicalIF":0.0,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143170454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global scenario of silica-associated diseases: A review on emerging pathophysiology of silicosis and potential therapeutic regimes","authors":"Prasad Sherekar ,&nbsp;Sanvidhan G. Suke ,&nbsp;Archana Dhok ,&nbsp;Srikant Malegaonkar ,&nbsp;Shrikrishna A. Dhale","doi":"10.1016/j.toxrep.2025.101941","DOIUrl":"10.1016/j.toxrep.2025.101941","url":null,"abstract":"<div><div>Silicosis is an occupational fibrotic lung disease caused by exposure to respirable crystalline silica dust particles produced during industrial activities. Other crystalline silica-induced pulmonary disorders include a predisposition to mycobacterial infections, obstructive airway diseases, idiopathic pulmonary fibrosis, and lung cancer. This review paper discusses the burden of silicosis and associated co-morbidities in developed as well as developing countries globally using the published data of various government agencies, related organizations, and epidemiological findings. Moreover, it sheds light on diverse mechanisms of silicosis, outlining molecular events and peculiar alterations in lung parenchyma leading to this occupational lung disease. Evaluation of pathophysiological mechanisms could aid in the identification of novel target molecules and treatments; to date, there is no curative treatment for silicosis. In recent periods, a lot of attention has been focused on the development and fabrication of suitable nanocarriers for improved and sustained drug delivery in the pulmonary system. Nanoparticle-based therapeutic modality has been evaluated in <em>in-vitro</em> and <em>ex-vivo</em> silicosis models for prolongation of drug activity and improved therapeutic outcomes. The preclinical findings open the doors to clinical trials for operational and regenerative nanoformulations, which eventually create a positive change in medical practice. The following review summarizes various therapeutic approaches available and in the pipe line for silicosis and also stresses the preventive practices for effectively combating this occupational hazard.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101941"},"PeriodicalIF":0.0,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143103971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental lead exposure and aggression in male rats: Influences of maternal care and environmental enrichment","authors":"Shamaila Zafar ,&nbsp;Courtney Williams ,&nbsp;Jaehyun Joo ,&nbsp;Blanca E. Himes ,&nbsp;Jay S. Schneider","doi":"10.1016/j.toxrep.2025.101937","DOIUrl":"10.1016/j.toxrep.2025.101937","url":null,"abstract":"<div><div>Developmental lead (Pb) exposure results in a variety of cognitive deficits and behavioral issues including increased antisocial behavior and aggression. This study investigated the effect of developmental Pb exposure on aggression and violent behavior in male rats and the potential modulatory influences of quality of maternal care and enriched/non-enriched housing conditions. Long-Evans male rats with or without Pb exposure (perinatal or early postnatal) from low or high maternal care mothers (based on amounts of licking/grooming and arched-back nursing) were randomly assigned to live in enriched or non-enriched environments at weaning. At postnatal day 120–190, offensive aggression was assessed using a resident intruder test. Clinch attack (CAK) frequency and latency, and occurrence of biting events were observed to determine violent behavior. Both perinatal and postnatal Pb-exposed rats were significantly more aggressive and showed more violent behavior, compared to non-Pb-exposed animals, regardless of level of maternal care and environmental enrichment. High maternal care significantly lowered the proportion of animals with short CAK latencies and enriched housing significantly lowered the occurrence of biting events. These results suggest that high maternal care and enriched housing may potentially modify expression of violent aggressive behavior in rats with early life Pb exposure.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101937"},"PeriodicalIF":0.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143104087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microplastics: A threat to Fetoplacental unit and Reproductive systems","authors":"Abass Toba Anifowoshe ,&nbsp;Md Noor Akhtar ,&nbsp;Abisola Majeed ,&nbsp;Asem Sanjit Singh ,&nbsp;Toyyibah Funmilayo Ismail ,&nbsp;Upendra Nongthomba","doi":"10.1016/j.toxrep.2025.101938","DOIUrl":"10.1016/j.toxrep.2025.101938","url":null,"abstract":"<div><div>Plastic pollution has become a pressing global environmental and public health challenge, raising significant concerns about its potential effects on human health. While extensive research has been conducted on micro- and nanoplastics (MNPs), there remains a critical gap in understanding how these plastic particles traverse the maternal-fetal interface and contribute to reproductive anomalies. This review aims to address this knowledge gap by examining the effects of MNPs on the fetoplacental unit, a vital structure that serves as the interface between the mother and fetus during pregnancy, as well as on the broader reproductive system. Traditionally viewed as a protective barrier safeguarding the fetus, emerging evidence suggests that the placenta may also act as a site for the accumulation of plastic particles, thereby compromising its function. A literature search was conducted using a combination of keywords on Google Scholar and PubMed including ’plastic particles affect the fetoplacental unit’, ’how plastic particles traverse the maternal-fetal contact’, and reproductive abnormalities induced by micro/nano-plastics’. Key studies show that plastic particles can traverse the maternal-fetal interface, potentially exposing developing fetuses to various harmful chemicals present in plastics, such as endocrine disruptors and persistent organic pollutants. Once in contact with the fetoplacental unit, these particles may trigger inflammatory responses, oxidative stress, and even epigenetic modifications. They also bioaccumulate in testes, altering spermatogenesis, spermatozoa morphology, testosterone production, body weights, and inflammation as reported in mice. Such disruptions can increase the risk of developmental and reproductive disorders in the fetus, suggesting that exposure to plastic particles may carry long-term health implications. Further studies highlight the particular vulnerability of the fetoplacental unit to plastic particles. The placenta has limited detoxifying capabilities and unique immunological regulation, making it especially sensitive to foreign particles. Identifying critical windows of susceptibility during pregnancy is germane, as exposure to plastic particles during these periods could have heightened effects on fetal development. This growing concern underscores the urgent need for comprehensive research into the mechanisms through which plastic particles impact the fetoplacental unit. Additionally, this review calls for stronger measures to mitigate plastic pollution and recommends health strategies aimed at protecting future generations from potential harm. It synthesizes recent findings on the ways in which these particles influence the fetoplacental unit and the broader reproductive system.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101938"},"PeriodicalIF":0.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143351134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valerenic acid ameliorates amphetamine-related neurotoxicity by improving hypothalamus tyrosine hydroxylase and histamine-N-methyl transferase enzymes","authors":"Khaled M.M. Koriem ,&nbsp;Ammar H.A. Naiem","doi":"10.1016/j.toxrep.2025.101936","DOIUrl":"10.1016/j.toxrep.2025.101936","url":null,"abstract":"<div><h3>Background</h3><div>Narcolepsy, obesity, and attention deficit hyperactivity disorder are all treated with amphetamine (a central nervous system stimulant) while valerenic acid (VA) has a pharmacological effect in the central nervous system.</div></div><div><h3>Objectives</h3><div>The purpose of this study was to ascertain whether VA is able to make amends for neurotoxicity by modifying hypothalamus expressions of the enzymes <em>tyrosine hydroxylase and histamine-N-methyl transferase</em> in rats orally administered with methamphetamine (METH).</div></div><div><h3>Methods</h3><div>There were thirty-six male albino rats split up into six equal groups, Control, VA (5 mg/kg)-treated, and VA (10 mg/kg)-treated groups: For four weeks, normal rats received oral administration of 1 ml of distilled water, 5 mg/kg of VA, and 10 ml/kg of VA once daily. METH-treated, VA (5 mg/kg) prior to METH-treated, and VA (10 mg/kg) before METH-treated groups: normal rats were oral administrated with METH (2.5 mg/kg), 3 days/week for 3 weeks, where the last two groups were oral administrated daily during four weeks at 5 mg/kg and 10 mg/kg VA, starting one week prior to METH administration.</div></div><div><h3>Results</h3><div>METH decreased superoxide dismutase, glutathione peroxidase, catalase, NADPH oxidase, interleukin-10, sucrose preference test, distance traveled test, and center square entries test, ATPase activity and the enzymes <em>tyrosine hydroxylase</em> and <em>histamine-N-methyl transferase</em> but increased malondialdehyde, conjugated dienes, oxidative index, serotonin, dopamine, norepinephrine, γ-aminobutyric acid, tumor necrosis factor-α, interleukin-1β, interleukin-6, nuclear factor kappa B levels, the center square duration test, tail suspension test, and forced swimming test. in the METH-treated animals' brain in contrast to the control group. After four weeks of oral administration of VA to METH-treated rats, all of these parameters returned to levels that were nearly control, indicating that a higher dose was more effective than a lower one.</div></div><div><h3>Conclusion</h3><div>VA ameliorated METH-related neurotoxicity by improving hypothamalus expressions of the enzymes <em>tyrosine hydroxylase</em> and <em>histamine-N-methyl transferase</em>.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101936"},"PeriodicalIF":0.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143104085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low molecular weight chitosan attenuates acrylamide-induced toxicity in Drosophila melanogaster","authors":"Swetha Senthil Kumar ,&nbsp;Sahabudeen Sheik Mohideen","doi":"10.1016/j.toxrep.2025.101933","DOIUrl":"10.1016/j.toxrep.2025.101933","url":null,"abstract":"<div><div>Acrylamide (ACR), a toxic by-product of high-temperature food processing, poses significant health risks due to its oxidative, neurotoxic, and genotoxic properties. Regulatory measures focus on limiting ACR in commercial food products, yet daily cooking practices often result in unnoticed exposure, threatening vulnerable populations such as children. This study evaluates the protective role of low and medium molecular-weight (MW) chitosan against ACR-induced toxicity using <em>Drosophila melanogaster</em>. Chitosan, a natural polysaccharide with antioxidant and prebiotic properties, was supplemented alongside ACR exposure in larvae and adult flies. Developmental metrics such as pupation rates, fecundity, and adult emergence were assessed, alongside oxidative stress markers and neurobehavioral outcomes. ACR exposure impaired development, increased oxidative stress, and reduced locomotor activity. Supplementation with low and medium MW chitosan alleviated these effects, with low MW chitosan demonstrating greater efficacy. These findings reveal the potential of low MW chitosan as a dietary intervention to counteract the toxic effects of contaminants like ACR. By reducing oxidative stress, preserving mitochondrial function, and supporting developmental processes, chitosan offers a promising avenue for mitigating the overall toxicity of heat-processed toxins. These findings further highlight chitosan's molecular weight-dependent protective potential against ACR toxicity, offering insights into its application as a dietary mitigator of heat-processed toxins.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101933"},"PeriodicalIF":0.0,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143104086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fumonisin B1 neurotoxicity: Preclinical evidence, biochemical mechanisms and therapeutic strategies","authors":"Blessing A. Obafemi ,&nbsp;Isaac A. Adedara ,&nbsp;Cássia Pereira Delgado ,&nbsp;Olabisi T. Obafemi ,&nbsp;Michael Aschner ,&nbsp;Joao B.T. Rocha","doi":"10.1016/j.toxrep.2025.101931","DOIUrl":"10.1016/j.toxrep.2025.101931","url":null,"abstract":"<div><div>The neurotoxic effects of fungal toxins in both humans and animals have been well documented. Fumonisin B1 (FB1), a mycotoxin produced by fungi of the <em>Fusarium</em> species, is the most toxic fumonisin variant whose neurotoxic effect is still being elucidated. This review highlights the biochemical aspects of FB1 neurotoxicity, such as its mechanisms of action as well as therapeutic strategies. Both <em>in vitro</em> and <em>in vivo</em> studies have demonstrated that alteration in sphingolipid metabolism is a major event in FB-induced neurotoxicity. Studies have also shown that neurotoxicity due to FB1 involves dysregulation of several biochemical events in the brain, such as induction of oxidative stress and inflammation, mitochondrial dysfunction and associated programmed cell death, inhibition of acetylcholinesterase and alteration of neurotransmitter levels, decreased activity of Na⁺K⁺ ATPase, as well as disruption of blood-brain barrier. This review highlights the potential public health effects of FB1-induced neurotoxicity and the need to limit human and animal exposure to FB1in order to prevent its neurotoxic effect. Moreover, it is hoped that this review would stimulate studies aimed at filling the current research gaps such as delineating the effect of FB1 on the blood-brain barrier and appropriate therapies for neurotoxicity caused by FB1.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101931"},"PeriodicalIF":0.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143170450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Highly-sensitive quantification of carbamazepine and identification of its degradation and metabolism products in human liver by high performance liquid chromatography – High resolution mass spectrometry","authors":"Andrei Pirogov ,&nbsp;Ekaterina Shirokova ,&nbsp;Samvel Barsegyan ,&nbsp;Nikita Gandlevskiy ,&nbsp;Valeriya Akimova ,&nbsp;Alessandro Barge ,&nbsp;Aleksander Nosyrev","doi":"10.1016/j.toxrep.2025.101923","DOIUrl":"10.1016/j.toxrep.2025.101923","url":null,"abstract":"<div><div>A method for the qualitative and quantitative determination of carbamazepine in human <em>post mortem</em> liver tissues using high-performance liquid chromatography coupled with high-resolution mass spectrometry has been developed. Validation has been carried out and the main analytical characteristics of the developed method have been determined. The limit of detection (LOD) is 1 ng/g, and the lower limit of quantification (LLOQ) is 5 ng/g. The range of working concentrations for the calibration curve is 5–2000 ng/g. When assessing analyte carryover, the analyte signal of the sample does not exceed 20 % of the signal at the LLOQ level. Degradation products of carbamazepine in model solutions were studied under the presence of hydrochloric acid, sodium hydroxide, and hydrogen peroxide oxidation. Twenty-two degradation products were identified. It was found that the most intensive degradation process of carbamazepine, resulting in various degradation products, is observed during its oxidation with an acidified solution of 3 % hydrogen peroxide at pH= 1–2. The stability of carbamazepine in liver tissues was studied during storage under ambient conditions over various periods. The maximum concentration decline is observed during the first week of storage (on average by 20 %), and then the concentration approximately halves over 8 weeks. Based on the analysis of forensic samples from human liver, 2 out of the 22 carbamazepine degradation products described in this study were detected.</div></div>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"Article 101923"},"PeriodicalIF":0.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143170434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}