Toxicology Research最新文献

{"title":"Metagenomic analysis and bioactive profiling of kombucha fermentation: antioxidant, antibacterial activities, and molecular docking insights into gastric cancer therapeutics.","authors":"Thavasiaanatham Seenivasan Shalini, Ragothaman Prathiviraj, Poomalai Senthilraja","doi":"10.1093/toxres/tfae224","DOIUrl":"10.1093/toxres/tfae224","url":null,"abstract":"<p><p>Kombucha is fermented and produced with a biofilm called a symbiotic culture of bacteria and yeast, which is drunk all over the world for its beneficial effects on human health and energy levels. The metagenomic study of kombucha frequently detected microorganisms in proteobacteria, firmicutes, and actinobacteria. And also, yeast and fungi are Ascomycota and Basidiomycota is present in green leaf and sugarcane juice fermented kombucha. The kombucha extracts' biological activities were assessed using pH, total phenolic content, antioxidant, antibacterial, and anticancer activity. Fermentation may enhance biological activity and the generation of bioactive substances. These results showed the pH -3.1 ± 0.2 and TPC -0.721 μg/mL of gallic acid equivalent. The antioxidant radicals scavenging activity of kombucha was evaluated by DPPH, ABTS, H₂O₂ and TAC. The bioactive chemicals identified by FT-IR and HR-LC/MS analysis of Kombucha totaled 45 components. The identified compounds were further move on to perform molecular docking study against gastric cancer target proteins 4H9M, 2DQ7 and 1TVO are binding with Nequinate compounds showing best LibDock scores 105.12, 114.49, and 108.97. So, this study suggests that knowledge can potentially active bioactive compounds are present in kombucha and it's stimulated the mechanism of gastrointestinal transit. Additionally, the metagenomic analysis gives strength to understand the bacterial and fungal distribution and its molecular mechanism from Kombucha.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae224"},"PeriodicalIF":2.2,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing renal protection against cadmium toxicity: the role of herbal active ingredients.","authors":"Ahmad Safari Maleki, A Wallace Hayes, Gholamreza Karimi","doi":"10.1093/toxres/tfae222","DOIUrl":"https://doi.org/10.1093/toxres/tfae222","url":null,"abstract":"<p><strong>Background: </strong>Rapid industrialization globally has led to a notable increase in the production and utilization of metals, including cadmium (Cd), consequently escalating global metal pollution worldwide. Cd, characterized as a persistent environmental contaminant, poses significant health risks, particularly impacting human health, notably the functionality of the kidneys. The profound effects of Cd stem primarily from its limited excretion capabilities and extended half-life within the human body. Mechanisms underlying its toxicity encompass generating reactive oxygen species (ROS), disrupting calcium-signaling pathways and impairing cellular antioxidant defense mechanisms. This review focuses on the protective effects of various herbal active ingredients against Cd-induced nephrotoxicity.</p><p><strong>Aim: </strong>This study aims to investigate the mechanisms of action of herbal active ingredients, including ant-oxidative, anti-inflammatory and anti-apoptotic pathways, to elucidate potential therapeutic strategies for reducing nephrotoxicity caused by Cd exposure.</p><p><strong>Methods: </strong>A comprehensive search of scientific databases, including Web of Science, PubMed, Scopus and Google Scholar, used relevant keywords to identify studies published up to October 2024.</p><p><strong>Results: </strong>Research illustrates that herbal active ingredients protect against Cd nephrotoxicity by reducing oxidative stress, enhancing antioxidant enzyme activity, inhibiting inflammation, preventing apoptosis, alleviating endoplasmic reticulum (ER) stress, enhancing autophagy and improving mitochondrial function in the kidney.</p><p><strong>Conclusion: </strong>The present study indicates that an extensive understanding of the protective effects of herbal active ingredients holds promise for the development of innovative approaches to safeguard human health and environmental integrity against the detrimental effects of Cd exposure.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae222"},"PeriodicalIF":2.2,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemical study of the risk of diabetes, prediabetic and insulin resistance in car painters and its association with mercury exposure: a retrospective case-control study.","authors":"Ahmad Tarik Numan, Nada Kadum Jawad, Hayder Adnan Fawzi","doi":"10.1093/toxres/tfae221","DOIUrl":"10.1093/toxres/tfae221","url":null,"abstract":"<p><strong>Purpose: </strong>There is controversy about the effect of mercury (Hg) exposure on developing diabetes and insulin resistance. This study aimed to assess the risk of diabetes and insulin resistance in car painters using biochemical markers and serum Hg levels.</p><p><strong>Methods: </strong>A retrospective case-control study involving 210 male participants aged between 25 and 50 years. The participants were divided into two groups: Car painters for at least one year and healthy people who had not worked as car painters and had no health concerns or chronic diseases.</p><p><strong>Results: </strong>The serum levels of Hg, MDA (malondialdehyde), interleukin (IL)-1β, visfatin, fasting insulin, and fasting blood glucose (FBG) were evaluated. Serum Hg levels were significantly higher in car painters compared to the control group (19.00 ± 7.20 vs. 8.339 ± 3.916 μg/L, <i>P</i>-value < 0.001). Serum levels of visfatin, MDA, insulin, FBG, and IL-1β were significantly higher in the car painter compared to the control (<i>P</i>-value < 0.001). There was a significantly higher proportion of people with diabetes in car painters compared to control (8.6% vs. 0%) and higher prediabetic (30.5% vs. 13.3%, <i>P</i>-value < 0.001). In car painter workers, levels of Hg were significantly higher in DM compared to prediabetic and normoglycemic car painter workers (27.01 ± 1.59, 23.98 ± 4.31, and 15.39 ± 6.41 μg/mL, respectively, <i>P</i>-value < 0.001); additionally, levels of Hg were significantly higher car painter with insulin resistance compared to non-insulin resistance workers (21.18 ± 7.29 vs. 16.79 ± 16.7 μg/mL, <i>P</i>-value < 0.001).</p><p><strong>Conclusions: </strong>Increased serum Hg in car painters increases the risk of insulin resistance and diabetes/prediabetes status.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae221"},"PeriodicalIF":2.2,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of circTLK1 improves the impairments in learning and memory induced by anesthetics via regulating miR-374b-5p expression and reducing neuroinflammation.","authors":"Xiaoli Zhu","doi":"10.1093/toxres/tfae220","DOIUrl":"10.1093/toxres/tfae220","url":null,"abstract":"<p><strong>Background: </strong>Sevoflurane (Sev) is a common anesthetic used during surgery, but research on its induction of neurotoxicity and learning memory impairment is insufficient. This study aimed to explore the role of Circular RNA tousled like kinase 1 (circTLK1) and its target microRNA (miR)-374b-5p in Sev-induced neurotoxicity and learning memory impairment.</p><p><strong>Methods: </strong>Mouse hippocampal neuronal HT22 cells and SD rats were treated with Sev. Levels of circTLK1 and miR-374b-5p were detected using RT-qPCR. The concentration of inflammatory factors was determined using ELISA. Cell viability and apoptosis were analyzed using CCK-8 and flow cytometry. Targeting relationship between circTLK1 and miR-374b-5p was validated using dual-luciferase reporter assays and RIP experiments. The Morris water maze test was used to assess the learning and spatial memory abilities of rats.</p><p><strong>Results: </strong>The results indicated that Sev treatment stimulated neuroinflammation and oxidative stress while increasing circTLK1 levels and decreasing miR-374b-5p levels in both rats and HT22 cells. Silencing circTLK1 alleviated the decrease in cell viability, increased apoptosis rates, and raised concentrations of inflammatory factors caused by Sev treatment. In in vivo experiments, silencing circTLK1 was also found to counteract the oxidative stress, neuroinflammation, and learning and memory impairment induced by Sev treatment in rats. Additionally, circTLK1 was shown to interact with miR-374b-5p, and inhibiting miR-374b-5p could counteract the neuroprotective effects of si-circTLK1.</p><p><strong>Conclusion: </strong>This research suggested that silencing circTLK1 can mitigate Sev-induced neurotoxicity and learning memory impairment by modulating miR-374b-5p.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae220"},"PeriodicalIF":2.2,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury by regulating miR-4454.","authors":"Jianxing Chen, Gaofeng Zhang, Aili Guo, Changliang Mou, Meiqing Du, Shuang Zhai, Mingshan Huang","doi":"10.1093/toxres/tfae219","DOIUrl":"10.1093/toxres/tfae219","url":null,"abstract":"<p><strong>Background: </strong>Sevoflurane (Sevo) prevents hypoxia/reoxygenation (H/R)-induced cardiomyocytes injury. The expression of miR-4,454 was increased in individuals experiencing an acute myocardial infarction.</p><p><strong>Objective: </strong>The purpose of current investigation was to delved into whether the effects of Sevo on cardiomyocytes are mediated through regulation of miR-4,454 expression.</p><p><strong>Method: </strong>In this study, the expression levels of miR-4,454 and BAG5 were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability was detected by cell counting kit-8 (CCK-8). The levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI) were detected by enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were detected using various commercially available kits to assess the level of oxidative stress in the cells. The luciferase reporter gene assay was used to verify the interaction of miR-4,454 with downstream target genes.</p><p><strong>Results: </strong>There was a notable upregulation of miR-4,454 expression in H/R-induced cardiomyocyte models. This was accompanied by a decrease in the viability of myocardial cells induced by H/R and an intensification of the extent of myocardial injury and oxidative stress. However, the detrimental effects were mitigated by the administration of Sevo. miR-4,454 had a target site for binding to BAG5, and its expression was negatively modulated by miR-4,454. An increase in the expression of BAG5 was shown to directly offset the exacerbation of cardiomyocyte damage induced by the overexpression of miR-4,454.</p><p><strong>Conclusion: </strong>Sevo may attenuate H/R-induced cardiomyocyte injury by regulating miR-4454.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae219"},"PeriodicalIF":2.2,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect of Auraptene, a novel acetylcholinesterase inhibitor, on hydrogen peroxide-induced cell toxicity in PC12 cells.","authors":"Elham Hadipour, Mahdi Khodadadi, Seyed Ahmad Emami, Samaneh Rahamouz Haghighi, Elham Ramazani, Zahra Tayarani-Najaran","doi":"10.1093/toxres/tfae217","DOIUrl":"10.1093/toxres/tfae217","url":null,"abstract":"<p><strong>Objective: </strong>Alzheimer's disease (ad) is a progressive and degenerative disorder of the central nervous system that is associated with cognitive and memory impairment. The main factors which have been implicated in neurodegeneration of ad are oxidative stress and cholinergic neurons dysfunction. Here, we examined the effects of auraptene, a novel acetylcholinesterase (AChE) inhibitor, on hydrogen peroxide (H₂O₂)-induced cell death in PC12 cells.</p><p><strong>Methods: </strong>Thereby, we measured cell viability, intracellular reactive oxygen species (ROS) production, AChE inhibitory activity, cell damage and apoptosis with AlmarBlue, 2', 7'-dichlorodihydrofluorescein diacetate (DCFH-DA), Ellman method, lactate dehydrogenase (LDH) release, propidium iodide (PI) staining and western blot analysis, respectively.</p><p><strong>Results: </strong>H₂O₂ (150 μM) resulted in the cell death and apoptosis while, pretreatment with auraptene (10, 20 and 50 μM) significantly increased the viability (<i>P</i> < 0.01), and at 5-50 μM decreased ROS amount (<i>P</i> < 0.05 and <i>P</i> < 0.001). Pretreatment with auraptene (10, 20 and 50 μM) lessened AChE activity (<i>P</i> < 0.001), and at 20 and 50 μM reduced the release of LDH (<i>P</i> < 0.001), and at (10, 20 and 50 μM) diminished the percentage of apoptotic cells (<i>P</i> < 0.001). Also, pretreatment with auraptene at 10,20 and 50 μM prevented from poly (ADP-ribose) polymerase (PARP) cleavage (<i>P</i> < 0.001), and cytochrome c release (<i>P</i> < 0.01 and <i>P</i> < 0.001). The amount of caspase 3 activity (<i>P</i> < 0.001) and survivin (<i>P</i> < 0.001) were elevated after pretreatment of cells with auraptene at 10-50 μM and 10 and 50 μM.</p><p><strong>Conclusion: </strong>It seems that auraptene has the ability to slow down or stop H₂O₂-induced nerve cells death by reducing the activity of AChE and suppression of internal pathway of apoptosis.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae217"},"PeriodicalIF":2.2,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoxanthin alleviates the cytotoxic effects of cadmium and lead on a human osteoblast cell line.","authors":"Ekramy M Elmorsy, Ayat B Al-Ghafari, Huda A Al Doghaither","doi":"10.1093/toxres/tfae218","DOIUrl":"10.1093/toxres/tfae218","url":null,"abstract":"<p><strong>Objective: </strong>Cadmium (Cd) and lead (Pb) are non-biodegradable heavy metals (HMs) that persistently contaminate ecosystems and accumulate in bones, where they exert harmful effects. This study aimed to investigate the protective effect of fucoxanthin (FX) against the chemical toxicity induced by Cd and Pb in human bone osteoblasts in vitro, using various biochemical and molecular assays.</p><p><strong>Methods: </strong>The effect of metals and FX on osteoblasts viability was assayed by MTT, then the effect of Pb, Cd, and FX on the cells' mitochondrial parameters was studied via assays for ATP, mitochondrial membrane potential (MMP), mitochondrial complexes, and lactate production. Also, the effect of metals on oxidative stress was assessed by reactive oxygen species, lipid peroxidation and antioxidant enzymes assays. Also the effect of FX and metals on apoptosis caspases and related genes was assessed.</p><p><strong>Results: </strong>When Cd and Pb were added to human osteoblast cultures at concentrations ranging from 1-20 μM for 72 h, they significantly reduced osteoblast viability in a time and concentration-dependent manner. The cytotoxic effect of Cd on osteoblasts was greater than that of Pb, with estimated EC50 of 8 and 12 μM, respectively, after 72 h of exposure. FX (10 and 20 μM) alleviated the cytotoxicity of the metals. Bioenergetics assays, including ATP, MMP, and mitochondrial complexes I and III activities, revealed that HMs at 1 and 10 μM concentrations inhibited cellular bioenergetics after 72 h of exposure. Cd and Pb also increased lipid peroxidation and reactive oxygen species while reducing catalase and superoxide dismutase antioxidant activities and oxidative stress-related genes. This was accompanied by increased caspases -3, -8, and - 9 and Bax/bCl-2 ratio. Co-treatment with FX (10 and 20 μM) mitigated the disruption of bioenergetics, oxidative damage, and apoptosis induced by the metals, showing a concentration-dependent pattern to varying extents.</p><p><strong>Conclusion: </strong>These findings strongly support the role of FX in managing toxicities induced by environmental pollutants in bones and in addressing bone diseases associated with molecular bases of oxidative stress, apoptosis, and bioenergetic disruption.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae218"},"PeriodicalIF":2.2,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11655842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142875619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of quercetin against tongue injury and oxidative stress triggered by irinotecan: a histopathological, biochemical and molecular study.","authors":"Eman Mohamed Faruk, Fatma Ibrahim, Mahmoud M Hassan, Kamal M Kamal, Dina Allam Abdelmaksoud Hassan, Ayat Abu-Elnasr Awwad, Neama Mahmoud Taha, Mohamed Ghazy Attia Hablas, Ahmed Mohammed Zaazaa, Mai Hassan Ibrahim","doi":"10.1093/toxres/tfae214","DOIUrl":"https://doi.org/10.1093/toxres/tfae214","url":null,"abstract":"<p><strong>Introduction: </strong>About 80% of patients receiving chemotherapeutics suffer from side effects related to the gastrointestinal tract. Irinotecan (CPT-11) is a chemotherapeutic agent usually used in treating solid tumors. Quercetin (QRT), a bioflavonoid, is an antioxidant and scavenger reactive oxygen species scavenger.</p><p><strong>Objective: </strong>The current study explored the possible protective effects of QRT against mucosal tongue injury caused by CPT-11.</p><p><strong>Methods: </strong>The study included four equal groups: group 1/control, group 2/QRT, group 3/CPT-11, and group 4/CPT-11 + QRT.</p><p><strong>Results: </strong>CPT-11-induced tongue injury in the form of non-healed ulcers, absent lingual papillae, mononuclear cells infiltration, marked deposition of collagen fibers, and overexpression of CD86 and tumor necrosis factor- α (TNF-α). The increased malondialdehyde levels, decreased superoxide dismutase and total antioxidant capacity revealed that there was an oxidative stress. Also, there was a decreased countenance of Ki-67 and Bcl-2 and an increased countenance of NF-κB. The QRT-treated group showed complete ulcer healing, with histological features almost like the control group, along with minimal collagen fiber deposition, decreased reactivity to CD86 and TNF-α and improvement of oxidative stress status and the molecular study results as well.</p><p><strong>Conclusion: </strong>QRT possess protective properties against CPT-11-triggered tongue injury.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae214"},"PeriodicalIF":2.2,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Determination of pesticide residues in bee honey and pollen grains with their potential human health risks in the Nile Delta, Egypt.","authors":"Asmaa El-Metwally Abd-Alla, Rasha Adel Salem, Abdulraouf Mohamed Amro","doi":"10.1093/toxres/tfae215","DOIUrl":"https://doi.org/10.1093/toxres/tfae215","url":null,"abstract":"<p><p>A growing trend in understanding human health involves looking at the bigger picture by examining all potential environmental exposures that may cause health risks, with a particular focus on dietary intake of anthropogenic chemicals. This study investigated the presence of pesticide residues in honey and pollen samples collected randomly from ten locations in four agricultural governorates during the spring season of 2023 in the Nile Delta, Egypt. A QuEChERS extraction was employed for sample preparation before GC-MS analysis for pesticide residues. The human health risk associated with these residues were evaluated using hazard quotient (HQ). Our findings indicate that the detection rate and levels of pesticide residues are greater than previously reported. Giza governorate exhibited the highest content of residues in both honey and pollen samples, followed by El-Dakahlia, El-Qalyubia and Gharbia. Also, honey samples from El-Dakahlia, El-Qalyubia, and Giza contained the highest concentrations of aldrin, hexachlorocyclohexane (HCH) and chlorpyrifos, ranging from 10.45 to 19.6 μg kg ^<b>-1</b> , 21.70 to 62.23 μg kg ^<b>-1</b> , and 167.55 to 190.74 μg kg ^<b>-1</b> , respectively. Pollen grain samples from Giza and El-Dakahlia showed high levels of chlorpyrifos (76.20 μg kg ^<b>-1</b> ) and HCH (33.60 μg kg ^<b>-1</b> ), respectively. Health hazard and quotient studies indicate that the residue levels of pesticides in all tested honey did not pose a significant risk for human consumption. Out of all pesticides, aldrin is the only one that requires further risk assessment to determine its potential impact on honeybee colonies.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae215"},"PeriodicalIF":2.2,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemical Alterations and Motor Dysfunctions in Corpus Striatum of Rats Brain Exposed to Azo Dyes.","authors":"Pronit Biswas, Juli Jain, Whidul Hasan, Devasish Bose, Rajesh Singh Yadav","doi":"10.1093/toxres/tfae216","DOIUrl":"https://doi.org/10.1093/toxres/tfae216","url":null,"abstract":"<p><p>Azo food dyes are prohibited in most countries, but their injudicious use is still reported particularly in the developing Nations. Continuous use of contaminated food raises health concerns and given this the present study designed to investigate the effects of 3 non-permitted azo dyes (metanil yellow - MY, malachite green - MG, and sudan III - SIII) on neurobehavioral, neurochemicals, mitochondrial dysfunction, oxidative stress, and histopathological changes in the corpus striatum of rats. Rats were grouped and treated with MY (430 mg/kg), MG (13.75 mg/kg), SIII (250 mg/kg) & mixture (YGR) (MY 143.33 + MG 4.52 + SIII 83.33 mg/kg) p.o. for 60 days showed a significant decrease in grip strength and motor activity, the activity of acetylcholinesterase (AChE), monoamine oxidase - B (MAO-B), and mitochondrial complex I and II compared to the control. The treated groups showed a significant increase in lipid peroxidation and a decrease in the level of reduced glutathione, superoxide dismutase, and catalase as compared to the control. Histopathology of the corpus striatum revealed immense damage. Data from the present study correlate between azo dyes and changes in the behavior of rats which have been associated with the altered biochemicals and neurochemicals activities. In conclusion, exposure to azo dyes caused neurotoxicity involving motor impairments associated with enhanced oxidative stress, mitochondrial dysfunctions, AChE and MAO-B inhibition, and neuronal damage in the corpus striatum of rats.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 6","pages":"tfae216"},"PeriodicalIF":2.2,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11652610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142862615","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}