Human & experimental toxicology最新文献_第3页

Protocatechuic acid mitigates 5-fluorouracil-triggered renal and hepatic injury in rats. 原儿茶酸减轻5-氟尿嘧啶引起的大鼠肾和肝损伤。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-04-14 DOI: 10.1177/09603271251332914

Alhomedy M Alharbi, Hoda E Kafl, Rania R Abdelaziz, Ghada M Suddek

{"title":"Protocatechuic acid mitigates 5-fluorouracil-triggered renal and hepatic injury in rats.","authors":"Alhomedy M Alharbi, Hoda E Kafl, Rania R Abdelaziz, Ghada M Suddek","doi":"10.1177/09603271251332914","DOIUrl":"https://doi.org/10.1177/09603271251332914","url":null,"abstract":"IntroductionNephrotoxicity and hepatotoxicity are substantial side effects triggered in individuals injected with 5-fluorouracil (5-FU), an anticancer drug. This study aimed to investigate the impact of the natural antioxidant and anti-inflammatory phenolic compound; protocatechuic acid (PCA) on 5-FU-provoked renal and hepatic injury in rats.MethodsRats were allocated to 4 groups: control, 5-FU, 5-FU + PCA (50 mg/kg), and 5-FU + PCA (100 mg/kg). Rats were intraperitoneally injected 5-FU (75 mg/kg; once a week for 21 days. Protocatechuic acid (50 and 100 mg/kg/day; orally) was administered for 3 weeks.ResultsRats co-treated with PCA had lower serum kidney and liver function markers than those receiving 5-FU alone. Furthermore, co-treatment with PCA successfully modulated kidney and liver contents of TNF-α, NF-κB p65, active caspase-1, IL-1β, p-p38 MAPK, SOD, GSH, Nrf-2, HO-1 and MDA. Moreover, PCA improved histopathological alterations of both kidney and liver tissues.ConclusionPCA exerts its hepatoprotective and nephroprotective effects against 5-FU-triggered toxicity through modulation of oxidative stress and inflammatory pathways, particularly via Nrf-2 activation and NF-κB inhibition.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251332914"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144034989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanism of triiodothyronine alleviating acute alcoholic liver injury and delaying alcoholic liver fibrosis progression. 三碘甲状腺原氨酸减轻急性酒精性肝损伤和延缓酒精性肝纤维化进展的机制。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-04-02 DOI: 10.1177/09603271251332505

Renli Luo, Sanqiang Li, Mengli Yang, Junfei Wu, Jiayang Feng, Yue Sun, Yadi Zhao, Longfei Mao

{"title":"Mechanism of triiodothyronine alleviating acute alcoholic liver injury and delaying alcoholic liver fibrosis progression.","authors":"Renli Luo, Sanqiang Li, Mengli Yang, Junfei Wu, Jiayang Feng, Yue Sun, Yadi Zhao, Longfei Mao","doi":"10.1177/09603271251332505","DOIUrl":"10.1177/09603271251332505","url":null,"abstract":"IntroductionAlcoholic liver disease poses a severe threat to human health. The thyroid hormone Triiodothyronine (T3) is closely related to liver metabolism. This study investigated the effect and mechanism of T3 in alcoholic liver injury.MethodsAcute alcoholic liver injury model was established in mice by alcohol administration. Alcoholic liver fibrosis models were established in vivo and in vitro using hepatic stellate cells (HSC)-T6 cells and mice. The role and regulatory mechanism of T3 in the occurrence and progression of alcoholic acute liver injury and fibrosis were analyzed by evaluating key factors involved in cell proliferation and apoptosis, inflammatory response, oxidative stress, and autophagy using histopathological staining.ResultsThe results showed that T3 at low and medium concentrations reduced inflammation and oxidative damage in acute alcoholic liver injury and inhibited HSC activation and delayed the onset and progression of alcoholic liver fibrosis in mice. T3 inhibited the PI3K/AKT and NF-κB signal pathway, increased Nrf2 expression levels, and restored liver autophagy. However, high T3 concentrations had the opposite effect.DiscussionOptimal T3 concentrations protects the liver from alcoholic liver injury by inhibiting inflammatory response and oxidative stress injury and by restoring hepatocyte proliferation, apoptosis, and autophagy.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251332505"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pedunculoside inhibits cardiomyocyte inflammatory biomarkers via Nrf2/HO-1 pathway in high glucose-induced H9c2 cells and diabetic cardiomyopathy model rats. 在高糖诱导的H9c2细胞和糖尿病性心肌病模型大鼠中，足跖草苷通过Nrf2/HO-1途径抑制心肌细胞炎症生物标志物。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-03-11 DOI: 10.1177/09603271251322186

Yuanben Lu, Jianqiang Meng, Dewen Zhu, Zhenhua Jiang, Hailiang Ma

{"title":"Pedunculoside inhibits cardiomyocyte inflammatory biomarkers via Nrf2/HO-1 pathway in high glucose-induced H9c2 cells and diabetic cardiomyopathy model rats.","authors":"Yuanben Lu, Jianqiang Meng, Dewen Zhu, Zhenhua Jiang, Hailiang Ma","doi":"10.1177/09603271251322186","DOIUrl":"10.1177/09603271251322186","url":null,"abstract":"IntroductionDiabetic cardiomyopathy (DCM) is a complication of diabetes mellitus (DM) that can lead to heart failure and increase the risk of mortality. Pedunculoside (PE), a novel triterpenoid saponin, exhibits anti-inflammatory and anti-oxidative stress (OS) properties. However, its role in DCM remains unexplored.MethodsDCM models were established and treated with PE or the Nrf2 inhibitor (ML385). In vitro, cell function was evaluated using CCK-8, flow cytometry, qRT-PCR, and ELISA. In vivo, fasting blood glucose and insulin levels in rats were measured. The effects of PE on DCM were assessed using HE staining, TUNEL staining, and corresponding kits. Additionally, Nrf2/HO-1 pathway proteins were analyzed by western blot.ResultsLow doses of PE (2.5, 5, 10, and 20 μM) did not affect the viability of H9c2 cells. PE (10 and 20 μM) improved cell viability and prevented apoptosis, inflammation, and OS in high glucose (HG)-stimulated H9c2 cells. PE also upregulated Nrf2 in the nucleus and enhanced HO-1 and NQO1 expression in HG-treated H9c2 cells. Furthermore, the Nrf2 inhibitor (ML385) reversed PE's protective effects on HG-induced cell injury. In vivo, PE reduced blood glucose, increased insulin, alleviated myocardial injury, inhibited apoptosis, decreased levels of inflammatory factors and OS, and upregulated Nrf2, HO-1, and NQO1 in DCM model rats.DiscussionPE alleviates DCM injury by activating the Nrf2/HO-1 pathway. These findings support the potential therapeutic application of PE in DCM.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251322186"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143606777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNF216 inhibits ferroptosis in lung adenocarcinoma by promoting p53 ubiquitination. RNF216通过促进p53泛素化抑制肺腺癌铁下垂。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-06-12 DOI: 10.1177/09603271251336793

Jiasheng Wu, Weiqiang Mo, Haiqin Wang, Jianping Jiang, Jing Zhao

{"title":"RNF216 inhibits ferroptosis in lung adenocarcinoma by promoting p53 ubiquitination.","authors":"Jiasheng Wu, Weiqiang Mo, Haiqin Wang, Jianping Jiang, Jing Zhao","doi":"10.1177/09603271251336793","DOIUrl":"https://doi.org/10.1177/09603271251336793","url":null,"abstract":"PurposeLung adenocarcinoma (LUAD) is the most prevalent subtype of non-small cell lung cancer and a leading cause of cancer-related mortality worldwide. This study investigates the role of Ring Finger Protein 216 (RNF216) in LUAD progression.MethodsRNF216 expression was evaluated in LUAD tissues and cells. Functional assays evaluated cell viability, migration, invasion, and ferroptosis in vitro. Mechanistic investigations defined RNF216's role in regulating p53 ubiquitination and stability. In vivo, xenograft models evaluated tumor growth and ferroptosis.ResultsRNF216 was markedly overexpressed in LUAD tissues and cell lines. Functional studies demonstrated that silencing RNF216 suppressed LUAD cell proliferation, migration, and invasion while inducing ferroptosis, characterized by increased reactive oxygen species (ROS), lipid peroxidation (LPO), and intracellular Fe2+ accumulation. Mechanistically, RNF216 knockdown stabilized p53 by reducing its ubiquitination, thereby promoting ferroptosis. These findings were corroborated in vivo, where RNF216 silencing significantly inhibited tumor growth and enhanced ferroptosis in xenograft models.ConclusionsOur results establish RNF216 as a pivotal oncogenic driver that accelerates LUAD progression by suppressing ferroptosis through p53 ubiquitination. Targeting RNF216 may represent a promising therapeutic strategy to induce ferroptosis and combat LUAD.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251336793"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144287651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuroinflammatory chemokine networks in transgenic models of Alzheimer's disease: A comparative multi-compartmental analysis. 阿尔茨海默病转基因模型中的神经炎症趋化因子网络：一项比较多室分析。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-06-05 DOI: 10.1177/09603271251348723

Yangyan Sun, Xinhua Xie, Xiaoqin Zou, Futao Zhou

{"title":"Neuroinflammatory chemokine networks in transgenic models of Alzheimer's disease: A comparative multi-compartmental analysis.","authors":"Yangyan Sun, Xinhua Xie, Xiaoqin Zou, Futao Zhou","doi":"10.1177/09603271251348723","DOIUrl":"https://doi.org/10.1177/09603271251348723","url":null,"abstract":"BackgroundAlzheimer's disease (AD) progression is critically modulated by neuroinflammatory cascades involving chemokine-mediated glial activation.ObjectiveThis study aimed to systematically compare compartment-specific chemokine signatures between two distinct AD mouse models (2×Tg-AD [APPswe/PS1dE9] and 3×Tg-AD [APPswe/PS1M146V/TauP301L]), hypothesizing that differential chemokine expression patterns would emerge in a model- and brain region-specific manner, correlating with glial activation profiles.ResultsUsing a Luminex liquid suspension chip assay, we quantified 22 chemokines in serum and brain tissues from transgenic and non-transgenic controls, complemented by Western blot analysis of microglial and astrocytic markers. Twenty-two chemokines were quantitatively analyzed with three key findings: First, serum analysis revealed elevated levels of (i) CCL11, CCL17, CCL24, CCL27, and CXCL12 in 3×Tg-AD versus non-Tg mice; (ii) CCL22 in 2×Tg-AD versus non-Tg mice; and (iii) CCL5, CCL11, CCL17, CCL24, CCL27, and CXCL12 in 3×Tg-AD versus 2×Tg-AD mice. Second, hippocampal changes showed upregulation of CCL3/CCL12 in 2×Tg-AD and CXCL16 in 3×Tg-AD mice, with cortical alterations demonstrating distinct CCL3/CCL12/CCL4 increases in 2×Tg-AD versus elevated CCL1/CXCL13 in 3×Tg-AD mice. Third, Western blot confirmed enhanced hippocampal microglial activation specifically in 3×Tg-AD mice. ConclusionOur findings establish model-specific chemokine signatures that differentially engage neuroinflammatory pathways, suggesting that 3×Tg-AD mice may better replicate human AD's complex chemokine-glia interactions. This compartmentalized profiling provides a framework for targeting chemokine networks in model-specific therapeutic development and biomarker discovery. Further studies are needed to determine whether elevated chemokine expression directly contributes to microglial activation.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251348723"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144236286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rhynchophylline promotes microglia phenotypic transformation and repair of cerebral ischaemic injury through the JAK2/STAT3 pathway. 黄连素通过 JAK2/STAT3 通路促进小胶质细胞表型转化和脑缺血损伤的修复。

Human & experimental toxicology Pub Date : 2025-01-01 DOI: 10.1177/09603271251324582

Peng Bai, Caixia Li, Luwei Yin, Yao Li, Meng Ju, Laicang Wang

{"title":"Rhynchophylline promotes microglia phenotypic transformation and repair of cerebral ischaemic injury through the JAK2/STAT3 pathway.","authors":"Peng Bai, Caixia Li, Luwei Yin, Yao Li, Meng Ju, Laicang Wang","doi":"10.1177/09603271251324582","DOIUrl":"10.1177/09603271251324582","url":null,"abstract":"Background: Rhynchophylline (RIN) is an alkaloid known for its ability to effectively block signal transduction related to various neurodegenerative diseases. However, the specific mechanism by which RIN regulates microglial activation and cerebral ischemia remains unexplored. This study aims to investigate the function and molecular pathways through which RIN activates the JAK2/STAT3 signaling cascade, promoting the transformation of microglial phenotypes that contribute to recovery from cerebral ischemic injury.Methods: By establishing a microglia oxygen glucose deprivation/reoxygenation (OGD/R) model and a middle cerebral artery occlusion animal model, we assessed changes in the expression of phenotype-specific marker factors for M1 and M2 microglia, as well as key proteins in the JAK2/STAT3 pathway, utilizing ELISA and Western blot techniques. Histological examination, including HE staining, TUNEL assay, and immunofluorescence, was employed to evaluate pathological changes in brain tissue, along with cell apoptosis and proliferation.Results: The results indicated that microglial activity was significantly reduced and shifted towards the M1 phenotype following OGD/R. However, RIN treatment reversed these changes. When JAK2/STAT3 inhibitors were combined with RIN, it inhibited RIN's protective effect. Animal studies have shown that RIN reduces histopathological changes associated with cerebral ischemia. Additionally, RIN inhibited microglial proliferation in ischemic cortical tissue and increased the expression of M2-type marker proteins, as well as the levels of phosphorylated JAK2 and STAT3 in the ischemic tissue.Conclusion: In conclusion, this study indicates that RIN may protect against cerebral ischemic injury by activating the JAK2/STAT3 pathway, which promotes the transition of microglia to the M2 phenotypic.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251324582"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

KLF9 mediates NLRP3 inflammasome and reactive oxygen species to mediate pyroptosis in trophoblasts. KLF9介导NLRP3炎性体和活性氧介导滋养细胞焦亡。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-03-11 DOI: 10.1177/09603271251324702

Qian Li, Min Chen

{"title":"KLF9 mediates NLRP3 inflammasome and reactive oxygen species to mediate pyroptosis in trophoblasts.","authors":"Qian Li, Min Chen","doi":"10.1177/09603271251324702","DOIUrl":"10.1177/09603271251324702","url":null,"abstract":"IntroductionThe objective of this study was to explore the effect of KLF9 on oxidative stress (OS) and NLRP3-mediated inflammation in preeclampsia (PE).MethodsLipopolysaccharide (LPS)+adenosine triphosphate (ATP)-induced HTR-8/SVneo cells were used as an in vitro PE inflammation cell model. shRNA was used to interfere with KLF9 expression (sh-KLF9) to assess the transfection efficiency and the effect of KLF9 on cell proliferation, migration, and invasion. ELISA was performed to detect OS-related factors and inflammatory cytokines. Reactive oxygen species (ROS) levels and pyroptosis were analyzed using DCFH-DA and TUNEL staining. LPS and ATP induced HTR-8/SVneo cells were co-transfected with sh-PRDX6/sh-KLF9 to explore the potential regulatory effect of KLF9 on PRDX6.ResultsLPS+ATP stimulation increased KLF9 expression in the PE cell model. Specifically, reducing KLF9 levels alleviated morphological damage and enhanced proliferation, migration, and invasion in the in vitro PE cell models. Moreover, inhibiting KLF9 expression decreased protein expression of NLRP3, GSDMD-N, cleaved caspase-1, and cleaved-IL-1β, suppressing cell death in LPS+ATP-induced HTR-8/SVneo cells. Analysis of OS indicators revealed that downregulating KLF9 expression restrained intracellular ROS production, decreased MDA expression, and increased SOD and CAT levels. KLF9 regulated the transcription of PRDX6 to attenuate OS and pyroptosis. Knockdown of PRDX6 partially abolished the effect of KLF9 downregulation on OS and pyroptosis of LPS+ATP-induced HTR-8/SVneo cells, as evidenced by the inhibition of cell proliferation, migration, and invasion, as well as the enhanced activity of the NLRP3 inflammasome.ConclusionDownregulation of KLF9 enhances trophoblast cell invasion and reduces OS and NLRP3 inflammasome activation-mediated pyroptosis.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251324702"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143606773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The safety assessment of N-trans-feruloyltyramine using In vitro genotoxicity studies and 90-day toxicity study in rats. 用体外遗传毒性研究和大鼠90天毒性研究评价n -反式阿魏乙胺的安全性。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-04-18 DOI: 10.1177/09603271251334452

Sungwon Lee, Srinivas Seekallu, Suresh Babu Venkataramaiah, Chandrashekar Mataguru Doreswamy, Mohan Cheluru Umesh, Sandeep Malleshappa, Sajeev Justin Dev, Ganadhal Puttaramaiah Chethankumara, Nagaraju Lohith, Gajanan Rajpal Deshmukh, Brian Premkumar, Brinda Mahadevan

{"title":"The safety assessment of N-trans-feruloyltyramine using In vitro genotoxicity studies and 90-day toxicity study in rats.","authors":"Sungwon Lee, Srinivas Seekallu, Suresh Babu Venkataramaiah, Chandrashekar Mataguru Doreswamy, Mohan Cheluru Umesh, Sandeep Malleshappa, Sajeev Justin Dev, Ganadhal Puttaramaiah Chethankumara, Nagaraju Lohith, Gajanan Rajpal Deshmukh, Brian Premkumar, Brinda Mahadevan","doi":"10.1177/09603271251334452","DOIUrl":"https://doi.org/10.1177/09603271251334452","url":null,"abstract":"IntroductionN-trans-feruloyltyramine (NFT) is a bioactive compound present in many plant sources. The purpose of the studies was to investigate adverse effects, if any, of NFT produced through precision fermentation.MethodsAn in vitro Ames test was performed with NFT using bacterial strains at concentrations up to 1580 µg/plate with and without S9. The in vitro micronucleus assay was performed in human peripheral blood cells in culture, with and without, metabolic activation at three different doses. In the subchronic toxicity study, adult Sprague Dawley rats (10/sex/group) were fed diets prepared with target doses of 0, 5000, 10,000 or 20,000 ppm of NFT for 90 days.ResultsIn the Ames assay, there were no NFT-related or concentration dependent increases in revertant colony numbers in any of the tester strains. In the in vitro micronucleus assay, there was no statistically significant increase in the number of binucleated cells with micronuclei compared to the vehicle control. NFT was found to be non-genotoxic when evaluated in the in vitro Ames and micronucleus assays. In the 90-day rodent study, NFT was well tolerated, with no related adverse findings observed at any of the dose levels tested. There were no NFT related adverse histopathological changes observed in the high dose group of both the sexes.ConclusionThe No observed adverse effect level of NFT was determined as 1474 mg/kg body weight/day in males and 1958 mg/kg body weight/day in females based on the actual intake at the dose levels tested and under the experimental conditions employed.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251334452"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144045203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "Effect of grape seed extract ondoxorubicin-induced testicular andepididymal damage in rats". “葡萄籽提取物对多柔比星诱导的大鼠睾丸和附睾损伤的影响”的更正。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-05-08 DOI: 10.1177/09603271251341390

引用次数: 0

Human health risk assessment of heavy metals in different compartments of vegetables from Erbil City-Iraq. 伊拉克埃尔比勒市不同蔬菜中重金属的人体健康风险评估。

Human & experimental toxicology Pub Date : 2025-01-01 Epub Date: 2025-06-17 DOI: 10.1177/09603271251351421

Bashdar Abuzed Sadee

{"title":"Human health risk assessment of heavy metals in different compartments of vegetables from Erbil City-Iraq.","authors":"Bashdar Abuzed Sadee","doi":"10.1177/09603271251351421","DOIUrl":"https://doi.org/10.1177/09603271251351421","url":null,"abstract":"IntroductionThe consumption of vegetables is a key route for increasing the content of potentially toxic heavy metals in the food chain. This article aimed to quantify the concentrations of As, Se, Cd, Cr, Co, Cu, Ni, and Pb in different parts of vegetables harvested from Erbil city.MethodologyThe total concentrations of As, Cd, Cr, Co, Cu, Ni, and Pb in various vegetable parts were pursued by ICP-MS analysis.ResultsThe values of heavy metals in different parts of the analyzed vegetables ranged from 0.052 to 2.106 mg/kg for As, 0.024 to 5.899 mg/kg for Se, 0.014 to 0.753 mg/kg for Cd, 0.441 to 89.400 mg/kg for Cr, 0.052 to 2.693 mg/kg for Co, 0.737 to 39.120 mg/kg for Cu, 0.301 to 63.880 mg/kg for Ni, and 0.032 to 1.782 mg/kg for Pb. The Hazard Quotient (HQ) values for As, Cr, Cu, and Ni in the edible parts of most vegetables exceeded one, while those for Se, Co, Cd, and Pb were below one.DiscussionIn contrast to Se, Co, Cd, and Pb, the HQ values for As, Cr, and Pb indicate a potential health risk when consuming these edible parts of the vegetables. The Hazard Index (HI) for all edible parts of the analyzed vegetable samples exceeded one. The cancer risk (CR) of As, Cd, Cr and Ni were higher than 1.0 × 10-4 which indicating carcinogenic risk. As a result, regular consumption of these vegetables is regarded as unsafe and not advisable.","PeriodicalId":94029,"journal":{"name":"Human & experimental toxicology","volume":"44 ","pages":"9603271251351421"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0