Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115208
Adrian Frydrych , Kamil Jurowski
Elemental analysis of solid candy and wrapper samples from Polish flea markets was conducted using portable X-ray fluorescence (pXRF), a fast, cost-effective, and non-destructive technique. Hazardous elements were detected in candies, including Ni (5.20 ± 0.56 μg/g), Fe (17.28 ± 1.03 μg/g), Ba (41.23 ± 7.10 μg/g), Cr (9.63 ± 2.30 μg/g), Cd (0.56 ± 0.33 μg/g), and Cu (7.30 ± 1.15 μg/g), while wrappers contained high levels of Ti (13073.31 ± 106.80 μg/g), Sb (158.29 ± 5.28 μg/g), and Ba (2081.01 ± 36.42 μg/g). Health risk assessments showed Ni and Cd exceeding acceptable limits, posing risks for children consuming three candies daily. Non-carcinogenic risks from Ba and Cd also surpassed provisional tolerable weekly intake (PTWI) values. Minimal migration between wrappers and candies was observed, but extreme conditions may increase contamination. The study highlights the need for stricter food safety regulations and adoption of pXRF for rapid, non-invasive detection of hazardous elements.
{"title":"Direct, rapid, non-destructive and ‘white’ multielemental toxicological analysis of hazardous elements with health risk assessment in candies and wrappers from Polish flea markets using portable XRF spectroscopy","authors":"Adrian Frydrych , Kamil Jurowski","doi":"10.1016/j.fct.2024.115208","DOIUrl":"10.1016/j.fct.2024.115208","url":null,"abstract":"<div><div>Elemental analysis of solid candy and wrapper samples from Polish flea markets was conducted using portable X-ray fluorescence (pXRF), a fast, cost-effective, and non-destructive technique. Hazardous elements were detected in candies, including Ni (5.20 ± 0.56 μg/g), Fe (17.28 ± 1.03 μg/g), Ba (41.23 ± 7.10 μg/g), Cr (9.63 ± 2.30 μg/g), Cd (0.56 ± 0.33 μg/g), and Cu (7.30 ± 1.15 μg/g), while wrappers contained high levels of Ti (13073.31 ± 106.80 μg/g), Sb (158.29 ± 5.28 μg/g), and Ba (2081.01 ± 36.42 μg/g). Health risk assessments showed Ni and Cd exceeding acceptable limits, posing risks for children consuming three candies daily. Non-carcinogenic risks from Ba and Cd also surpassed provisional tolerable weekly intake (PTWI) values. Minimal migration between wrappers and candies was observed, but extreme conditions may increase contamination. The study highlights the need for stricter food safety regulations and adoption of pXRF for rapid, non-invasive detection of hazardous elements.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115208"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142870799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115200
Yuming Kuang , Zuoyao Wu , Yuqin Liu
Deoxynivalenol (DON), a Fusarium mycotoxin, causes spleen apoptosis and inflammation, which damage the organ. Curcumin (Cur) is a member of the ginger family. It has anti-apoptotic and anti-inflammatory effects that maintain the health of the organism's immune system. Here, the protective effects of Cur against DON-induced spleen damage were explored. First, we found DON (2.4 mg/kg body weight) decreased the expression of manganese superoxide dismutase, mitochondrial membrane potential, adenosine triphosphate, and disturbed hematoxylin and eosin staining in mice spleen. The results confirmed that DON causes mitochondrial reactive oxygen species (mtROS) overproduction leading to spleen damage. Second, we found DON decreased the expression of mitochondrial apoptosis-inducing factor (AIF) and B-cell lymphoma-2 (Bcl-2), and increased the expression of nuclear AIF, Bcl2-associated X (Bax), cysteine-aspartate protease-3 (caspase-3), caspase-9. Mitoquinone is a mitochondria-targeted antioxidant that can prevent of mitochondrial oxidative damage. These expression increases were not observed in the mitoquinone-treated group, confirming that mtROS was an upstream regulatory target of apoptosis and inflammation in DON-exposed mice spleens. Finally, we confirmed that Cur (50 or 100 mg/kg body weight) attenuated DON-induced apoptosis and inflammation by inactivating mtROS. Collectively, these results confirm that DON causes spleen damage by increasing mtROS, and the protective effects of curcumin.
脱氧雪腐镰刀菌烯醇（DON）是一种镰刀菌霉菌毒素，会导致脾脏凋亡和炎症，从而损害器官。姜黄素（Cur）是姜科植物。它具有抗凋亡和抗炎作用，能维持机体免疫系统的健康。在此，我们探讨了姜黄素对 DON 诱导的脾脏损伤的保护作用。首先，我们发现 DON（2.4 毫克/千克体重）会降低小鼠脾脏中超氧化物歧化酶锰、线粒体膜电位、三磷酸腺苷的表达，并干扰苏木精和伊红染色。结果证实，DON 会导致线粒体活性氧（mtROS）过度产生，从而导致脾脏损伤。其次，我们发现DON降低了线粒体凋亡诱导因子（AIF）和B细胞淋巴瘤-2（Bcl-2）的表达，增加了核AIF、Bcl2相关X（Bax）、半胱氨酸-天门冬氨酸蛋白酶-3（caspase-3）、caspase-9的表达。线醌是一种线粒体靶向抗氧化剂，可防止线粒体氧化损伤。这些表达的增加在线粒体醌处理组中没有观察到，证实了mtROS是DON暴露小鼠脾脏中细胞凋亡和炎症的上游调控靶点。最后，我们证实 Cur（50 或 100 毫克/千克体重）通过使 mtROS 失活而减轻了 DON 诱导的细胞凋亡和炎症。总之，这些结果证实了 DON 通过增加 mtROS 导致脾脏损伤，以及姜黄素的保护作用。
{"title":"Deoxynivalenol induces spleen damage, apoptosis, and inflammation in mice by increasing mitochondrial reactive oxygen species: Protective effects of curcumin","authors":"Yuming Kuang , Zuoyao Wu , Yuqin Liu","doi":"10.1016/j.fct.2024.115200","DOIUrl":"10.1016/j.fct.2024.115200","url":null,"abstract":"<div><div>Deoxynivalenol (DON), a <em>Fusarium</em> mycotoxin, causes spleen apoptosis and inflammation, which damage the organ. Curcumin (Cur) is a member of the ginger family. It has anti-apoptotic and anti-inflammatory effects that maintain the health of the organism's immune system. Here, the protective effects of Cur against DON-induced spleen damage were explored. First, we found DON (2.4 mg/kg body weight) decreased the expression of manganese superoxide dismutase, mitochondrial membrane potential, adenosine triphosphate, and disturbed hematoxylin and eosin staining in mice spleen. The results confirmed that DON causes mitochondrial reactive oxygen species (mtROS) overproduction leading to spleen damage. Second, we found DON decreased the expression of mitochondrial apoptosis-inducing factor (AIF) and B-cell lymphoma-2 (Bcl-2), and increased the expression of nuclear AIF, Bcl2-associated X (Bax), cysteine-aspartate protease-3 (caspase-3), caspase-9. Mitoquinone is a mitochondria-targeted antioxidant that can prevent of mitochondrial oxidative damage. These expression increases were not observed in the mitoquinone-treated group, confirming that mtROS was an upstream regulatory target of apoptosis and inflammation in DON-exposed mice spleens. Finally, we confirmed that Cur (50 or 100 mg/kg body weight) attenuated DON-induced apoptosis and inflammation by inactivating mtROS. Collectively, these results confirm that DON causes spleen damage by increasing mtROS, and the protective effects of curcumin.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115200"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Electronic cigarettes (e-cigarettes) have emerged as a potential alternative to traditional smoking and may aid in tobacco harm reduction and smoking cessation. E-cigarette use has notably increased, especially among young non-tobacco users, raising concerns due to the unknown long-term health effects. The oral cavity is the first and one of the most crucial anatomical sites for the deposition of e-cigarette aerosols. E-cigarette aerosols contain nicotine, flavors, volatile organic compounds, heavy metals, carcinogens, and other hazardous substances. These aerosols impact the oral cavity, disrupting host-microbial interactions and triggering gingivitis and systemic diseases. Furthermore, oral inflammation and periodontitis can be caused by proinflammatory cytokines induced by e-cigarette aerosols. The toxic components of e-cigarette aerosols increase the cellular reactive oxygen species (ROS) levels, reduce antioxidant capacity, increase DNA damage, and disrupt repair processes, which may further contribute to harmful effects on oral epithelum, leading to inflammatory and pre-malignant oral epithelial lesions. In this review, we analyze the toxicological properties of compounds in e-cigarette aerosols, exploring their cytotoxic, genotoxic, and inflammatory effects on oral health and delving into the underlying molecular mechanisms. Further research is essential to understand the impact of e-cigarettes on oral health and make informed regulatory decisions based on reliable scientific evidence.
{"title":"E-Cigarette effects on oral health: A molecular perspective","authors":"Vengatesh Ganapathy , Ravindran Jaganathan , Mayilvanan Chinnaiyan , Gautham Chengizkhan , Balaji Sadhasivam , Jimmy Manyanga , Ilangovan Ramachandran , Lurdes Queimado","doi":"10.1016/j.fct.2024.115216","DOIUrl":"10.1016/j.fct.2024.115216","url":null,"abstract":"<div><div>Electronic cigarettes (e-cigarettes) have emerged as a potential alternative to traditional smoking and may aid in tobacco harm reduction and smoking cessation. E-cigarette use has notably increased, especially among young non-tobacco users, raising concerns due to the unknown long-term health effects. The oral cavity is the first and one of the most crucial anatomical sites for the deposition of e-cigarette aerosols. E-cigarette aerosols contain nicotine, flavors, volatile organic compounds, heavy metals, carcinogens, and other hazardous substances. These aerosols impact the oral cavity, disrupting host-microbial interactions and triggering gingivitis and systemic diseases. Furthermore, oral inflammation and periodontitis can be caused by proinflammatory cytokines induced by e-cigarette aerosols. The toxic components of e-cigarette aerosols increase the cellular reactive oxygen species (ROS) levels, reduce antioxidant capacity, increase DNA damage, and disrupt repair processes, which may further contribute to harmful effects on oral epithelum, leading to inflammatory and pre-malignant oral epithelial lesions. In this review, we analyze the toxicological properties of compounds in e-cigarette aerosols, exploring their cytotoxic, genotoxic, and inflammatory effects on oral health and delving into the underlying molecular mechanisms. Further research is essential to understand the impact of e-cigarettes on oral health and make informed regulatory decisions based on reliable scientific evidence.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115216"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Exposure to high levels of fluoride leads to brain developmental and functional damage. Motor performance deficits, learning and memory dysfunctions are related to fluoride neurotoxicity in human and rodent studies.
Materials and methods
Here, we evaluated the effects of Quercetin treatment (25 mg/kg) against sodium fluoride-induced neurotoxicity (NaF, 200 ppm) in the medial prefrontal cortex (mPFC) of male adult rats based on oxidative markers, behavioral performances, mRNA expressions, and stereological parameters. After a 4-week experimental period, the brains of rats were collected and used for molecular and histological analysis.
Results
We found that 4 weeks of NaF exposure decreased body weight, working memory, Brain-derived neurotrophic factor (BDNF) mRNA expression, total volume of mPFC, number of neurons and non-neuronal cells in the mPFC, and anti-oxidative markers (CAT, SOD, and GSH-Px), while increased lipid peroxidation, P53 mRNA expression and anxiety. Quercetin treatment could significantly reverse the neurotoxic effect of NaF in the mPFC.
Conclusions
In summary, Quercetin could decrease the detrimental effects of NaF in the mPFC of adult rats by improving antioxidant potency and consequently decreasing neuronal and non-neuronal apoptosis.
{"title":"Effects of Quercetin against fluoride-induced neurotoxicity in the medial prefrontal cortex of rats: A stereological, histochemical and behavioral study","authors":"Parinaz Javanbakht , Afshin Talebinasab , Reza Asadi-Golshan , Maryam Shabani , Iraj Ragerdi Kashani , Sina Mojaverrostami","doi":"10.1016/j.fct.2024.115126","DOIUrl":"10.1016/j.fct.2024.115126","url":null,"abstract":"<div><h3>Background</h3><div>Exposure to high levels of fluoride leads to brain developmental and functional damage. Motor performance deficits, learning and memory dysfunctions are related to fluoride neurotoxicity in human and rodent studies.</div></div><div><h3>Materials and methods</h3><div>Here, we evaluated the effects of Quercetin treatment (25 mg/kg) against sodium fluoride-induced neurotoxicity (NaF, 200 ppm) in the medial prefrontal cortex (mPFC) of male adult rats based on oxidative markers, behavioral performances, mRNA expressions, and stereological parameters. After a 4-week experimental period, the brains of rats were collected and used for molecular and histological analysis.</div></div><div><h3>Results</h3><div>We found that 4 weeks of NaF exposure decreased body weight, working memory, Brain-derived neurotrophic factor (BDNF) mRNA expression, total volume of mPFC, number of neurons and non-neuronal cells in the mPFC, and anti-oxidative markers (CAT, SOD, and GSH-Px), while increased lipid peroxidation, P53 mRNA expression and anxiety. Quercetin treatment could significantly reverse the neurotoxic effect of NaF in the mPFC.</div></div><div><h3>Conclusions</h3><div>In summary, Quercetin could decrease the detrimental effects of NaF in the mPFC of adult rats by improving antioxidant potency and consequently decreasing neuronal and non-neuronal apoptosis.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115126"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115159
Junxia Liu , Peng Li , Xiao Li , Yanli Xie , Fred Mwabulili , Shumin Sun , Yuhui Yang , Weibin Ma , Qian Li , Hang Jia
Deoxynivalenol (DON) contamination in cereals and their products poses a potential threat to animal and human health, however, physical and chemical detoxification methods deplete nutrients and cannot specifically remove DON. This study aims to identify novel and efficient DON-degrading enzymes, providing practical support for their application in biodegradation. A novel DON-degrading aldo-keto reductase named AKR11A2 was identified from Bacillus velezensis Vel-HNGD-F2 through BlastP comparison. AKR11A2, an enzyme with a molecular mass of 34.8 kDa encoded by a 933 bp gene, exhibited optimal activity at pH 9 and 40 °C, while demonstrating remarkable thermal and alkaline stability by retaining over 90% of its activity. UPLC-MS/MS analysis revealed that the m/z of the DON degradation product was 295.1, identified as 3-epi-DON, formed through the direct isomerization of DON. Notably, zebrafish experiments demonstrated that the liver toxicity of the degradation product was significantly lower than that of DON. AKR11A2 effectively degraded 50.69% of the DON in contaminated corn, highlighting its practical application in food safety. These findings indicate that the study achieved the biodegradation of DON and provide a promising theoretical and technological support for the application of DON detoxifying enzymes in food and feed products.
谷物及其制品中的脱氧雪腐镰刀菌醇（DON）污染对动物和人类健康构成潜在威胁，然而，物理和化学解毒方法消耗营养物质，不能特异性去除DON。本研究旨在寻找新型高效的don降解酶，为其在生物降解中的应用提供实践支持。通过BlastP比较，从velezensis wel - hngd - f2中鉴定出一种新的don降解醛酮还原酶AKR11A2。AKR11A2是一种分子量为34.8 kDa，由933 bp基因编码的酶，在pH 9和40°C条件下具有最佳活性，同时保持90%以上的活性，表现出良好的热碱性稳定性。UPLC-MS/MS分析表明，DON降解产物的m/z为295.1，鉴定为3-epi-DON，由DON直接异构化形成。值得注意的是，斑马鱼实验表明，降解产物的肝毒性明显低于DON。AKR11A2能有效降解污染玉米中50.69%的DON，突出了其在食品安全方面的实际应用。上述结果表明，本研究实现了DON的生物降解，为DON解毒酶在食品和饲料产品中的应用提供了良好的理论和技术支持。
{"title":"Expression, characterization, and application of an aldo-keto reductase mined from Bacillus velezensis Vel-HNGD-F2 for deoxynivalenol biodegradation","authors":"Junxia Liu , Peng Li , Xiao Li , Yanli Xie , Fred Mwabulili , Shumin Sun , Yuhui Yang , Weibin Ma , Qian Li , Hang Jia","doi":"10.1016/j.fct.2024.115159","DOIUrl":"10.1016/j.fct.2024.115159","url":null,"abstract":"<div><div>Deoxynivalenol (DON) contamination in cereals and their products poses a potential threat to animal and human health, however, physical and chemical detoxification methods deplete nutrients and cannot specifically remove DON. This study aims to identify novel and efficient DON-degrading enzymes, providing practical support for their application in biodegradation. A novel DON-degrading aldo-keto reductase named AKR11A2 was identified from <em>Bacillus velezensis</em> Vel-HNGD-F2 through BlastP comparison. AKR11A2, an enzyme with a molecular mass of 34.8 kDa encoded by a 933 bp gene, exhibited optimal activity at pH 9 and 40 °C, while demonstrating remarkable thermal and alkaline stability by retaining over 90% of its activity. UPLC-MS/MS analysis revealed that the <em>m/z</em> of the DON degradation product was 295.1, identified as 3-<em>epi</em>-DON, formed through the direct isomerization of DON. Notably, zebrafish experiments demonstrated that the liver toxicity of the degradation product was significantly lower than that of DON. AKR11A2 effectively degraded 50.69% of the DON in contaminated corn, highlighting its practical application in food safety. These findings indicate that the study achieved the biodegradation of DON and provide a promising theoretical and technological support for the application of DON detoxifying enzymes in food and feed products.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115159"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142754411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115145
Albert Sebastià , Carmen Fernández-Matarredona , Juan Manuel Castagnini , Francisco J. Barba , Houda Berrada , Juan Carlos Moltó , Olga Pardo , Francesc A. Esteve-Turrillas , Emilia Ferrer
Snacks, including popcorn, are increasingly consumed in Spain and are susceptible to acrylamide (AA) formation. AA, classified as a probable human carcinogen by the International Agency for Research on Cancer (IARC), is produced via the Maillard reaction between reducing sugars and amino acids, particularly glucose, and asparagine, when foods are heated above 120 °C. This study aims to analyze the AA content in 91 popcorn samples, categorized by flavor (salted, butter, caramel, flavored, colored, unflavored) and cooking method (ready-to-eat, popcorn maker, microwave), and assess dietary AA exposure in the Spanish population. Samples were collected from supermarkets, grocery stores, and cinemas across Spain and analyzed using solid-liquid extraction (SLE) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). The average AA concentration in the samples was 277 ± 119 μg kg−1, with only two samples below the limit of quantification (LOQ, 60 μg kg−1). At the same time, no significant correlation between flavor and AA content was found. Whereas microwave cooking notably increased AA levels. Estimated AA intake for adults and children ranged from 0.011 to 0.045 μg kg⁻1 day⁻1, depending on the exposure scenario. In children, a margin of exposure (MOE) below 10,000 was observed for Harderian gland tumors in realistic and pessimistic scenario.
包括爆米花在内的零食在西班牙的消费量越来越大，容易产生丙烯酰胺（AA）。AA被国际癌症研究机构（IARC）列为可能的人类致癌物，当食物加热到120°C以上时，它是通过还原糖和氨基酸，特别是葡萄糖和天冬酰胺之间的美拉德反应产生的。本研究旨在分析91种爆米花样品的AA含量，按风味（咸味、黄油、焦糖、调味、有色、无风味）和烹饪方法（即食、爆米花机、微波）进行分类，并评估西班牙人群的膳食AA暴露情况。样品从西班牙各地的超市、杂货店和电影院收集，并使用固液萃取（SLE）和液相色谱-串联质谱（LC-MS/MS）进行分析。样品中AA的平均浓度为277±119 μg kg-1，仅有2个样品低于定量限（定量限为60 μg kg-1）。同时，风味与AA含量之间无显著相关。而微波烹饪明显增加了AA水平。据估计，成人和儿童的AA摄入量在0.011到0.045 μg kg - 1天，这取决于暴露的情况。在儿童中，在现实和悲观的情况下，观察到哈德氏腺肿瘤的暴露边际（MOE）低于10,000。
{"title":"Acrylamide content in popcorn from Spanish market: Risk assessment","authors":"Albert Sebastià , Carmen Fernández-Matarredona , Juan Manuel Castagnini , Francisco J. Barba , Houda Berrada , Juan Carlos Moltó , Olga Pardo , Francesc A. Esteve-Turrillas , Emilia Ferrer","doi":"10.1016/j.fct.2024.115145","DOIUrl":"10.1016/j.fct.2024.115145","url":null,"abstract":"<div><div>Snacks, including popcorn, are increasingly consumed in Spain and are susceptible to acrylamide (AA) formation. AA, classified as a probable human carcinogen by the International Agency for Research on Cancer (IARC), is produced via the Maillard reaction between reducing sugars and amino acids, particularly glucose, and asparagine, when foods are heated above 120 °C. This study aims to analyze the AA content in 91 popcorn samples, categorized by flavor (salted, butter, caramel, flavored, colored, unflavored) and cooking method (ready-to-eat, popcorn maker, microwave), and assess dietary AA exposure in the Spanish population. Samples were collected from supermarkets, grocery stores, and cinemas across Spain and analyzed using solid-liquid extraction (SLE) and liquid chromatography-tandem mass spectrometry (LC-MS/MS). The average AA concentration in the samples was 277 ± 119 μg kg<sup>−1</sup>, with only two samples below the limit of quantification (LOQ, 60 μg kg<sup>−1</sup>). At the same time, no significant correlation between flavor and AA content was found. Whereas microwave cooking notably increased AA levels. Estimated AA intake for adults and children ranged from 0.011 to 0.045 μg kg⁻<sup>1</sup> day⁻<sup>1</sup>, depending on the exposure scenario. In children, a margin of exposure (MOE) below 10,000 was observed for Harderian gland tumors in realistic and pessimistic scenario.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115145"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115194
Alisha Janiga-MacNelly , Tham C. Hoang , Ramon Lavado
Originally developed to conserve natural resources, plastic has become a global pollution issue due to inadequate waste management. The dispersion and weathering of plastic waste in the environment generate micro-sized particles. Despite extensive research on the toxicological effects of pristine polymers, the impact of microplastics (MPs) from consumer plastics is poorly understood. This study investigated the cytotoxic and genotoxic effects of cryo-milled single-use plastic products (fork and cup) on eight cell lines (Caco-2, HEK001, MRC-5, HMEC-1, HepaRG, HMC-3, and T47D) at concentrations from 0.01 to 100 μg/mL. Results showed that 100 μg/mL of MPs did not significantly affect cell viability in Caco-2, HEK001, MRC-5, and T47D. However, HMEC-1 and HMC-3 exhibited decreased viability with 10–100 μg/mL of fork particles, while HMC-3 and HepaRG showed reduced viability with 100 μg/mL of cup particles. Conversely, cup particles increased HMEC-1 proliferation at 0.1–100 μg/mL. Comet assay data indicated that both fork and cup exposure led to elevated DNA fragmentation in HMEC-1 and HMC-3 cells. These findings indicate that MPs from consumer-grade plastics may exhibit cytotoxic and genotoxic effects, with endothelial and microglial cells being particularly susceptible.
{"title":"Comparative toxicity of microplastics obtained from human consumer products on human cell-based models","authors":"Alisha Janiga-MacNelly , Tham C. Hoang , Ramon Lavado","doi":"10.1016/j.fct.2024.115194","DOIUrl":"10.1016/j.fct.2024.115194","url":null,"abstract":"<div><div>Originally developed to conserve natural resources, plastic has become a global pollution issue due to inadequate waste management. The dispersion and weathering of plastic waste in the environment generate micro-sized particles. Despite extensive research on the toxicological effects of pristine polymers, the impact of microplastics (MPs) from consumer plastics is poorly understood. This study investigated the cytotoxic and genotoxic effects of cryo-milled single-use plastic products (fork and cup) on eight cell lines (Caco-2, HEK001, MRC-5, HMEC-1, HepaRG, HMC-3, and T47D) at concentrations from 0.01 to 100 μg/mL. Results showed that 100 μg/mL of MPs did not significantly affect cell viability in Caco-2, HEK001, MRC-5, and T47D. However, HMEC-1 and HMC-3 exhibited decreased viability with 10–100 μg/mL of fork particles, while HMC-3 and HepaRG showed reduced viability with 100 μg/mL of cup particles. Conversely, cup particles increased HMEC-1 proliferation at 0.1–100 μg/mL. Comet assay data indicated that both fork and cup exposure led to elevated DNA fragmentation in HMEC-1 and HMC-3 cells. These findings indicate that MPs from consumer-grade plastics may exhibit cytotoxic and genotoxic effects, with endothelial and microglial cells being particularly susceptible.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115194"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115192
Pierre-Jean Ferron , Romain Pelletier , Julie Massart , Celine Narjoz , Vinh-Hoang-Lan Julie Tran , Marie-Anne Loriot , Angéline Kernalleguen , Marie Zins , Sofiane Kab , Isabelle Morel , Bruno Clément , Thomas Gicquel , Brendan Le Daré
Very few quantitative data exist on tramadol metabolites, which hampers our understanding of their role in efficacy and safety of tramadol. We aimed to provide quantitative data on tramadol and its 5 main metabolites in a patient cohort and to determine whether metabolite ratios can be predictive of a CYP2D6 metabolism phenotype. We also aimed to investigate the influence of co-medications and patient profile (BMI, glycemia, lipid levels) on tramadol metabolite ratios. Overall, 37 patient samples from the CONSTANCES cohort contained tramadol and its 5 metabolites. Mean concentrations found tramadol at 343.2 ± 223.2 μg/L, M1 at 62.4 ± 41.4 μg/L, M2 at 210.0 ± 272.3, M3 at 1.76 ± 3.0 μg/L, M4 at 1.8 ± 2.8 μg/L and M5 at 31.8 ± 28.4 μg/L. The most frequent CYP2D6 phenotype was extensive metabolizers (51.3%), followed by intermediate metabolizers (24.3%) and poor metabolizers (10.8%). CYP2D6-inhibiting co-medications impacted tramadol metabolism independently of CYP2D6 metabolism phenotype. Lipid parameters and glycemia were significantly associated with changes in tramadol metabolic ratios. Metabolic ratios are not sufficient to determine the CYP2D6 metabolic phenotype in patients. CYP2D6 inhibitors and obesity/NAFLD/diabetes impact tramadol metabolism. These factors are likely to impact the analgesic efficacy and safety profile of tramadol, justifying the need for further studies in this area.
{"title":"Role of CYP2D6 polymorphisms in tramadol metabolism in a context of co-medications and overweight","authors":"Pierre-Jean Ferron , Romain Pelletier , Julie Massart , Celine Narjoz , Vinh-Hoang-Lan Julie Tran , Marie-Anne Loriot , Angéline Kernalleguen , Marie Zins , Sofiane Kab , Isabelle Morel , Bruno Clément , Thomas Gicquel , Brendan Le Daré","doi":"10.1016/j.fct.2024.115192","DOIUrl":"10.1016/j.fct.2024.115192","url":null,"abstract":"<div><div>Very few quantitative data exist on tramadol metabolites, which hampers our understanding of their role in efficacy and safety of tramadol. We aimed to provide quantitative data on tramadol and its 5 main metabolites in a patient cohort and to determine whether metabolite ratios can be predictive of a CYP2D6 metabolism phenotype. We also aimed to investigate the influence of co-medications and patient profile (BMI, glycemia, lipid levels) on tramadol metabolite ratios. Overall, 37 patient samples from the CONSTANCES cohort contained tramadol and its 5 metabolites. Mean concentrations found tramadol at 343.2 ± 223.2 μg/L, M1 at 62.4 ± 41.4 μg/L, M2 at 210.0 ± 272.3, M3 at 1.76 ± 3.0 μg/L, M4 at 1.8 ± 2.8 μg/L and M5 at 31.8 ± 28.4 μg/L. The most frequent CYP2D6 phenotype was extensive metabolizers (51.3%), followed by intermediate metabolizers (24.3%) and poor metabolizers (10.8%). CYP2D6-inhibiting co-medications impacted tramadol metabolism independently of CYP2D6 metabolism phenotype. Lipid parameters and glycemia were significantly associated with changes in tramadol metabolic ratios. Metabolic ratios are not sufficient to determine the CYP2D6 metabolic phenotype in patients. CYP2D6 inhibitors and obesity/NAFLD/diabetes impact tramadol metabolism. These factors are likely to impact the analgesic efficacy and safety profile of tramadol, justifying the need for further studies in this area.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115192"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142816847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115177
Yiren Xiong , Jiayi He , Shanshan He , Zuqing Hu , Di Ouyang , Renyi Liu , Zhenjie Gao , Weiguang Zhang , Zhujun Kang , Shuyi Lan , Yang Wang , Fatoumata Diallo , Dalin Hu
Lead is a ubiquitous environmental chemical with various toxic damage to human body. This investigation aimed to explore the intervention effect of human umbilical cord mesenchymal stem cells derived exosomes (HUC-MSC-exo) on the neurotoxicity of lead and the relevant mechanism. Differential gradient ultracentrifugation was adopted to isolate HUC-MSC-exo. Nanoparticle tracking assay (NTA), Transmission electron microscope (TEM) technology and exosomal specific biomarkers CD9, CD63 and CD81 were adopted for exosomal characterization. Human neuroblastoma cell (SH-SY5Y) was used as the recipient cell. Confocal laser scanning microscope analysis was conducted to confirm the intake of HUC-MSC-exo by SH-SY5Y cells. Cell migration ability, apoptosis, IL-6, IL-1β and TNF-α were analyzed. The role of miR-26a-5p/PTEN axis was assessed. The result showed that the exposure of SH-SY5Y cells to lead activated the miR-26a-5p/PTEN pathway by down-regulating miR-26a-5p and up-regulating PTEN expression, which was related to the significantly decreased cell migration and increased apoptosis, as well as significantly enhanced levels of inflammatory cytokine as compared with the control. While HUC-MSC-exo could significantly alleviate the cytotoxicity, apoptosis and inflammatory effects induced by lead on SH-SY5Y cells via partially restoring miR-26a-5p/PTEN pathway. Herein, we conclude that HUC-MSC-exo can alleviate lead-induced toxic effects on SH-SY5Y cells partially through miR-26a-5p/PTEN pathway.
{"title":"The toxicity of lead on human neuroblastoma cells was alleviated by HUC-MSC-derived exosomes through miR-26a-5p/PTEN pathway","authors":"Yiren Xiong , Jiayi He , Shanshan He , Zuqing Hu , Di Ouyang , Renyi Liu , Zhenjie Gao , Weiguang Zhang , Zhujun Kang , Shuyi Lan , Yang Wang , Fatoumata Diallo , Dalin Hu","doi":"10.1016/j.fct.2024.115177","DOIUrl":"10.1016/j.fct.2024.115177","url":null,"abstract":"<div><div>Lead is a ubiquitous environmental chemical with various toxic damage to human body. This investigation aimed to explore the intervention effect of human umbilical cord mesenchymal stem cells derived exosomes (HUC-MSC-exo) on the neurotoxicity of lead and the relevant mechanism. Differential gradient ultracentrifugation was adopted to isolate HUC-MSC-exo. Nanoparticle tracking assay (NTA), Transmission electron microscope (TEM) technology and exosomal specific biomarkers CD9, CD63 and CD81 were adopted for exosomal characterization. Human neuroblastoma cell (SH-SY5Y) was used as the recipient cell. Confocal laser scanning microscope analysis was conducted to confirm the intake of HUC-MSC-exo by SH-SY5Y cells. Cell migration ability, apoptosis, IL-6, IL-1β and TNF-α were analyzed. The role of miR-26a-5p/PTEN axis was assessed. The result showed that the exposure of SH-SY5Y cells to lead activated the miR-26a-5p/PTEN pathway by down-regulating miR-26a-5p and up-regulating PTEN expression, which was related to the significantly decreased cell migration and increased apoptosis, as well as significantly enhanced levels of inflammatory cytokine as compared with the control. While HUC-MSC-exo could significantly alleviate the cytotoxicity, apoptosis and inflammatory effects induced by lead on SH-SY5Y cells via partially restoring miR-26a-5p/PTEN pathway. Herein, we conclude that HUC-MSC-exo can alleviate lead-induced toxic effects on SH-SY5Y cells partially through miR-26a-5p/PTEN pathway.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115177"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142790711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-01DOI: 10.1016/j.fct.2024.115199
Bryan Delaney Ph.D., DABT, Fellow, ATS ((Soon to be former) Editor-in-Chief)
{"title":"Editorial from the departing Editor-in-Chief","authors":"Bryan Delaney Ph.D., DABT, Fellow, ATS ((Soon to be former) Editor-in-Chief)","doi":"10.1016/j.fct.2024.115199","DOIUrl":"10.1016/j.fct.2024.115199","url":null,"abstract":"","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115199"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142816839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号