Food and Chemical Toxicology最新文献

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Aescin ameliorates alcohol-induced liver injury. A possible implication of ROS / TNF-alpha / p38MAPK / caspase-3 signaling

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-21 DOI: 10.1016/j.fct.2025.115270

Sherin Zakaria , Shimaa A. Abass , Mona Abdelatty , Sama Said , Samar Elsebaey

Alcoholic liver disease (ALD) is a commonly known liver disease mediated by prolonged alcohol consumption. Aescin is a triterpene saponin that can manage several conditions, including brain trauma, arthritis, venous congestion, stroke, and thrombophlebitis. Even so, studies illustrating the aescin role in ALD are scarce. Our study explored the potential effect of aescin in ALD in mice. In the current experiment, forty mice were utilized and sorted randomly into four groups: the control group received only vehicles, the alcohol group was given 5% alcohol in drinking water for four weeks, and the aescin-treated groups were given 5% alcohol in drinking water and aescin (10 and 20 mg/kg/day) for four weeks, then two doses of 60% alcohol (3g/kg) were given in the 29th and 30th day of the experiment. Our study revealed that aescin ameliorated alcohol-mediated liver damage, including reducing inflammatory cell infiltration and vascular dilatation. The serum concentrations of liver enzymes (ALT and AST) decreased in the aescin-treated groups. The apoptosis and oxidative stress also decreased, and the antioxidant enzyme activities were restored by aescin in alcohol-treated mice. Additionally, aescin decreased ethanol-induced inflammation by downregulating p38 MAPK and tumor necrosis factor-α (TNF-α), suggesting that aescin positively reduces alcohol-caused inflammation and oxidative stress. Consequently, aescin could ameliorate alcohol-induced hepatic damage by targeting the p38 MAPK/TNF-α signalling and could be developed as a novel health product that potentially ameliorates ALD.

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引用次数: 0

Therapeutic potential of rosmarinic acid in tramadol-induced hepatorenal toxicity: Modulation of oxidative stress, inflammation, RAGE/NLRP3, ER stress, apoptosis, and tissue functions parameters

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-21 DOI: 10.1016/j.fct.2025.115275

Onur Karaca , Nurhan Akaras , Hasan Şimşek , Cihan Gür , Mustafa İleritürk , Sefa Küçükler , Selman Gencer , Fatih Mehmet Kandemir

Aim

Tramadol (TRM), a widely used opioid analgesic for moderate to severe pain, is associated with liver and kidney toxicity at high doses or prolonged use. This study investigates the protective role of rosmarinic acid (RA), a natural phenolic compound known for its antioxidant, anti-inflammatory, and cell-protective properties, against TRM-induced hepatorenal toxicity.

Methods

Thirty-five male Wistar rats were divided into five groups: Control, TRM, RA, TRM + RA25, and TRM + RA50. Rats received TRM (50 mg/kg) and RA (25 or 50 mg/kg), with liver and kidney function tests, oxidative stress, inflammation, ER stress, apoptosis, and tissue damage indicators assessed through qRT-PCR, ELISA, Western blotting, H&E, and immunohistochemical analysis.

Results

TRM induced liver and kidney dysfunctions, evident from increased ALT, AST, ALP, urea, creatinine, nephrin, TIM-1 and 8-OHdG levels, along with activated oxidative stress, inflammation, ER stress, and apoptosis pathways. RA significantly reduced these effects, ameliorating histologic and immunohistochemical markers of tissue damage and inflammation.

Conclusion

RA demonstrates therapeutic potential by mitigating TRM-induced hepatorenal toxicity and preserving tissue integrity.

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引用次数: 0

The role of GSK3β signaling mediated lysosomal biosynthesis dysregulation in fluoride-induced neurological impairment

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-20 DOI: 10.1016/j.fct.2025.115267

Yi Cheng , Yuhui Du , Yue Hu , Xinying Wang , Qingyuan Li , Xi Yan , Ming Dou , Weihua Jia , Fangfang Yu , Yue Ba , Guoyu Zhou

Neurological dysfunction induced by fluoride is still one of major concern worldwide, yet the underlying mechanisms remain elusive. To explore whether fluoride disrupts lysosomal biosynthesis via the GSK3β signaling, leading to neurological damage, both in vivo rat models and in vitro PC12 cell models were conducted. Subsequent findings revealed reduced spatial learning and memory abilities, decreased hippocampal neurons, and disrupted neuronal arrangement in NaF-treated rats. In vitro, PC12 cells exhibited decreased cell viability and increased apoptosis rates after NaF treatment for 24 h. Moreover, immunofluorescence assays demonstrated that there is a reduction in the number of mature lysosomes and an increase in immature lysosomes in NaF-treated PC12 cells, evident by decreased co-localization of LAMP1 with Arl8b, and increased co-localization of LAMP1 with Rab7. Furthermore, both in vivo and in vitro, the protein expression of cleaved caspase-3 was upregulated, whereas the protein expressions of TFEB and CTSB were downregulated. The GSK3β signaling activation was detected, and this was confirmed by silencing GSK3β with siRNA in vitro. Collectively, these results indicate that NaF can impair lysosomal biosynthesis via GSK3β signaling, promoting neuronal apoptosis, and consequently impairing neurological function in rats.

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引用次数: 0

Aprepitant ameliorates vancomycin-induced kidney injury: Role of GPX4/system Xc− and oxidative damage 阿瑞吡坦改善万古霉素诱导的肾损伤：GPX4/系统Xc-和氧化损伤的作用

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-19 DOI: 10.1016/j.fct.2025.115264

Maha H. Sharawy , Ahmed M. Abdel-Rahman , Noha Abdel-Rahman

Vancomycin, a glycopeptide antibiotic, is used in cases of drug-resistant bacterial infections, but unfortunately is associated with acute kidney injury (AKI). We here explore the protective potential of aprepitant against vancomycin-induced AKI. Vancomycin (500 mg/kg/i.p) was given to rats for seven days and aprepitant (20 mg/kg/p.o) was administered one day before and for seven days concomitant with vancomycin. At the end of the experiment, kidney function, oxidative stress, autophagy and ferroptosis markers were assessed. We show that aprepitant reduced kidney/body weight ratio, serum creatinine and blood urea nitrogen levels. It improved renal structure and enhanced the antioxidant machinery as indicated by elevated catalase activity and GSH levels and reduced renal MDA. Aprepitant managed to inhibit ferroptosis by decreasing system Xc⁻ and GPX4 renal levels. As a result, levels of autophagic markers ATG3, LC3A and LC3B were attenuated. These results were confirmed by electron microscopy examination of cellular structures. In addition, aprepitant increased p62 protein expression. Moreover, aprepitant decreased the apoptotic marker cleaved caspase-3 levels. Our results suggest a new repurposed role for aprepitant in protecting against AKI. This protective effect relies on its antioxidant effect and the influence of inhibiting ferroptosis which resulted in downregulation of autophagy and apoptosis.

万古霉素是一种糖肽抗生素，用于耐药细菌感染的病例，但不幸的是与急性肾损伤（AKI）有关。我们在此探讨阿瑞吡坦对万古霉素诱导的AKI的保护潜力。万古霉素（500mg /kg/i.p）给药7 d，阿瑞吡坦（20mg /kg/p.o）给药1天，与万古霉素同时给药7 d。实验结束时，测定大鼠肾功能、氧化应激、自噬和铁下垂指标。我们发现阿瑞吡坦降低了肾/体重比、血清肌酐和血尿素氮水平。它改善了肾脏结构，增强了抗氧化机制，过氧化氢酶活性和谷胱甘肽水平升高，肾脏MDA降低。阿瑞吡坦通过降低系统Xc-和GPX4肾水平来抑制铁下垂。结果，自噬标志物ATG3、LC3A和LC3B水平降低。电镜检查细胞结构证实了这些结果。此外，阿瑞吡坦增加p62蛋白的表达。此外，阿瑞吡坦降低了凋亡标志物caspase-3裂解水平。我们的结果提示阿瑞吡坦在预防AKI中的新作用。这种保护作用依赖于其抗氧化作用和抑制铁下垂的作用，从而下调自噬和细胞凋亡。

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引用次数: 0

Corrigendum to “Maternal ochratoxin A exposure impairs meiosis progression and primordial follicle formation of F1 offspring” [Food and Chemical Toxicology 168 (2022) 113386] “母体赭曲霉毒素A暴露损害F1后代减数分裂进程和原始卵泡形成”的更正[食品与化学毒理学168(2022)113386]。

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-19 DOI: 10.1016/j.fct.2025.115257

Yue Song , Jinxin Zhao , Tian Qiao , Lan Li , Dachuan Shi , Yonghong Sun , Wei Shen , Xiaofeng Sun

引用次数: 0

Dexlansoprazole is an aryl hydrocarbon receptor agonist 右兰索拉唑是芳烃受体和ITE的干扰物。

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-19 DOI: 10.1016/j.fct.2025.115262

Kuo-Liang Wei , Shan-Chun Chen , Chih-Yi Lin , Yu-Ting Chou , Wei-Tin Kuo , Teik-Wei Chuah , Jyan-Gwo Joseph Su

Dexlansoprazole, a proton pump inhibitor, is commonly used to treat gastro-esophageal reflux disease and erosive esophagitis. The activated aryl hydrocarbon receptor (AhR) functions as a transcription factor by binding to the aryl hydrocarbon response element (AHRE) of its target genes, with cytochrome P450 (CYP) 1A1 being the most well-known target. In this study, we demonstrated that dexlansoprazole stimulates AhR activity, leading to increased CYP1A1 expression. Our findings indicate that treatment with 2 μM dexlansoprazole is sufficient to induce CYP1A1 mRNA and protein expression, as well as AHRE-mediated transcriptional activity, in both human and mouse cells. Using AhR signal-deficient mutant cells and specific AhR antagonists—SR1, GNF351, and CH-223191—we confirmed that AhR is required for dexlansoprazole-induced CYP1A1 expression. Additionally, we showed that dexlansoprazole promotes AhR nuclear translocation, acting as an AhR agonist. However, due to its lower potency compared to FICZ and ITE in activating AhR, dexlansoprazole suppresses FICZ- and ITE-induced CYP1A1 expression in human liver HepG2 and ovarian granulosa HO23 cell lines, suggesting that it functions as both an AhR agonist and a modulator. This study offers valuable insights into the potential clinical side effects of dexlansoprazole.

右兰索拉唑是一种质子泵抑制剂，常用于治疗胃食管反流病和糜烂性食管炎。活化芳烃受体（activated aryl hydrocarbon receptor, AhR）通过与靶基因的芳烃应答元件（aryl hydrocarbon response element， AHRE）结合而发挥转录因子的作用，其中细胞色素P450 (CYP) 1A1是最著名的靶基因。在本研究中，我们证明了右兰索拉唑刺激AhR活性，导致CYP1A1表达增加。我们的研究结果表明，在人和小鼠细胞中，2 μM右兰索拉唑足以诱导CYP1A1 mRNA和蛋白的表达，以及ahre介导的转录活性。利用AhR信号缺陷突变细胞和特异性AhR拮抗剂sr1、GNF351和ch -223191，我们证实了右兰索拉唑诱导的CYP1A1表达需要AhR。此外，我们发现右兰索拉唑促进AhR核易位，作为AhR激动剂。然而，由于其在激活AhR方面的效力低于FICZ和ITE，右兰索拉唑抑制了FICZ和ITE诱导的人肝脏HepG2和卵巢颗粒HO23细胞系中CYP1A1的表达，表明其同时具有AhR激动剂和调节剂的功能。本研究对右兰索拉唑的潜在临床副作用提供了有价值的见解。

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引用次数: 0

Ferulic acid protects rat offspring from maternal high-fat, high-fructose diet-induced toxicity and developmental retardation through a direct effect on pancreatic islets 阿魏酸通过对胰岛的直接作用，保护大鼠后代免受母体高脂肪、高果糖饮食引起的毒性和发育迟缓。

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-18 DOI: 10.1016/j.fct.2025.115265

Hekmat L. El-Gammal, Fatma Omar, Ayman Hyder

Maternal obesity predisposes offspring to type 2 diabetes (T2D) through a direct chronic effect of lipids on pancreatic β-cell neogenesis. β-cells produce FABP3 to bind and metabolize fatty acids. Ferulic acid (FA) is a natural product that may inhibit fatty acids' binding to FABP3, preventing their toxicity. It is aimed to evaluate the consequences of maternal feeding on high-fat, high fructose diet (HFFD) and the role of FA on the offspring. Four-week-old female rats were fed HFFD for 9 weeks prior to and throughout gestation and lactation to develop T2D. A group of them received 50 mg/kg FA daily. Offspring were sampled on gestational day 18 (GD18), and postnatal days (PND) 3 and 30. HFFD increased offspring's blood glucose, insulin, Homa-IR, HbA1c, triglycerides, cholesterol, intrahepatic and intra-insular lipid droplets. The mechanism of islet inflammation and apoptosis, detected by Il-1b and cleaved caspase3, involved the nuclear translocation of NFκB p65. Maternal HFFD caused developmental retardations in offspring's ovaries, testes, kidney and liver. Coupling FA treatment with the maternal HFFD maintained normoglycemia, lipidemia, and healthy islets, and prevented developmental retardations. FA administration to T2D mothers revealed positive effects on the offspring that is related to its direct protective effect on pancreatic β-cells.

母体肥胖通过脂质对胰腺β细胞新生的直接慢性影响，使后代易患2型糖尿病（T2D）。β-细胞产生FABP3结合和代谢脂肪酸。阿魏酸（FA）是一种天然产物，可以抑制脂肪酸与FABP3的结合，防止其毒性。本研究旨在评估高脂肪、高果糖饮食（HFFD）对后代的影响以及FA对后代的作用。4周龄的雌性大鼠在妊娠和哺乳期前和整个哺乳期喂养9周HFFD以形成T2D。每组饲喂50 mg/kg FA。子代在妊娠第18天（GD18）和产后第3和30天（PND）取样。HFFD增加子代血糖、胰岛素、Homa-IR、HbA1c、甘油三酯、胆固醇、肝内和岛内脂滴。通过Il-1b和cleaved caspase3检测，胰岛炎症和凋亡的机制与NFκB p65的核易位有关。母体HFFD导致子代卵巢、睾丸、肾脏和肝脏发育迟缓。将FA治疗与母亲HFFD结合，维持正常的血糖、血脂和健康的胰岛，并预防发育迟缓。给T2D母鼠服用FA对后代有积极作用，这与FA对胰腺β细胞的直接保护作用有关。

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引用次数: 0

Update to RIFM fragrance ingredient safety assessment, 4,8-dimethyl-7-nonen-2-ol, CAS Registry Number 40596-76-7 更新RIFM香料成分安全性评估，4,8-二甲基-7-壬烯-2-醇，CAS登记号40596-76-7。

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-18 DOI: 10.1016/j.fct.2025.115259

A.M. Api , A. Bartlett , D. Belsito , D. Botelho , M. Bruze , A. Bryant-Friedrich , G.A. Burton Jr. , M.A. Cancellieri , H. Chon , M.L. Dagli , W. Dekant , C. Deodhar , K. Farrell , A.D. Fryer , L. Jones , K. Joshi , A. Lapczynski , M. Lavelle , I. Lee , H. Moustakas , Y. Tokura

引用次数: 0

Safety and antioxidant assessments of BLR-E50, 50% ethanolic extract from red beans co-fermented by Bacillus subtilis and Lactobacillus bulgaricus 枯草芽孢杆菌与保加利亚乳杆菌共发酵红豆50%乙醇提取物BLR-E50的安全性及抗氧化性评价

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-17 DOI: 10.1016/j.fct.2025.115261

Su-Tze Chou , Yi-Hua Chen , Yi-Hung Chen , Yu‐Chen Tsai , Yun-Chin Chung , Ju-Pi Li

Since red beans have poor textural properties, fermentation is commonly used to help produce better pulse products. To obtain BLR-E50, red beans are fermented using a co-culture of Bacillus subtilis and Lactobacillus bulgaricus, followed by extraction with 50% ethanol. The present data demonstrate that BLR-E50 did not exhibit mutagenicity, genotoxicity, or subacute oral toxicity. BLR-E50 showed antioxidant abilities in vitro. Under H₂O₂-challenged conditions, the dietary addition of BLR-E50 extended the survival time of female Drosophila melanogaster (D. melanogaster). Meanwhile, BLR-E50 modulated the antioxidant system in H₂O₂-treated D. melanogaster. Oral administration of BLR-E50 also improved motor abilities and reduced tyrosine hydroxylase levels in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurodegeneration mouse model. Overall, this study presents that BLR-E50 is safe and possesses antioxidant, anti-aging, and neuroprotective capabilities, providing scientific evidence for the potential application of fermented red bean products as antioxidants in future dietary interventions.

由于红豆的质地较差，发酵通常用于生产更好的豆类产品。为了获得BLR-E50，红豆采用枯草芽孢杆菌和保加利亚乳杆菌共培养发酵，然后用50%乙醇提取。目前的数据表明，BLR-E50没有表现出诱变性、遗传毒性或亚急性口服毒性。BLR-E50具有体外抗氧化能力。在h2o2胁迫条件下，饲料中添加BLR-E50可延长雌性黑腹果蝇的存活时间。同时，BLR-E50调节了h2o2处理的黑胃的抗氧化系统。在1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）诱导的神经变性小鼠模型中，口服BLR-E50还能改善运动能力，降低酪氨酸羟化酶水平。总之，本研究表明BLR-E50是安全的，具有抗氧化、抗衰老和神经保护功能，为发酵红豆制品作为抗氧化剂在未来饮食干预中的潜在应用提供了科学依据。

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引用次数: 0

Gold nanoparticles and induction of structural alteration and enhanced oxidative stress in rat lens 金纳米颗粒与诱导大鼠晶状体结构改变和氧化应激增强。

IF 3.9 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology

Pub Date : 2025-01-17 DOI: 10.1016/j.fct.2025.115263

Samaa Samir Kamar , Lobna A. Elkhateb , Asmaa Mohammed ShamsEldeen , Randa Mohamed Abdel-Moneim El-Mofty , Mohamed Mahmoud Elsebaie , Nermin Nabil Fayed , Hala Hassan Mohamed

There is an emerging wide use of nanotechnology in the medical fields. The information regarding distribution and clearance of gold nanoparticles (AuNPs) in the ocular tissue is insufficient. We investigated the cumulative effect of AuNPs on rat lens structure and their effect on the redox state and aquaporin-0 (AQP0) expression. Thirty-six male rats were distributed as follow: control, AuNPs-200 (200 μg/kg/rat for 4-weeks) and AuNPs-500 (500 μg/kg/rat for 4-weeks) groups. Rats were euthanized after 4-weeks, and the eye lenses were investigated for histological studies, transmission and scanning electron microscopic studies, immunohistochemistry for AQP0 and morphometric measures. Lens homogenates were investigated for tumour necrosis factor-alpha (TNF-α) and total reactive oxygen species levels by ELISA and for p-c-SRC by western-blot. AuNPs administration induced morphological and ultrastructural changes in rat lens. Degenerative changes in the lens epithelium, cytoplasmic vacuoles, distorted separated cortical lens fibers and loss of ball-and-socket junctions were observed. A significant reduction of AQP0-immune-staining with a significant elevation of TNF-α, total ROS and p-c-SRC content in rat lens homogenates were detected as compared to the control group. Repetitive spherical 20 nm-sized AuNPs administration, especially at 500 μg/kg/rat, induced structural changes in lens fibers of rats and increased oxidative stress level in the lens tissue.

纳米技术在医学领域的应用越来越广泛。关于金纳米颗粒（AuNPs）在眼组织中的分布和清除的信息是不充分的。我们研究了AuNPs对大鼠晶状体结构的累积效应及其对氧化还原状态和水通道蛋白-0 （AQP0）表达的影响。雄性大鼠36只，随机分为对照组、AuNPs-200组（200 μg/kg/大鼠，持续4周）和AuNPs-500组（500 μg/kg/大鼠，持续4周）。4周后处死大鼠，对眼晶状体进行组织学、透射电镜、扫描电镜、AQP0免疫组化及形态计量学检测。通过ELISA检测晶状体匀浆中肿瘤坏死因子-α (TNF-α)和总活性氧含量，western-blot检测p-c-SRC含量。AuNPs诱导大鼠晶状体形态和超微结构改变。晶状体上皮退行性改变，胞浆空泡，分离的皮质晶状体纤维变形，球窝连接丢失。与对照组相比，大鼠晶状体匀浆中aqp0免疫染色显著降低，TNF-α、总ROS和p-c-SRC含量显著升高。重复给药20 nm球形AuNPs，特别是500 μg/kg/大鼠，可引起大鼠晶状体纤维结构改变和晶状体组织氧化应激水平升高。

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引用次数: 0

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