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Preclinical safety evaluation of SloIron CFTN-PS 5: A pea-derived ferritin product
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2025.115291
Bradley J. Lampe , Margitta Dziwenka , Vincent P. Hackel
Ferritins are proteins present in plants and animals that are highly effective in storing iron and maintaining iron homeostasis. Iron deficiency anemia is a widespread nutritional disorder, and plant ferritins (phytoferritin) are potential sources of bioavailable iron with slow-release characteristics that prevent oxidative damage. These characteristics are related to receptor mediated endocytosis, the primary absorption mechanism in humans. However, the available toxicological data are insufficient to determine whether the use of phytoferritin as a nutritional supplement to enhance iron consumption in human populations is safe. Therefore, several GLP-compliant toxicology studies have been conducted with phytoferritin prepared from the seed of Psium sativum (trade name: SloIron CFTN-PS5). SloIron CFTN-PS5 was non-mutagenic and non-clastogenic in vitro and did not induce the formation of micronuclei in vivo. SloIron CFTN-PS5 was well-tolerated in a 90-day subchronic toxicity studies conducted in Sprague-Dawley rats at doses up to 1950 mg/kg bw/day. These findings suggest that the oral consumption of SloIron CFTN-PS5 is of low toxicological concern, with a 90-day oral subchronic No Observed Adverse Effect Level (NOAEL) of 1950 mg/kg-day, the highest dose tested.
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引用次数: 0
Atractylenolide III ameliorates DSS-induced colitis by improving intestinal epithelial barrier via suppressing the NF-κB-Mediated MLCK-pMLC signaling pathway 苍术内酯III通过抑制NF-κ b介导的MLCK-pMLC信号通路改善肠上皮屏障,改善dss诱导的结肠炎。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2024.115158
Ting-ting Dai , Wei Fang , Wen-tao Zhu , Zhi-li Han , Nian-xia Sun , Gang Yin , Dian-lei Wang
This study is to demonstrate the protection of atractylenolide III (AT III) on intestinal barrier dysfunction in ulcerative colitis (UC). UC model was established by 3% dextran sulfate sodium (DSS), and TNF-α was used to induce dysfunction in the intestinal epithelial barrier. TEER, FD-4 transmembrane flux and DAI were measured. Histopathological changes was identified by H&E staining, TJ structure changes were observed by TEM, IL-1β and TNF-α contents were measured by ELISA, bacterial translocation was investigated by FISH. The expressions of ZO-1, occludin, and the proteins in the MLCK/p-MLC and NF-κB pathways were analyzed by Western blotting or immunofluorescence. The results indicated that AT III alleviate the symptoms of DSS-induced colitis, reduce the disruption of intestinal epithelial barrier, and decrease FD4. Moreover, AT III inhibited the destruction of intestinal epithelial TJ structure and bacterial translocation in UC mice. AT III reversed the high levels of IL-1β and TNF-α, the decrease of occludin, ZO-1 expressions. Furthermore, AT III showed similar effects to PDTC (pyrrolidinedithiocarbamate) in ameliorating the disruption of the TNF-α-induced TEER and FD-4 disruption, MLCK protein expression, and MLC2 phosphorylation. In conclusion, AT III mitigates the dysfunction of intestinal epithelial barrier in UC through the NF-κB-mediated MLCK/p-MLC signaling pathway.
本研究旨在证明白术内酯III (atiii)对溃疡性结肠炎(UC)患者肠道屏障功能障碍的保护作用。用3%葡聚糖硫酸钠(DSS)建立UC模型,用TNF-α诱导肠上皮屏障功能障碍。测定TEER、FD-4跨膜通量和DAI。H&E染色观察组织病理变化,TEM观察TJ结构变化,ELISA检测IL-1β和TNF-α含量,FISH观察细菌易位。Western blotting或免疫荧光法检测ZO-1、occludin及MLCK/p-MLC、NF-κB通路蛋白的表达。结果表明,AT III可减轻dss诱导结肠炎的症状,减轻肠上皮屏障的破坏,降低FD4。此外,AT III抑制UC小鼠肠上皮TJ结构的破坏和细菌易位。AT III逆转高水平IL-1β、TNF-α, occludin、ZO-1表达降低。此外,AT III在改善TNF-α-诱导的TEER和FD-4破坏、MLCK蛋白表达和MLC2磷酸化方面表现出与PDTC(吡罗烷二硫代氨基甲酸酯)相似的效果。综上所述,AT III通过NF-κ b介导的MLCK/p-MLC信号通路减轻UC肠上皮屏障功能障碍。
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引用次数: 0
Molecular insights of T-2 toxin exposure-induced neurotoxicity and the neuroprotective effect of dimethyl fumarate T-2毒素暴露诱导的神经毒性和富马酸二甲酯的神经保护作用的分子机制。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2024.115166
Xingyao Pei , Shuhui Ma , Liang Hong , Zonghui Zuo , Gang Xu , Chun Chen , Yao Shen , Dingkuo Liu , Cun Li , Daowen Li
T-2 toxin, a potent environmental pollutant, has been proved to stimulate neuroinflammation, while the connection between T-2 toxin and pyroptosis remain elusive. Dimethyl fumarate (DMF), recently identified as a neuroprotectant and pyroptosis inhibitor, has potential therapeutic applications that are underexplored. Based on present study in vitro and vivo, we demonstrated that T-2 toxin induced the activation of NLRP3-Caspase-1 inflammasome in hippocampal neurons. In addition to proinflammatory mediator overexpression, gasdermin D (GSDMD)-dependently pyroptosis in the mouse hippocampal neuron cell line (HT22) treated by T-2 toxin was determined in our study. Moreover, the palliative effect of knockdown sequence of high mobility group B1 protein (HMGB1) provided more details for T-2 toxin-initiated pyroptosis. Importantly, we confirmed that DMF, as a novel inhibitor of GSDMD, could alleviate pyroptosis induced by T-2 toxin in an GSDMD targeting manner. In summary, our studies exposed the evidence that T-2 toxin could induce NLRP3 inflammasome activation and hippocampal neuronal pyroptosis. More notably, DMF was turn out to be a critical executioner for attenuating GSDMD-mediated pyroptosis. Our data found a new function of DMF and suggested a novel therapy strategy against mycotoxin-triggered neuronal inflammation, which leads to varieties of neurological diseases.
T-2毒素是一种强效的环境污染物,已被证明可刺激神经炎症,但T-2毒素与焦亡之间的联系尚不明确。富马酸二甲酯(DMF),最近被确定为神经保护剂和焦亡抑制剂,具有潜在的治疗应用尚未开发。在体外和体内实验的基础上,我们证实了T-2毒素诱导海马神经元NLRP3-Caspase-1炎症小体的激活。除促炎介质过表达外,本研究还检测了T-2毒素处理小鼠海马神经元细胞系(HT22)中gasdermin D (GSDMD)依赖性焦亡。此外,高迁移率组B1蛋白(HMGB1)敲低序列的缓解作用为T-2毒素引发的焦亡提供了更多的细节。重要的是,我们证实了DMF作为一种新的GSDMD抑制剂,能够以GSDMD靶向的方式减轻T-2毒素诱导的焦亡。总之,我们的研究揭示了T-2毒素可诱导NLRP3炎性体活化和海马神经元焦亡的证据。更值得注意的是,DMF被证明是减弱gsdmd介导的焦亡的关键刽子手。我们的数据发现了DMF的新功能,并提出了一种新的治疗策略,用于治疗真菌毒素引发的神经元炎症,这导致了各种神经系统疾病。
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引用次数: 0
Heavy metal contamination in cow and buffalo milk from industrial and residential areas of raipur, India: A health risk assessment 印度赖布尔工业区和居民区牛奶和水牛奶中的重金属污染:健康风险评估。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2024.115178
Anuradha Sharma , Shashi Gupta , Kamlesh Shrivas , Suryakant Chakradhari , Shamsh Pervez , Manas Kanti Deb
This study investigated heavy metal contamination in cow and buffalo milk from industrial and residential areas of Raipur, India, assessing health risks and identifying contamination sources. Milk samples were collected from seven sites and analyzed for Zn, Ni, Fe, Mn, Cu, Cr, Cd, Pb, and As using inductively coupled plasma-optical emission spectroscopy (ICP-OES) and atomic absorption spectroscopy (AAS). Results revealed higher contamination in industrial areas, with fodder being a primary source for Zn, Ni, Fe, and Cu, while water contributed to Mn, Cr, and As. Estimated daily intake (EDI), target hazard quotient (THQ), and carcinogenic risk (CR) determination highlighted non-carcinogenic risks for Ni, Fe, and Pb, and significant carcinogenic risks for Pb and As. The concentrations of Zn, Ni, Fe, Mn, Cu, Cr, Cd, Pb, and As in milk samples were ranged from 1.708 to 3.243, 0.078–0.295, 1.480–4.450, 0.119–0.472, 0.032–0.461, 0.007–0.040, 0.006–0.032, 0.040–0.204, and 0.006–0.023 mg/kg, respectively. The principal component analysis (PCA) identified fodder as a source of Zn, Ni, Fe, Cu, and Cd, while water contributed to Mn, Cr, and As. This study needed monitoring and regulation to mitigate health risks from contaminated milk in Raipur.
本研究调查了来自印度赖布尔工业区和居民区的牛奶和水牛奶中的重金属污染,评估了健康风险并确定了污染源。采用电感耦合等离子体发射光谱(ICP-OES)和原子吸收光谱(AAS)分析了7个地点的牛奶样品中Zn、Ni、Fe、Mn、Cu、Cr、Cd、Pb和As的含量。结果显示,工业区的污染程度较高,饲料是锌、镍、铁和铜的主要来源,而水是锰、铬和砷的主要来源。估计每日摄入量(EDI)、目标危害商(THQ)和致癌风险(CR)测定强调了Ni、Fe和Pb的非致癌风险,以及Pb和As的显著致癌风险。Zn、Ni、Fe、Mn、Cu、Cr、Cd、Pb和As的浓度分别为1.708 ~ 3.243、0.078 ~ 0.295、1.480 ~ 4.450、0.119 ~ 0.472、0.032 ~ 0.461、0.007 ~ 0.040、0.006 ~ 0.032、0.040 ~ 0.204和0.006 ~ 0.023 mg/kg。主成分分析(PCA)发现饲料是Zn、Ni、Fe、Cu和Cd的主要来源,而水是Mn、Cr和as的主要来源。这项研究需要监测和监管,以减轻赖布尔受污染牛奶带来的健康风险。
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引用次数: 0
Renoprotective effect of berberine in cisplatin-induced acute kidney injury: Role of Klotho and the AMPK/mtor/ULK1/Beclin-1 pathway 小檗碱在顺铂诱导的急性肾损伤中的肾保护作用:Klotho和AMPK/mTOR/ULK1/Beclin-1通路的作用
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2024.115179
Tasneem M. Salah, Mostafa A. Rabie, Nesrine S. El Sayed
Cisplatin (Cisp) is a potent cancer drug, but its use is limited by acute kidney injury (AKI). Autophagy, a process that removes damaged proteins and maintains cellular homeostasis, has been shown to alleviate Cisp-induced AKI. The balance between autophagy and apoptosis is crucial to kidney protection. Treatment with Berberine, known for its antioxidant and anti-inflammatory effects in nephrotoxicity models, was studied for its potential to enhance autophagy in Cisp-induced AKI.
Treatment with Berberine (Berb) upregulated Klotho gene expression, enhancing autophagy as indicated by elevated protein levels of pS486-AMPK, pS638-ULK1, and Beclin-1, accompanied by a decrease in pS248-mTOR protein expression. Also, Berb mitigated oxidative stress by reducing elevated MDA levels and boosting SOD activity, which in turn suppressed inflammation by down-regulating HMGB1 and RAGE gene expression, as well as reducing pS536-NF-κB and IL-6 protein contents. Additionally, Berb reduced apoptosis by increasing Bcl-2 and decreasing Bax. This coordinated action preserved kidney function, evidenced by reductions in early injury markers (cystatin C, KIM-1, NGAL) and late markers (creatinine, BUN), along with attenuation of histopathological alterations. The use 3-MA, autophagy inhibitor, nullified these protective effects, highlighting Berb's role in promoting autophagy, reducing oxidative stress, inflammation, and apoptosis, and preserving renal health in Cisp-induced AKI.
顺铂(Cisp.)是一种有效的抗癌药物,但其使用受到急性肾损伤(AKI)的限制。自噬,一种去除受损蛋白和维持细胞稳态的过程,已被证明可以减轻cisp诱导的AKI。自噬和细胞凋亡之间的平衡对肾脏保护至关重要。小檗碱在肾毒性模型中具有抗氧化和抗炎作用,研究了其在cisp诱导的AKI中增强自噬的潜力。小檗碱(Berberine, Berb)可上调Klotho基因表达,增强自噬,pS486-AMPK、pS638-ULK1和Beclin-1蛋白水平升高,同时pS248-mTOR蛋白表达降低。此外,小檗通过降低MDA水平和提高SOD活性来减轻氧化应激,从而通过下调HMGB1和RAGE基因表达以及降低pS536-NF-κB和IL-6蛋白含量来抑制炎症。此外,小檗通过增加Bcl-2和降低Bax来减少细胞凋亡。这种协同作用保留了肾功能,早期损伤标志物(胱抑素C、KIM-1、NGAL)和晚期标志物(肌酐、BUN)的减少以及组织病理学改变的减弱证明了这一点。自噬抑制剂3-MA的使用抵消了这些保护作用,强调了小檗在cisp诱导的AKI中促进自噬、减少氧化应激、炎症和细胞凋亡以及保持肾脏健康方面的作用。
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引用次数: 0
18β-glycyrrhetinic acid Mitigates bisphenol A-induced liver and renal damage: Inhibition of TNF-α/NF-κB/p38-MAPK, JAK1/STAT1 pathways, oxidative stress and apoptosis 18β-甘草次酸减轻双酚a诱导的肝脏和肾脏损害:抑制TNF-α/NF-κB/p38-MAPK, JAK1/STAT1通路,氧化应激和细胞凋亡。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2024.115218
Ekrem Darendelioglu , Cuneyt Caglayan , Sefa Küçükler , İbrahim Bayav , Fatih Mehmet Kandemir , Adnan Ayna , Sevda Sağ
Bisphenol A (BPA) has been commonly used in various consumer products, including water bottles, food containers, and canned food linings. However, there are concerns about its potential toxicity to human health, particularly its impact on the liver and kidneys. The objective of this research was to investigate the potential ameliorative effects of 18β-glycyrrhetinic acid (GA) against BPA-induced hepatotoxicity and nephrotoxicity in rats. The animals were supplemented with BPA (250 mg/kg b.w.) alone or with GA (50 and 100 mg/kg b.w.) for 14 days. GA treatment alleviated the BPA-induced hepato-renal tissue injuries through reducing the serum ALT, AST and ALP levels, and urea and creatinine levels. GA co-treatment also increased activities of SOD, CAT and GPx enzymes and levels of GSH, and suppressed MDA levels in BPA induced tissues. BPA also induced inflammation by increasing the levels of TNF-α, NF-κB, JAK1, STAT1, P38 MAPK and JNK in liver and kidney tissues and GA treatment ameliorated these effects. BPA triggered apoptosis by increasing caspase-3, Bax, and cytochrome c at protein levels and also by decreasing the antiapoptotic Bcl-2 level. However, treatment with GA (50 and 100 mg/kg) decreased apoptosis. Overall, our results have revealed the potential ameliorative mechanisms of GA, as a possible agent for BPA-induced hepatotoxicity and nephrotoxicity.
双酚A (BPA)通常用于各种消费品,包括水瓶、食品容器和罐头食品衬里。然而,人们担心其对人体健康的潜在毒性,特别是对肝脏和肾脏的影响。本研究旨在探讨18β-甘草次酸(GA)对bpa诱导的大鼠肝毒性和肾毒性的潜在改善作用。各组分别添加BPA (250 mg/kg b.w)或GA(50和100 mg/kg b.w),为期14 d。GA通过降低血清ALT、AST、ALP水平及尿素、肌酐水平减轻bpa所致的肝肾组织损伤。GA共处理提高了BPA诱导组织中SOD、CAT、GPx酶活性和GSH水平,抑制了MDA水平。BPA还通过增加肝脏和肾脏组织中TNF-α、NF-κB、JAK1、STAT1、P38 MAPK和JNK的水平诱导炎症,而GA治疗改善了这些作用。BPA通过增加caspase-3、Bax和细胞色素c蛋白水平以及降低抗凋亡Bcl-2水平触发细胞凋亡。然而,GA(50和100 mg/kg)可减少细胞凋亡。总的来说,我们的研究结果揭示了GA作为bpa诱导的肝毒性和肾毒性的可能药物的潜在改善机制。
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引用次数: 0
Chemopreventive effect of Pistacia vera leaf extract against mammary carcinoma induced by dimethyl-benz(a)anthracene in vivo and in vitro: Potential role of antioxidant, antiinflammatory and immune mechanisms 黄连木叶提取物对二甲苯(a)蒽致乳腺癌的体内外化学预防作用:抗氧化、抗炎和免疫机制的潜在作用
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2024.115229
Ali G. Alkhathami , Esmail M. El-Fakharany , Mohamed H. El-Sayed , Ahmed Atwa , Fatma Khairallah Ali , Nashwa Hamad , Hussam Askar , Mahmoud Ashry
This study aimed to define the antitumor effect of ethanolic extract of Pistacia vera leaves (PEE) toward breast cancer both in vitro and in vivo using dimethyl-benz(a)anthracene (DMBA)-induced breast tumor in adult female rats. PEE showed a potent antioxidant effect toward both DPPH (1,1-diphenyl-2-picrylhydrazyl) and ABTS (2,2′-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid) radicals with IC50 values of 72.6 and 107.4 μg/mL, respectively. PEE exerted its cytotoxicity in dose-dependent manners with favorable selectivity toward MCF-7 and MDA cancer cells, sparing normal WI-38 cells. Through considerable decreases in blood CA15.3, CEA, CA19.9, TNF-α, IL1β, IL-4, IL-6, and IL-10 levels, as well as mammary MDA and NO levels, PEE administration effectively improved the damage caused by breast cancer. Additionally, PEE exhibited remarkable increasing in mammary GSH content, GPx, SOD and CAT activities. The histopathological findings demonstrated the therapeutic potential of PEE that successfully improved the mammary gland alterations induced by DMBA and aborted cancer development. PEE has shown intriguing potential as an anti-inflammatory and antioxidant drug by targeting the expression of pro-inflammatory cytokines and oxidative stress indicators, which has helped to successfully treat malignancies in clinical settings. Collectively, our findings support chemo-preventive potential of PEE against DMBA-induced breast tumor in rats via enhancing apoptosis and immune response.
本研究旨在通过对二甲苯并蒽(DMBA)诱导的成年雌性大鼠乳腺肿瘤的体外和体内研究,确定黄连叶乙醇提取物(PEE)对乳腺癌的抗肿瘤作用。PEE对DPPH(1,1-二苯基-2-吡啶肼基)和ABTS(2,2'-氮基-双(3-乙基苯并噻唑-6-磺酸)自由基均有较强的抗氧化作用,IC50值分别为72.6和107.4 μg/mL。PEE以剂量依赖的方式发挥其细胞毒性,对MCF-7和MDA癌细胞具有良好的选择性,保留正常的WI-38细胞。PEE通过显著降低血CA15.3、CEA、CA19.9、TNF-α、il -1 β、IL-4、IL-6、IL-10水平以及乳腺MDA、NO水平,有效改善乳腺癌损伤。此外,PEE显著提高了乳腺GSH含量、GPx、SOD和CAT活性。组织病理学结果表明,PEE能够成功改善DMBA诱导的乳腺改变,并阻止癌症的发展。通过靶向促炎细胞因子和氧化应激指标的表达,PEE作为一种抗炎和抗氧化药物显示出了令人感兴趣的潜力,这有助于在临床环境中成功治疗恶性肿瘤。总的来说,我们的研究结果支持PEE通过增强细胞凋亡和免疫反应来预防dmba诱导的大鼠乳腺肿瘤的化学预防潜力。
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引用次数: 0
Evaluation of 9,10-anthraquinone contamination in tea products from Indonesian manufacturers and its carcinogenic risk to consumer health 印尼茶叶产品中9,10-蒽醌污染评价及其对消费者健康的致癌风险。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2025.115239
Harmoko Harmoko , Rahmana Emran Kartasasmita , Hasim Munawar , Dadan Rohdiana , Fransiska Kurniawan , Daryono Hadi Tjahjono , Amadeo R. Fernández-Alba
This study aimed to determine 9,10-anthraquinone (AQ) levels in Indonesian tea products from different manufacturers and assess the AQ's associated health risks. AQ levels increased significantly during withering and drying stages, using pinewood as a heat source. Generally, black tea was highly contaminated by AQ followed by green tea, oolong tea, and white tea. Out of a total of 116 samples from manufacturers using wood pellets as a heat source, 13% (15/116) of samples were contaminated with AQ exceeding the EU maximum residue level (MRL), and after accounting for measurement uncertainty, this value decreased to only 2% (2/116) that were deemed non-compliant. In contrast, 88% (57/65) and 50% (7/14) of tea samples were contaminated with AQ exceeding the EU MRL when manufacturers used pinewood and palm kernel shells as heat sources, respectively. However, based on our estimation, the risk level due to AQ exposure from Indonesian tea is still manageable, as indicated by calculating incremental lifetime cancer risk, <10⁻⁶ across all conditions studied (age group, type of tea, and heat source).
本研究旨在测定印尼不同厂家茶叶产品中9,10-蒽醌(AQ)的含量,并评估其相关的健康风险。以松木为热源,在干燥和枯干阶段,AQ水平显著升高。一般来说,红茶受空气污染的程度最高,其次是绿茶、乌龙茶和白茶。在使用木屑颗粒作为热源的制造商的116个样本中,13%(15/116)的样本被污染的AQ超过了欧盟最大残留水平(MRL),在考虑了测量不确定度之后,这个值下降到只有2%(2/116)被认为是不合规的。相比之下,88%(57/65)和50%(7/14)的茶叶样品在使用松木和棕榈仁壳作为热源时,污染的AQ分别超过了欧盟的MRL。然而,根据我们的估计,从印尼茶中暴露于空气毒素的风险水平仍然是可控的,正如计算终生癌症风险的增量所表明的那样,< 10⁻26在所有研究条件下(年龄组、茶的类型和热源)。
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引用次数: 0
Polysorbate 80 and carboxymethylcellulose: A different impact on epithelial integrity when interacting with the microbiome 聚山梨酯80和羧甲基纤维素:与微生物群相互作用时对上皮完整性的不同影响。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2025.115236
Alicia Bellanco, Teresa Requena, M. Carmen Martínez-Cuesta
The consumption of dietary emulsifiers, including polysorbate 80 (P80) and sodium carboxymethylcellulose (CMC), has raised safety concerns due to its interaction with the intestinal microbiome. This study demonstrated that increasing concentrations of P80 and CMC added to a dynamic four-stage gut microbiota model (BFBL gut simulator) altered the microbiome composition and impacted epithelial integrity in a dose-dependent manner. 16S rDNA amplicon-based metagenomics analysis revealed that these emulsifiers increased microbial groups with proinflammatory capacities while decreasing microbial taxa known to enhance barrier function. Increasing doses of P80 significantly decreased Bacteroides dorei and Akkermansia, taxa associated with anti-inflammatory potential, while increasing doses of CMC were linked to a higher abundance of Ruminococcus torques and Hungatella, which negatively impact barrier function. Both emulsifiers displayed a different impact on epithelial integrity when interacting with the microbiome. On one hand, supernatants from the BFBL simulator fed with P80 disrupted epithelial integrity to a lesser extent than the additive alone. On the other hand, both the microbiota and the supernatants from the BFBL simulator fed with CMC diminished the epithelial integrity, though the additive itself did not. These findings highlight the need to incorporate the gut microbiome in the risk assessment of these additives.
食用乳化剂,包括聚山梨酸酯80 (P80)和羧甲基纤维素钠(CMC),由于其与肠道微生物群的相互作用而引起了安全问题。该研究表明,在动态四阶段肠道微生物群模型(BFBL肠道模拟器)中添加P80和CMC浓度的增加会以剂量依赖的方式改变微生物组组成并影响上皮完整性。基于16S rDNA扩增子的宏基因组学分析显示,这些乳化剂增加了具有促炎能力的微生物群,同时减少了已知具有增强屏障功能的微生物群。增加P80剂量可显著降低与抗炎潜力相关的多拟杆菌和Akkermansia类群,而增加CMC剂量可增加Ruminococcus torques和Hungatella的丰度,从而对屏障功能产生负面影响。当乳化剂与微生物群相互作用时,两种乳化剂对上皮完整性的影响不同。一方面,添加P80的BFBL模拟器上清液对上皮完整性的破坏程度低于单独添加添加剂。另一方面,添加CMC的微生物群和BFBL模拟器的上清液都降低了上皮的完整性,但添加剂本身没有降低上皮的完整性。这些发现强调了在这些添加剂的风险评估中纳入肠道微生物组的必要性。
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引用次数: 0
Coconut oil reduces steroidogenic enzymes and imbalances estrogen receptors in the adrenal cortex of Mongolian gerbils 椰子油减少类固醇酶和失衡雌激素受体在蒙古沙鼠肾上腺皮质。
IF 3.9 3区 医学 Q2 FOOD SCIENCE & TECHNOLOGY Pub Date : 2025-02-01 DOI: 10.1016/j.fct.2025.115248
Vitor Grigio , Luiz Henrique Alves Guerra , Thalles Fernando Rocha Ruiz , Sebastião Roberto Taboga , Patrícia Simone Leite Vilamaior
This study aims to verify the effects of prolonged ingestion of coconut oil on the adrenal glands of Mongolian gerbils. Mongolian gerbils were used as an experimental model due to the morphological similarity of the adrenal glands to those of primates. Male Mongolian gerbils, 3 months of age, were divided into three experimental groups (n = 12): an intact control group, which received no treatment, a gavage control group, which received 0.1 ml of water daily by gavage, and a coconut oil-treated group, which received 0.1 ml of coconut oil daily for 12 months. The results showed that prolonged consumption of coconut oil caused an increase in cell area and thickness of the zona reticularis and the accumulation of lipid droplets, as well as reducing the amount of steroidogenic enzymes, such as CYP17, 3BHSD, and 17BHSD. It was also observed that the oil increased the expression of estrogen receptor alpha and their isoforms. These alterations allow us to conclude that changes in the lipid diet can cause alterations in the morphophysiology of the adrenal gland and, consequently, impact its functionality.
本研究旨在验证长期摄入椰子油对蒙古沙鼠肾上腺的影响。由于蒙古沙鼠的肾上腺形态与灵长类动物相似,我们选择蒙古沙鼠作为实验模型。选取3月龄雄性蒙古沙鼠,分为3个实验组(n=12):完整对照组,不进行任何处理;灌食对照组,每天灌食0.1 ml水;椰子油处理组,每天灌食0.1 ml椰子油,连续12个月。结果表明,长时间食用椰子油导致网状带细胞面积和厚度增加,脂滴积聚,并导致CYP17、3BHSD、17BHSD等甾体生成酶的数量减少。还观察到精油增加了雌激素受体α及其同型异构体的表达。这些改变使我们得出结论,脂质饮食的改变会导致肾上腺形态生理的改变,从而影响其功能。
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引用次数: 0
期刊
Food and Chemical Toxicology
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