Pub Date : 2025-02-01DOI: 10.1016/j.fct.2025.115243
Jinghua Shen , Jingjing Gao , Xinyi Wang , Dongying Yan , Ying Wang , Hong Li , Dawei Chen , Jie Wu
Flame retardant polybrominated diphenyl ethers (PBDEs) accumulate in human bodies through food and dust ingestion, and cause neurobehavioral deficits with obscure mechanism. We aimed to investigate NMDAR-CaMKⅡγ-mediated synapse-to-nuclear communication involved in BDE-209-induced cognitive impairment, and alleviation from exogenous melatonin. Decreased NMDAR subunits GluN2A and 2B, autophosphorylation of CaMKⅡα, and postsynaptic GluA1 trafficking were observed in the hippocampus of juvenile rats after maternal BDE-209 exposure. Moreover, nuclear shuttling of CaMKⅡγ with CaM, as well as downstream nuclear p-CaMKIV and p-CREB-dependent genes (Bdnf, c-Fos, Arc) expression were all causally down-regulated. These resulted in less dendritic spines in CA1 area and poor spatial learning and memory. Importantly, elevated miR-219a-5p in transcriptome sequencing was identified together with its targets Grin2b and Camk2g mRNA, further elucidated the reduction in GluN2B and CaMKⅡγ protein. These changes on synaptic plasticity caused by BDE-209 were reversed correspondingly under pretreatment of melatonin, partially via miR-219a inhibition. Collectively, our findings suggest that synaptonuclear signaling alterations potentially mediated neurobehavioral deficits induced by early-life BDE-209 exposure and the neuroprotection from melatonin, therefore provided a novel perspective for prevention.
{"title":"Melatonin attenuates BDE-209-caused spatial memory deficits in juvenile rats through NMDAR-CaMKⅡγ-mediated synapse-to-nucleus signaling","authors":"Jinghua Shen , Jingjing Gao , Xinyi Wang , Dongying Yan , Ying Wang , Hong Li , Dawei Chen , Jie Wu","doi":"10.1016/j.fct.2025.115243","DOIUrl":"10.1016/j.fct.2025.115243","url":null,"abstract":"<div><div>Flame retardant polybrominated diphenyl ethers (PBDEs) accumulate in human bodies through food and dust ingestion, and cause neurobehavioral deficits with obscure mechanism. We aimed to investigate NMDAR-CaMKⅡγ-mediated synapse-to-nuclear communication involved in BDE-209-induced cognitive impairment, and alleviation from exogenous melatonin. Decreased NMDAR subunits GluN2A and 2B, autophosphorylation of CaMKⅡα, and postsynaptic GluA1 trafficking were observed in the hippocampus of juvenile rats after maternal BDE-209 exposure. Moreover, nuclear shuttling of CaMKⅡγ with CaM, as well as downstream nuclear p-CaMKIV and p-CREB-dependent genes (<em>Bdnf</em>, <em>c-Fos</em>, <em>Arc</em>) expression were all causally down-regulated. These resulted in less dendritic spines in CA1 area and poor spatial learning and memory. Importantly, elevated miR-219a-5p in transcriptome sequencing was identified together with its targets <em>Grin2b</em> and <em>Camk2g</em> mRNA, further elucidated the reduction in GluN2B and CaMKⅡγ protein. These changes on synaptic plasticity caused by BDE-209 were reversed correspondingly under pretreatment of melatonin, partially via miR-219a inhibition. Collectively, our findings suggest that synaptonuclear signaling alterations potentially mediated neurobehavioral deficits induced by early-life BDE-209 exposure and the neuroprotection from melatonin, therefore provided a novel perspective for prevention.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115243"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942072","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.2025.115244
Renner Philipe Rodrigues Carvalho , Rosiany Vieira da Costa , Isadora Ribeiro de Carvalho , Arabela Guedes Azevedo Viana , Camilo Ramirez Lopez , Mariana Souza Oliveira , Luiz Otavio Guimarães-Ervilha , Wassali Valadares de Sousa , Daniel Silva Sena Bastos , Edgar Diaz Miranda , Fábio César Sousa Nogueira , Mariana Machado-Neves
Eugenol has pharmacological properties, but its impact on renal function is limitedly studied. Thus, this study evaluated the effects of eugenol at 10, 20, and 40 mg kg−1, administered via gavage for 60 days, on histological, biochemical, oxidative, and proteomic parameters in rat kidneys. Adult Wistar rats treated with 10 mg kg−1 of eugenol had kidneys with low total antioxidant capacity, high nitric oxide content, and high percentual of blood vessels, with no damage to renal function or morphology. The kidney proteome revealed an upregulation of proteins associated with energy metabolism, oxidative stress, and mitochondrial function. Eugenol at 20 mg kg−1 did not alter kidney histology but inhibited Na+/K+ ATPase activity. This dose elicited an upregulation of proteins associated with mitochondrial function and cellular defense. Finally, 40 mg kg−1 eugenol had more pronounced effects on the kidney, increasing serum sodium, potassium, and chloride levels, inhibiting Na+/K+ ATPase activity, triggering an adaptive response to oxidative stress, and showing apical brush border thinness in proximal tubules. We concluded that eugenol exerted dose-dependent effects on kidney function and morphology. These findings highlight the importance of careful consideration of eugenol's dosage in therapeutic applications.
{"title":"Dose-related effects of eugenol: Exploring renal functionality and morphology in healthy Wistar rats","authors":"Renner Philipe Rodrigues Carvalho , Rosiany Vieira da Costa , Isadora Ribeiro de Carvalho , Arabela Guedes Azevedo Viana , Camilo Ramirez Lopez , Mariana Souza Oliveira , Luiz Otavio Guimarães-Ervilha , Wassali Valadares de Sousa , Daniel Silva Sena Bastos , Edgar Diaz Miranda , Fábio César Sousa Nogueira , Mariana Machado-Neves","doi":"10.1016/j.fct.2025.115244","DOIUrl":"10.1016/j.fct.2025.115244","url":null,"abstract":"<div><div>Eugenol has pharmacological properties, but its impact on renal function is limitedly studied. Thus, this study evaluated the effects of eugenol at 10, 20, and 40 mg kg<sup>−1</sup>, administered via gavage for 60 days, on histological, biochemical, oxidative, and proteomic parameters in rat kidneys. Adult Wistar rats treated with 10 mg kg<sup>−1</sup> of eugenol had kidneys with low total antioxidant capacity, high nitric oxide content, and high percentual of blood vessels, with no damage to renal function or morphology. The kidney proteome revealed an upregulation of proteins associated with energy metabolism, oxidative stress, and mitochondrial function. Eugenol at 20 mg kg<sup>−1</sup> did not alter kidney histology but inhibited Na<sup>+</sup>/K<sup>+</sup> ATPase activity. This dose elicited an upregulation of proteins associated with mitochondrial function and cellular defense. Finally, 40 mg kg<sup>−1</sup> eugenol had more pronounced effects on the kidney, increasing serum sodium, potassium, and chloride levels, inhibiting Na<sup>+</sup>/K<sup>+</sup> ATPase activity, triggering an adaptive response to oxidative stress, and showing apical brush border thinness in proximal tubules. We concluded that eugenol exerted dose-dependent effects on kidney function and morphology. These findings highlight the importance of careful consideration of eugenol's dosage in therapeutic applications.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115244"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963335","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.2024.115201
Si-Yao Cheng , Yi-Fan Yang , Ya-Long Wang , Zhao-Ping Yue , Yan-Zhu Chen , Wen-Ke Wang , Zhi-Ran Xu , Lin-Feng Li , Hao Shen , Zhi-Min Qi , Chang-Long Xu , Yu Liu
Triptolide (TPL), a prominent bioactive constituent derived from the Chinese herb Tripterygium wilfordii, exhibits diverse pharmacological effects such as anti-tumor and anti-immune properties. Despite its extensive clinical application for the treatment of arthritis and immune disorders, TPL has been associated with multiorgan toxicity, including adverse effects on the female reproductive system. However, the precise mechanisms underlying TPL-induced ovarian damage remain poorly understood. In this study, employing a mouse toxicological model, exposure to TPL was observed to result in decreased ovarian coefficient and fertility. Subsequent research demonstrated TPL exposure affected mitochondrial function, increased mitochondrial outer membrane permeability, resulted in mtDNA releasing into the cytoplasm. These events subsequently activated cGAS-STING pathway, leading to ovarian inflammation. Furthermore, TPL exposure has been found to disrupt the meiotic maturation of oocytes, which is mechanistically associated with suboptimal morphology of spindle and microtubule organizing centers (MTOCs). This association has been further confirmed through the use of reduced representation bisulfite sequencing (RRBS). In conclusion, our study demonstrates that TPL exposure can hinder follicular development, resulting in ovarian inflammation and reduced oocyte quality.
{"title":"Triptolide exposure triggers ovarian inflammation by activating cGAS-STING pathway and decrease oocyte quality in mouse","authors":"Si-Yao Cheng , Yi-Fan Yang , Ya-Long Wang , Zhao-Ping Yue , Yan-Zhu Chen , Wen-Ke Wang , Zhi-Ran Xu , Lin-Feng Li , Hao Shen , Zhi-Min Qi , Chang-Long Xu , Yu Liu","doi":"10.1016/j.fct.2024.115201","DOIUrl":"10.1016/j.fct.2024.115201","url":null,"abstract":"<div><div>Triptolide (TPL), a prominent bioactive constituent derived from the Chinese herb <em>Tripterygium wilfordii</em>, exhibits diverse pharmacological effects such as anti-tumor and anti-immune properties. Despite its extensive clinical application for the treatment of arthritis and immune disorders, TPL has been associated with multiorgan toxicity, including adverse effects on the female reproductive system. However, the precise mechanisms underlying TPL-induced ovarian damage remain poorly understood. In this study, employing a mouse toxicological model, exposure to TPL was observed to result in decreased ovarian coefficient and fertility. Subsequent research demonstrated TPL exposure affected mitochondrial function, increased mitochondrial outer membrane permeability, resulted in mtDNA releasing into the cytoplasm. These events subsequently activated cGAS-STING pathway, leading to ovarian inflammation. Furthermore, TPL exposure has been found to disrupt the meiotic maturation of oocytes, which is mechanistically associated with suboptimal morphology of spindle and microtubule organizing centers (MTOCs). This association has been further confirmed through the use of reduced representation bisulfite sequencing (RRBS). In conclusion, our study demonstrates that TPL exposure can hinder follicular development, resulting in ovarian inflammation and reduced oocyte quality.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115201"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821581","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.2024.115202
Ozge Kandemir , Sefa Kucukler , Selim Comakli , Cihan Gur , Mustafa İleriturk
Approximately 20 million new cancer cases have occurred worldwide, and dose limitation occurs because of the liver and kidney toxicity of chemotherapeutic agents. Inflammation/apoptosis/ROS pathways appear to be activated in the liver and kidney toxicity of chemotherapeutic agents. This study was conducted to investigate the potential effects of silymarin (SLY) use against docetaxel (DTX)-induced liver and kidney damage in rats. For this purpose, 30 mg/kg DTX was administered intraperitoneally to Sprague Dawley rats on the first day of the study, followed by SLY (25 or 50 mg/kg/day) orally for 7 days. Then, various analyses were performed on liver and kidney tissues using biochemical, molecular and histological methods. The data obtained showed that DTX administration suppressed antioxidant markers and increased lipid peroxidation in liver and kidney tissues. It was also determined that DTX administration triggered markers of endoplasmic reticulum stress, inflammation, apoptosis and autophagy. On the other hand, SLY treatment increased enzymatic and non-enzymatic antioxidant levels and decreased malondialdehyde levels. Additionally, SLY alleviated DTX-induced endoplasmic reticulum stress, inflammation, apoptosis and autophagy in liver and kidney tissues. Immunohistochemical analyses showed that DTX increased the density of 8-OHdG positive cells in liver and kidney tissues, while oxidative DNA damage decreased after SLY administration. ALT, AST, ALP, Urea and Creatinine levels increased in the DTX group and decreased in the SLY treatment groups. In conclusion, DTX administration caused toxicity in liver and kidney tissues and damaged tissue integrity, while SLY treatment alleviated DTX-induced toxicity.
{"title":"Docetaxel-induced liver and kidney toxicity in rats can be alleviated by suppressing oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis and autophagy signaling pathways after Silymarin treatment","authors":"Ozge Kandemir , Sefa Kucukler , Selim Comakli , Cihan Gur , Mustafa İleriturk","doi":"10.1016/j.fct.2024.115202","DOIUrl":"10.1016/j.fct.2024.115202","url":null,"abstract":"<div><div>Approximately 20 million new cancer cases have occurred worldwide, and dose limitation occurs because of the liver and kidney toxicity of chemotherapeutic agents. Inflammation/apoptosis/ROS pathways appear to be activated in the liver and kidney toxicity of chemotherapeutic agents. This study was conducted to investigate the potential effects of silymarin (SLY) use against docetaxel (DTX)-induced liver and kidney damage in rats. For this purpose, 30 mg/kg DTX was administered intraperitoneally to Sprague Dawley rats on the first day of the study, followed by SLY (25 or 50 mg/kg/day) orally for 7 days. Then, various analyses were performed on liver and kidney tissues using biochemical, molecular and histological methods. The data obtained showed that DTX administration suppressed antioxidant markers and increased lipid peroxidation in liver and kidney tissues. It was also determined that DTX administration triggered markers of endoplasmic reticulum stress, inflammation, apoptosis and autophagy. On the other hand, SLY treatment increased enzymatic and non-enzymatic antioxidant levels and decreased malondialdehyde levels. Additionally, SLY alleviated DTX-induced endoplasmic reticulum stress, inflammation, apoptosis and autophagy in liver and kidney tissues. Immunohistochemical analyses showed that DTX increased the density of 8-OHdG positive cells in liver and kidney tissues, while oxidative DNA damage decreased after SLY administration. ALT, AST, ALP, Urea and Creatinine levels increased in the DTX group and decreased in the SLY treatment groups. In conclusion, DTX administration caused toxicity in liver and kidney tissues and damaged tissue integrity, while SLY treatment alleviated DTX-induced toxicity.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115202"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142826940","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.2025.115237
Diane C. Mitchell , Megan Trout , Ross Smith , Robyn Teplansky , Harris R. Lieberman
Caffeine is a popular stimulant, predominantly consumed from beverages. The caffeinated beverage marketplace is continually evolving resulting in considerable interest in understanding the impact caffeinated beverages have on levels of intakes. Therefore, estimates of caffeine intakes in the U.S. population were calculated using a recent 2022 beverage survey, the Kantar Worldpanel Enhanced Beverage Service. A nationally representative sample of 49,700 consumers (aged ≥2 years) completed a 1-day beverage intake survey which collected data on beverage type/category, amount and brand. Approximately 69% of the U.S. population consumed at least one caffeinated beverage per day. The mean (±SE) daily caffeine intake of caffeine consumers (age >2 years) from all beverages was 210 ± 1.5 mg. Caffeine intake was highest in consumers aged 50–64 years (246 ± 4.5 mg/day) and lowest in children aged 2–5 (42 ± 2.4 mg/day). At the 90th percentile intake was 520 mg/day for all ages combined. Coffee was the largest contributor (69%) to caffeine intake across all age groups followed by carbonated soft drinks (15.4%), tea (8.8%), and energy drinks (6.3%). This study indicates that an increase in caffeine intake has occurred with a corresponding shift in beverage consumption patterns compared to previous surveys.
{"title":"An update on beverage consumption patterns and caffeine intakes in a representative sample of the US population","authors":"Diane C. Mitchell , Megan Trout , Ross Smith , Robyn Teplansky , Harris R. Lieberman","doi":"10.1016/j.fct.2025.115237","DOIUrl":"10.1016/j.fct.2025.115237","url":null,"abstract":"<div><div>Caffeine is a popular stimulant, predominantly consumed from beverages. The caffeinated beverage marketplace is continually evolving resulting in considerable interest in understanding the impact caffeinated beverages have on levels of intakes. Therefore, estimates of caffeine intakes in the U.S. population were calculated using a recent 2022 beverage survey, the Kantar Worldpanel Enhanced Beverage Service. A nationally representative sample of 49,700 consumers (aged ≥2 years) completed a 1-day beverage intake survey which collected data on beverage type/category, amount and brand. Approximately 69% of the U.S. population consumed at least one caffeinated beverage per day. The mean (±SE) daily caffeine intake of caffeine consumers (age >2 years) from all beverages was 210 ± 1.5 mg. Caffeine intake was highest in consumers aged 50–64 years (246 ± 4.5 mg/day) and lowest in children aged 2–5 (42 ± 2.4 mg/day). At the 90th percentile intake was 520 mg/day for all ages combined. Coffee was the largest contributor (69%) to caffeine intake across all age groups followed by carbonated soft drinks (15.4%), tea (8.8%), and energy drinks (6.3%). This study indicates that an increase in caffeine intake has occurred with a corresponding shift in beverage consumption patterns compared to previous surveys.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115237"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942069","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.2024.115232
Hong Huang , Ziyan Li , Zhanghua Qi , Linxi Ma , Gang Hu , Changwei Zou , Tingtao Chen
The highly toxic aflatoxin B1 (AFB1) is considered one of the primary risk factors for hepatocellular carcinoma, while effective measures after AFB1 exposure remain to be optimized. This study utilized cell-surface-display technique to construct an engineered S. cerevisiae-pYD1-ScFv-AFB1 (S.C-AF) that specifically binds AFB1, and verified the potential mechanism of S.C-AF in vivo through AFB1-induced (gastric perfused with 0.3 mg/kg/d AFB1 per day) liver injury mouse model. In this experiment, the C57BL/6 mouse model of AFB1-induced liver injury was treated with S.C (gastric perfused with 1 × 109 CFU/mL S.C per day) and S.C-AF (gastric perfused with 1 × 109 CFU/mL S.C-AF per day) for 4 weeks, respectively. With probiotic properties optimized, S.C.-AF achieved an in vitro AFB1 binding capacity 1.7 times higher than S. cerevisiae. Furthermore, S.C-AF could alleviate AFB1-induced liver injury by reducing proinflammatory cytokine secretion and apoptotic protein expression, enhancing antioxidative capacity via Nrf2 activation, and simultaneously reversing intestinal tight junction protein deficiency, increasing intestinal barrier permeability, and improving intestinal dysbiosis caused by AFB1 exposure. S.C-AF alleviates AFB1-induced liver lesions, which might be a novel intervention to mitigate aflatoxin toxicity.
{"title":"Engineered S. cerevisiae-pYD1-ScFv-AFB1 mitigates aflatoxin B1 toxicity via bio-binding and intestinal microenvironment repair","authors":"Hong Huang , Ziyan Li , Zhanghua Qi , Linxi Ma , Gang Hu , Changwei Zou , Tingtao Chen","doi":"10.1016/j.fct.2024.115232","DOIUrl":"10.1016/j.fct.2024.115232","url":null,"abstract":"<div><div>The highly toxic aflatoxin B1 (AFB1) is considered one of the primary risk factors for hepatocellular carcinoma, while effective measures after AFB1 exposure remain to be optimized. This study utilized cell-surface-display technique to construct an engineered <em>S. cerevisiae</em>-pYD1-ScFv-AFB1 (S.C-AF) that specifically binds AFB1, and verified the potential mechanism of S.C-AF <em>in vivo</em> through AFB1-induced (gastric perfused with 0.3 mg/kg/d AFB1 per day) liver injury mouse model. In this experiment, the C57BL/6 mouse model of AFB1-induced liver injury was treated with S.C (gastric perfused with 1 × 10<sup>9</sup> CFU/mL S.C per day) and S.C-AF (gastric perfused with 1 × 10<sup>9</sup> CFU/mL S.C-AF per day) for 4 weeks, respectively. With probiotic properties optimized, S.C.-AF achieved an <em>in vitro</em> AFB1 binding capacity 1.7 times higher than <em>S. cerevisiae.</em> Furthermore, S.C-AF could alleviate AFB1-induced liver injury by reducing proinflammatory cytokine secretion and apoptotic protein expression, enhancing antioxidative capacity <em>via</em> Nrf2 activation, and simultaneously reversing intestinal tight junction protein deficiency, increasing intestinal barrier permeability, and improving intestinal dysbiosis caused by AFB1 exposure. S.C-AF alleviates AFB1-induced liver lesions, which might be a novel intervention to mitigate aflatoxin toxicity.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115232"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142918713","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.2024.115234
Fernanda Santos Portela , Lara Fabiana Luz Malheiro , Caroline Assunção Oliveira , Érika Azenathe Barros Mercês , Lais Mafra De Benedictis , Júlia Mafra De Benedictis , Ana Jullie Veiga Fernandes , Bruna Santos Silva , Júlia Spínola Ávila , Thiago Macêdo Lopes Correia , Márcio Vasconcelos Oliveira , Patrícia da Silva Oliveira , Amélia Cristina Mendes de Magalhães , Telma de Jesus Soares , Fabrício Freire de Melo , Liliany Souza de Brito Amaral
Cisplatin (CP) is an antineoplastic drug associated with various cytotoxic adverse effects, including hepatotoxicity. Exercise training may offer hepatoprotection by improving redox status. This study compared the effects of light-intensity continuous training (LICT), moderate-intensity continuous training (MICT), and high-intensity interval training (HIIT) on CP-induced hepatotoxicity in female Wistar rats. The rats were divided into five groups (n = 7): sedentary control (C + S), CP and sedentary (CP + S), CP with LICT (CP + LICT), CP with MICT (CP + MICT), and CP with HIIT (CP + HIIT). The training protocols involved eight weeks of treadmill exercise before CP administration (5 mg/kg). Seven days after CP injection, the rats were euthanized to collect blood and liver tissue samples. Our findings demonstrate that HIIT was the most effective protocol in preventing histopathological alterations and reducing oxidative and nitrosative damage markers in macromolecules, including 4-HNE (lipids), nitrotyrosine (proteins), and 8-OHdG (DNA). The reduction in these markers appears to be linked to decreased CYP2E1 levels. Moreover, HIIT activated the Nrf2 pathway and upregulated its downstream antioxidant enzymes, including SOD1, catalase, GPx, and HO-1. In conclusion, HIIT emerged as the most effective protocol for mitigating hepatic damage, likely through CYP2E1 suppression and enhancement of antioxidant defenses via Nrf2 signaling pathway activation.
{"title":"High-intensity interval training improves hepatic redox status via Nrf2 downstream pathways and reduced CYP2E1 expression in female rats with cisplatin-induced hepatotoxicity","authors":"Fernanda Santos Portela , Lara Fabiana Luz Malheiro , Caroline Assunção Oliveira , Érika Azenathe Barros Mercês , Lais Mafra De Benedictis , Júlia Mafra De Benedictis , Ana Jullie Veiga Fernandes , Bruna Santos Silva , Júlia Spínola Ávila , Thiago Macêdo Lopes Correia , Márcio Vasconcelos Oliveira , Patrícia da Silva Oliveira , Amélia Cristina Mendes de Magalhães , Telma de Jesus Soares , Fabrício Freire de Melo , Liliany Souza de Brito Amaral","doi":"10.1016/j.fct.2024.115234","DOIUrl":"10.1016/j.fct.2024.115234","url":null,"abstract":"<div><div>Cisplatin (CP) is an antineoplastic drug associated with various cytotoxic adverse effects, including hepatotoxicity. Exercise training may offer hepatoprotection by improving redox status. This study compared the effects of light-intensity continuous training (LICT), moderate-intensity continuous training (MICT), and high-intensity interval training (HIIT) on CP-induced hepatotoxicity in female Wistar rats. The rats were divided into five groups (n = 7): sedentary control (C + S), CP and sedentary (CP + S), CP with LICT (CP + LICT), CP with MICT (CP + MICT), and CP with HIIT (CP + HIIT). The training protocols involved eight weeks of treadmill exercise before CP administration (5 mg/kg). Seven days after CP injection, the rats were euthanized to collect blood and liver tissue samples. Our findings demonstrate that HIIT was the most effective protocol in preventing histopathological alterations and reducing oxidative and nitrosative damage markers in macromolecules, including 4-HNE (lipids), nitrotyrosine (proteins), and 8-OHdG (DNA). The reduction in these markers appears to be linked to decreased CYP2E1 levels. Moreover, HIIT activated the Nrf2 pathway and upregulated its downstream antioxidant enzymes, including SOD1, catalase, GPx, and HO-1. In conclusion, HIIT emerged as the most effective protocol for mitigating hepatic damage, likely through CYP2E1 suppression and enhancement of antioxidant defenses via Nrf2 signaling pathway activation.</div></div>","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"196 ","pages":"Article 115234"},"PeriodicalIF":3.9,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142918748","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 : 2025-01-31DOI: 10.1016/j.fct.2025.115303
Rahma F. Ezz El-Arab , Hanan S.A. Waly , M. Bassam Al-Salahy , Moustafa A. Saleh , Shaimaa M.M. Saleh
Tartrazine (Tz) is one of the most commonly used artificial food colorants in the food industry, found in a wide array of products. This study investigates the protective role of gallic acid (GA), a powerful antioxidant, against the adverse effects of Tz on the liver. Over a 30-day period, 40 rats were divided into two groups: Group 1 (control group, 10 rats) received a daily administration of a vehicle, while Group 2 (30 rats) received Tz (30 mg/kg body weight). Group 2 was further subdivided into three subgroups of 10 rats each: Subgroup 1 served as a positive control for Tz; Subgroup 2 received GA (200 mg/kg body weight); and Subgroup 3 was left untreated for an additional 30 days as a recovery group (TR). Our study revealed that GA normalized liver functions markers (ALT, AST, and bilirubin), regulated lipids (cholesterol, HDL, LDL, and TG), and ameliorated the redox potentials activity of liver tissue (Catalase, GSH, SOD, LPO, Total peroxide, and Carbonyl protein), revealing its potential in mitigating the negative impact of Tz administration. Moreover, histopathological examinations, including the TUNEL assay, and histological and histochemical studies, demonstrated that GA effectively prevented the histological damage caused by Tz administration.
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Pub Date : 2025-01-31DOI: 10.1016/j.fct.2025.115283
A.M. Api , A. Bartlett , D. Belsito , D. Botelho , M. Bruze , A. Bryant-Friedrich , G.A. Burton Jr. , M.A. Cancellieri , H. Chon , M. Cronin , S. Crotty , M.L. Dagli , W. Dekant , C. Deodhar , K. Farrell , A.D. Fryer , L. Jones , K. Joshi , A. Lapczynski , D.L. Laskin , Y. Thakkar
{"title":"RIFM fragrance ingredient safety assessment, β-methyl-benzenepentanal, CAS registry number 55066-49-4","authors":"A.M. Api , A. Bartlett , D. Belsito , D. Botelho , M. Bruze , A. Bryant-Friedrich , G.A. Burton Jr. , M.A. Cancellieri , H. Chon , M. Cronin , S. Crotty , M.L. Dagli , W. Dekant , C. Deodhar , K. Farrell , A.D. Fryer , L. Jones , K. Joshi , A. Lapczynski , D.L. Laskin , Y. Thakkar","doi":"10.1016/j.fct.2025.115283","DOIUrl":"10.1016/j.fct.2025.115283","url":null,"abstract":"","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"197 ","pages":"Article 115283"},"PeriodicalIF":3.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072992","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 : 2025-01-31DOI: 10.1016/j.fct.2025.115284
A.M. Api , A. Bartlett , D. Belsito , D. Botelho , M. Bruze , A. Bryant-Friedrich , G.A. Burton Jr. , M.A. Cancellieri , H. Chon , M. Cronin , S. Crotty , M.L. Dagli , W. Dekant , C. Deodhar , K. Farrell , A.D. Fryer , L. Jones , K. Joshi , A. Lapczynski , D.L. Laskin , Y. Thakkar
{"title":"RIFM fragrance ingredient safety assessment, trans-4-decen-1-al, CAS Registry Number 65405-70-1","authors":"A.M. Api , A. Bartlett , D. Belsito , D. Botelho , M. Bruze , A. Bryant-Friedrich , G.A. Burton Jr. , M.A. Cancellieri , H. Chon , M. Cronin , S. Crotty , M.L. Dagli , W. Dekant , C. Deodhar , K. Farrell , A.D. Fryer , L. Jones , K. Joshi , A. Lapczynski , D.L. Laskin , Y. Thakkar","doi":"10.1016/j.fct.2025.115284","DOIUrl":"10.1016/j.fct.2025.115284","url":null,"abstract":"","PeriodicalId":317,"journal":{"name":"Food and Chemical Toxicology","volume":"197 ","pages":"Article 115284"},"PeriodicalIF":3.9,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072990","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}
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