Jennifer Barbosa Dos Santos, Rodrigo Brasil Choueri, Francisco Eduardo Melo Dos Santos, Laís Adrielle de Oliveira Santos, Letícia Fernanda da Silva, Caio Rodrigues Nobre, Milton Alexandre Cardoso, Renata de Britto Mari, Fábio Ruiz Simões, Tomas Angel Delvalls, Paloma Kachel Gusso-Choueri
The rise of "fast fashion" has driven up the production of low-cost, short-lived clothing, significantly increasing global textile fiber production and, consequently, exacerbating environmental pollution. This study investigated the ecotoxicological effects of different types of anthropogenic microfibers-cotton, polyester, and mixed fibers (50% cotton: 50% polyester)-on marine organisms, specifically sea urchin embryos. All tested fibers exhibited toxicity, with cotton fibers causing notable effects on embryonic development even at environmentally relevant concentrations. The research also simulated a scenario where microfibers were immersed in seawater for 30 days to assess changes in toxicity over time. The results showed that the toxicity of microfibers increased with both concentration and exposure duration, with polyester being the most toxic among the fibers tested. Although synthetic fibers have been the primary focus of previous research, this study highlights that natural fibers like cotton, which are often overlooked, can also be toxic due to the presence of harmful additives. These natural fibers, despite decomposing faster than synthetic ones, can persist in aquatic environments for extended periods. The findings underline the critical need for further research on both natural and synthetic microfibers to understand their environmental impact and potential threats to marine ecosystems and sea urchin populations.
{"title":"Are Microfibers a Threat to Marine Invertebrates? A Sea Urchin Toxicity Assessment.","authors":"Jennifer Barbosa Dos Santos, Rodrigo Brasil Choueri, Francisco Eduardo Melo Dos Santos, Laís Adrielle de Oliveira Santos, Letícia Fernanda da Silva, Caio Rodrigues Nobre, Milton Alexandre Cardoso, Renata de Britto Mari, Fábio Ruiz Simões, Tomas Angel Delvalls, Paloma Kachel Gusso-Choueri","doi":"10.3390/toxics12100753","DOIUrl":"https://doi.org/10.3390/toxics12100753","url":null,"abstract":"<p><p>The rise of \"fast fashion\" has driven up the production of low-cost, short-lived clothing, significantly increasing global textile fiber production and, consequently, exacerbating environmental pollution. This study investigated the ecotoxicological effects of different types of anthropogenic microfibers-cotton, polyester, and mixed fibers (50% cotton: 50% polyester)-on marine organisms, specifically sea urchin embryos. All tested fibers exhibited toxicity, with cotton fibers causing notable effects on embryonic development even at environmentally relevant concentrations. The research also simulated a scenario where microfibers were immersed in seawater for 30 days to assess changes in toxicity over time. The results showed that the toxicity of microfibers increased with both concentration and exposure duration, with polyester being the most toxic among the fibers tested. Although synthetic fibers have been the primary focus of previous research, this study highlights that natural fibers like cotton, which are often overlooked, can also be toxic due to the presence of harmful additives. These natural fibers, despite decomposing faster than synthetic ones, can persist in aquatic environments for extended periods. The findings underline the critical need for further research on both natural and synthetic microfibers to understand their environmental impact and potential threats to marine ecosystems and sea urchin populations.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11510891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anthony Radzimirski, Michael Croft, Nicholas Ireland, Lydia Miller, Jennifer Newell-Caito, Samuel Caito
The lanthanide series elements are transition metals used as critical components of electronics, as well as rechargeable batteries, fertilizers, antimicrobials, contrast agents for medical imaging, and diesel fuel additives. With the surge in their utilization, lanthanide metals are being found more in our environment. However, little is known about the health effects associated with lanthanide exposure. Epidemiological studies as well as studies performed in rodents exposed to lanthanum (La) suggest neurological damage, learning and memory impairment, and disruption of neurotransmitter signaling, particularly in serotonin and dopamine pathways. Unfortunately, little is known about the neurological effects of heavier lanthanides. As dysfunctions of serotonergic and dopaminergic signaling are implicated in multiple neurological conditions, including Parkinson's disease, depression, generalized anxiety disorder, and post-traumatic stress disorder, it is of utmost importance to determine the effects of La and other lanthanides on these neurotransmitter systems. We therefore hypothesized that early-life exposure of light [La (III) or cerium (Ce (III))] or heavy [erbium (Er (III)) or ytterbium (Yb (III))] lanthanides in Caenorhabditis elegans could cause dysregulation of serotonergic and dopaminergic signaling upon adulthood. Serotonergic signaling was assessed by measuring pharyngeal pump rate, crawl-to-swim transition, as well as egg-laying behaviors. Dopaminergic signaling was assessed by measuring locomotor rate and egg-laying and swim-to-crawl transition behaviors. Treatment with La (III), Ce (III), Er (III), or Yb (III) caused deficits in serotonergic or dopaminergic signaling in all assays, suggesting both the heavy and light lanthanides disrupt these neurotransmitter systems. Concomitant with dysregulation of neurotransmission, all four lanthanides increased reactive oxygen species (ROS) generation and decreased glutathione and ATP levels. This suggests increased oxidative stress, which is a known modifier of neurotransmission. Altogether, our data suggest that both heavy and light lanthanide series elements disrupt serotonergic and dopaminergic signaling and may affect the development or pharmacological management of related neurological conditions.
镧系元素是过渡金属,可用作电子产品的关键成分,也可用作充电电池、肥料、抗菌剂、医学成像造影剂和柴油添加剂。随着镧系金属的使用量激增,在我们的环境中发现的镧系金属也越来越多。然而,人们对接触镧系元素对健康的影响知之甚少。流行病学研究以及对暴露于镧(La)的啮齿类动物进行的研究表明,镧(La)会对神经系统造成损害、影响学习和记忆,并破坏神经递质信号转导,尤其是在血清素和多巴胺通路中。遗憾的是,人们对较重的镧系元素对神经系统的影响知之甚少。由于血清素能和多巴胺能信号传导功能障碍与多种神经系统疾病有关,包括帕金森病、抑郁症、广泛性焦虑症和创伤后应激障碍,因此确定 La 和其他镧系元素对这些神经递质系统的影响至关重要。因此,我们假设,草履虫早期暴露于轻[La (III)或铈(Ce (III)]]或重[铒(Er (III))或镱(Yb (III)]]镧系元素可能会导致其成年后血清素能和多巴胺能信号传导失调。通过测量咽泵速率、爬行到游泳的转变以及产卵行为来评估血清素能信号传导。多巴胺能信号通过测量运动速率、产卵和游泳到爬行的过渡行为进行评估。在所有试验中,用 La (III)、Ce (III)、Er (III) 或 Yb (III) 处理都会导致血清素能或多巴胺能信号的缺失,这表明重镧系元素和轻镧系元素都会破坏这些神经递质系统。在神经传递失调的同时,所有四种镧系元素都增加了活性氧(ROS)的生成,降低了谷胱甘肽和 ATP 的水平。这表明氧化应激增加,而氧化应激是已知的神经传递调节因子。总之,我们的数据表明,重镧系元素和轻镧系元素都会破坏5-羟色胺能和多巴胺能信号传导,并可能影响相关神经系统疾病的发展或药物治疗。
{"title":"Dopaminergic- and Serotonergic-Dependent Behaviors Are Altered by Lanthanide Series Metals in <i>Caenorhabditis elegans</i>.","authors":"Anthony Radzimirski, Michael Croft, Nicholas Ireland, Lydia Miller, Jennifer Newell-Caito, Samuel Caito","doi":"10.3390/toxics12100754","DOIUrl":"https://doi.org/10.3390/toxics12100754","url":null,"abstract":"<p><p>The lanthanide series elements are transition metals used as critical components of electronics, as well as rechargeable batteries, fertilizers, antimicrobials, contrast agents for medical imaging, and diesel fuel additives. With the surge in their utilization, lanthanide metals are being found more in our environment. However, little is known about the health effects associated with lanthanide exposure. Epidemiological studies as well as studies performed in rodents exposed to lanthanum (La) suggest neurological damage, learning and memory impairment, and disruption of neurotransmitter signaling, particularly in serotonin and dopamine pathways. Unfortunately, little is known about the neurological effects of heavier lanthanides. As dysfunctions of serotonergic and dopaminergic signaling are implicated in multiple neurological conditions, including Parkinson's disease, depression, generalized anxiety disorder, and post-traumatic stress disorder, it is of utmost importance to determine the effects of La and other lanthanides on these neurotransmitter systems. We therefore hypothesized that early-life exposure of light [La (III) or cerium (Ce (III))] or heavy [erbium (Er (III)) or ytterbium (Yb (III))] lanthanides in <i>Caenorhabditis elegans</i> could cause dysregulation of serotonergic and dopaminergic signaling upon adulthood. Serotonergic signaling was assessed by measuring pharyngeal pump rate, crawl-to-swim transition, as well as egg-laying behaviors. Dopaminergic signaling was assessed by measuring locomotor rate and egg-laying and swim-to-crawl transition behaviors. Treatment with La (III), Ce (III), Er (III), or Yb (III) caused deficits in serotonergic or dopaminergic signaling in all assays, suggesting both the heavy and light lanthanides disrupt these neurotransmitter systems. Concomitant with dysregulation of neurotransmission, all four lanthanides increased reactive oxygen species (ROS) generation and decreased glutathione and ATP levels. This suggests increased oxidative stress, which is a known modifier of neurotransmission. Altogether, our data suggest that both heavy and light lanthanide series elements disrupt serotonergic and dopaminergic signaling and may affect the development or pharmacological management of related neurological conditions.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511074/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Alzheimer's disease (AD) is the most common cause of dementia and cognitive decline in the elderly. Although the etiology of AD is unknow, an increase in amyloid precursor protein (APP) leads to the toxic aggregation of Aβ plaques. Several factors, such as hypertension, diabetes, dyslipidemia, smoking, hormonal changes, and metal exposure, could increase the risk of developing AD. In this review, we will examine the role of copper (Cu) in the pathophysiology of AD, as well as the mechanisms involved in neurotoxicity and cognitive decline.
Methods: This review was conducted in accordance with PRISMA guidelines. We performed a comprehensive literature analysis over the last ten years on AD and Cu. Only late-onset Alzheimer's disease was considered; only studies on elderly people of both sexes were included.
Results: A total of seven articles were picked for this review, three studies focused on non-ceruloplasmin-bound Copper (non-Cp-Cu) and four on ceruloplasmin-bound Copper (Cp-Cu). The results showed higher Cu concentrations in patients compared to healthy controls.
Conclusions: Elevated concentrations of Cu may contribute to the progression of AD, potentially interacting with ATP7B mutations, oxidative stress (OS), and amyloid-β plaques. Future research is needed to provide more robust evidence and better characterize the relationship between AD and Cu.
背景:阿尔茨海默病(AD)是导致老年人痴呆和认知能力下降的最常见原因。虽然阿尔茨海默病的病因尚不清楚,但淀粉样前体蛋白(APP)的增加会导致 Aβ 斑块的毒性聚集。高血压、糖尿病、血脂异常、吸烟、荷尔蒙变化和金属接触等多种因素都可能增加罹患AD的风险。在这篇综述中,我们将研究铜(Cu)在AD病理生理学中的作用,以及参与神经毒性和认知能力下降的机制:本综述根据 PRISMA 指南进行。我们对过去十年间有关 AD 和铜的文献进行了全面分析。只考虑了晚发性阿尔茨海默病;只纳入了对男女老年人的研究:本综述共选取了七篇文章,其中三篇研究的重点是非髓磷蛋白结合铜(non-Cp-Cu),四篇研究的重点是髓磷蛋白结合铜(Cp-Cu)。结果显示,与健康对照组相比,患者体内的铜浓度更高:结论:铜浓度升高可能会与ATP7B突变、氧化应激(OS)和淀粉样蛋白-β斑块相互作用,导致AD进展。未来的研究需要提供更有力的证据,并更好地描述AD与铜之间的关系。
{"title":"The Role of Copper in Alzheimer's Disease Etiopathogenesis: An Updated Systematic Review.","authors":"Angela Sabalic, Veronica Mei, Giuliana Solinas, Roberto Madeddu","doi":"10.3390/toxics12100755","DOIUrl":"https://doi.org/10.3390/toxics12100755","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is the most common cause of dementia and cognitive decline in the elderly. Although the etiology of AD is unknow, an increase in amyloid precursor protein (APP) leads to the toxic aggregation of Aβ plaques. Several factors, such as hypertension, diabetes, dyslipidemia, smoking, hormonal changes, and metal exposure, could increase the risk of developing AD. In this review, we will examine the role of copper (Cu) in the pathophysiology of AD, as well as the mechanisms involved in neurotoxicity and cognitive decline.</p><p><strong>Methods: </strong>This review was conducted in accordance with PRISMA guidelines. We performed a comprehensive literature analysis over the last ten years on AD and Cu. Only late-onset Alzheimer's disease was considered; only studies on elderly people of both sexes were included.</p><p><strong>Results: </strong>A total of seven articles were picked for this review, three studies focused on non-ceruloplasmin-bound Copper (non-Cp-Cu) and four on ceruloplasmin-bound Copper (Cp-Cu). The results showed higher Cu concentrations in patients compared to healthy controls.</p><p><strong>Conclusions: </strong>Elevated concentrations of Cu may contribute to the progression of AD, potentially interacting with ATP7B mutations, oxidative stress (OS), and amyloid-β plaques. Future research is needed to provide more robust evidence and better characterize the relationship between AD and Cu.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Florin-Ioan Fechete, Maria Popescu, Sorin-Marian Mârza, Loredana-Elena Olar, Ionel Papuc, Florin-Ioan Beteg, Robert-Cristian Purdoiu, Andrei Răzvan Codea, Caroline-Maria Lăcătuș, Ileana-Rodica Matei, Radu Lăcătuș, Adela Hoble, Ioan Valentin Petrescu-Mag, Florin-Dumitru Bora
Heavy metal contamination in agricultural soils presents serious environmental and health risks. This study assessed the bioaccumulation and spatial distribution of nickel, cadmium, zinc, lead, and copper within a sheep-based food chain in the Baia Mare region, Romania, which includes soil, green grass, sheep serum, and dairy products. Using inductively coupled plasma mass spectrometry (ICP-MS), we analyzed the concentrations of these metals and calculated bioconcentration factors (BCFs) to evaluate their transfer through trophic levels. Spatial analysis revealed that copper (up to 2528.20 mg/kg) and zinc (up to 1821.40 mg/kg) exceeded permissible limits, particularly near former mining sites. Elevated lead (807.59 mg/kg) and cadmium (2.94 mg/kg) were observed in industrial areas, while nickel and cobalt showed lower concentrations, but with localized peaks. Zinc was the most abundant metal in grass, while cadmium transferred efficiently to milk and cheese, raising potential health concerns. The results underscore the complex interplay between soil properties, contamination sources, and biological processes in heavy metal accumulation. These findings highlight the importance of continuous monitoring, risk assessment, and mitigation strategies to protect public health from potential exposure through contaminated dairy products.
{"title":"Spatial and Bioaccumulation of Heavy Metals in a Sheep-Based Food System: Implications for Human Health.","authors":"Florin-Ioan Fechete, Maria Popescu, Sorin-Marian Mârza, Loredana-Elena Olar, Ionel Papuc, Florin-Ioan Beteg, Robert-Cristian Purdoiu, Andrei Răzvan Codea, Caroline-Maria Lăcătuș, Ileana-Rodica Matei, Radu Lăcătuș, Adela Hoble, Ioan Valentin Petrescu-Mag, Florin-Dumitru Bora","doi":"10.3390/toxics12100752","DOIUrl":"https://doi.org/10.3390/toxics12100752","url":null,"abstract":"<p><p>Heavy metal contamination in agricultural soils presents serious environmental and health risks. This study assessed the bioaccumulation and spatial distribution of nickel, cadmium, zinc, lead, and copper within a sheep-based food chain in the Baia Mare region, Romania, which includes soil, green grass, sheep serum, and dairy products. Using inductively coupled plasma mass spectrometry (ICP-MS), we analyzed the concentrations of these metals and calculated bioconcentration factors (BCFs) to evaluate their transfer through trophic levels. Spatial analysis revealed that copper (up to 2528.20 mg/kg) and zinc (up to 1821.40 mg/kg) exceeded permissible limits, particularly near former mining sites. Elevated lead (807.59 mg/kg) and cadmium (2.94 mg/kg) were observed in industrial areas, while nickel and cobalt showed lower concentrations, but with localized peaks. Zinc was the most abundant metal in grass, while cadmium transferred efficiently to milk and cheese, raising potential health concerns. The results underscore the complex interplay between soil properties, contamination sources, and biological processes in heavy metal accumulation. These findings highlight the importance of continuous monitoring, risk assessment, and mitigation strategies to protect public health from potential exposure through contaminated dairy products.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Minamata disease, caused by ingesting seafood contaminated with methylmercury dumped by corporations, was discovered in 1956; however, there has been no continued investigation to determine the full extent of the damage. Since 2004, it has been discovered that affected patients can be found in areas further away from Minamata than previously known. In the present study, we investigated various symptoms and somatosensory disturbances in western Miyanokawachi District, northern Himedo District, southwestern Nagashima District, and the uncontaminated Amami district and calculated the proportion of patients with sensory disturbances as a percentage of the population in each area. Both touch and pain sensations, with a predominance of the peripheral extremities, were observed in 58.6% of patients in Miyanokawachi, 53.9% in Himedo, 37.8% in Nagashima, and 1.4% in Amami. The lowest estimates of attributable fractions of the exposed group for four-limb-predominant sensory disturbance in the population of the contaminated districts were 94.1% in Miyanokawachi, 94.6% in Himedo, and 91.4% in Nagashima, and general and perioral sensory disturbances were also high. This suggests that the presence or absence of these sensory disturbances is useful in the diagnosis of Minamata disease, even in more distant parts of the Yatsushiro Sea area.
{"title":"Health Effects of Methylmercury in Coastal Areas of the Yatsushiro Sea, Far from Minamata.","authors":"Shigeru Takaoka, Tadashi Fujino, Shin-Ichi Shigeoka, Yaeko Itai","doi":"10.3390/toxics12100751","DOIUrl":"https://doi.org/10.3390/toxics12100751","url":null,"abstract":"<p><p>Minamata disease, caused by ingesting seafood contaminated with methylmercury dumped by corporations, was discovered in 1956; however, there has been no continued investigation to determine the full extent of the damage. Since 2004, it has been discovered that affected patients can be found in areas further away from Minamata than previously known. In the present study, we investigated various symptoms and somatosensory disturbances in western Miyanokawachi District, northern Himedo District, southwestern Nagashima District, and the uncontaminated Amami district and calculated the proportion of patients with sensory disturbances as a percentage of the population in each area. Both touch and pain sensations, with a predominance of the peripheral extremities, were observed in 58.6% of patients in Miyanokawachi, 53.9% in Himedo, 37.8% in Nagashima, and 1.4% in Amami. The lowest estimates of attributable fractions of the exposed group for four-limb-predominant sensory disturbance in the population of the contaminated districts were 94.1% in Miyanokawachi, 94.6% in Himedo, and 91.4% in Nagashima, and general and perioral sensory disturbances were also high. This suggests that the presence or absence of these sensory disturbances is useful in the diagnosis of Minamata disease, even in more distant parts of the Yatsushiro Sea area.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ivan Khokhlov, Leonid Legashev, Irina Bolodurina, Alexander Shukhman, Daniil Shoshin, Svetlana Kolesnik
Predicting the toxicity of nanoparticles plays an important role in biomedical nanotechnologies, in particular in the creation of new drugs. Safety analysis of nanoparticles can identify potentially harmful effects on living organisms and the environment. Advanced machine learning models are used to predict the toxicity of nanoparticles in a nutrient solution. In this article, we performed a comparative analysis of the current state of research in the field of nanoparticle toxicity analysis using machine learning methods; we trained a regression model for predicting the quantitative toxicity of nanoparticles depending on their concentration in the nutrient solution at a fixed point in time with the achieved metrics values of MSE = 2.19 and RMSE = 1.48; we trained a multi-class classification model for predicting the toxicity class of nanoparticles depending on their concentration in the nutrient solution at a fixed point in time with the achieved metrics values of Accuracy = 0.9756, Recall = 0.9623, F1-Score = 0.9640, and Log Loss = 0.1855. As a result of the analysis, we concluded the good predictive ability of the trained models. The optimal dosages for the nanoparticles under study were determined as follows: ZnO = 9.5 × 10-5 mg/mL; Fe3O4 = 0.1 mg/mL; SiO2 = 1 mg/mL. The most significant features of predictive models are the diameter of the nanoparticle and the nanoparticle concentration in the nutrient solution.
{"title":"Prediction of Dynamic Toxicity of Nanoparticles Using Machine Learning.","authors":"Ivan Khokhlov, Leonid Legashev, Irina Bolodurina, Alexander Shukhman, Daniil Shoshin, Svetlana Kolesnik","doi":"10.3390/toxics12100750","DOIUrl":"https://doi.org/10.3390/toxics12100750","url":null,"abstract":"<p><p>Predicting the toxicity of nanoparticles plays an important role in biomedical nanotechnologies, in particular in the creation of new drugs. Safety analysis of nanoparticles can identify potentially harmful effects on living organisms and the environment. Advanced machine learning models are used to predict the toxicity of nanoparticles in a nutrient solution. In this article, we performed a comparative analysis of the current state of research in the field of nanoparticle toxicity analysis using machine learning methods; we trained a regression model for predicting the quantitative toxicity of nanoparticles depending on their concentration in the nutrient solution at a fixed point in time with the achieved metrics values of MSE = 2.19 and RMSE = 1.48; we trained a multi-class classification model for predicting the toxicity class of nanoparticles depending on their concentration in the nutrient solution at a fixed point in time with the achieved metrics values of Accuracy = 0.9756, Recall = 0.9623, F1-Score = 0.9640, and Log Loss = 0.1855. As a result of the analysis, we concluded the good predictive ability of the trained models. The optimal dosages for the nanoparticles under study were determined as follows: ZnO = 9.5 × 10<sup>-5</sup> mg/mL; Fe<sub>3</sub>O<sub>4</sub> = 0.1 mg/mL; SiO<sub>2</sub> = 1 mg/mL. The most significant features of predictive models are the diameter of the nanoparticle and the nanoparticle concentration in the nutrient solution.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human exposure to arsenic and other toxic elements such as cadmium, lead and mercury may lead to a wide range of adverse health effects. In relation to this, it is well established that the diet is the main route of exposure to both essential and toxic trace elements. In recent years, the levels of toxic elements in foodstuffs have been measured in numerous studies conducted all over the world. Scientific databases show that, in the current century, China and Spain have been the countries where the most surveys on this topic have been carried out. Regarding Spain, Catalonia is the region where most studies aimed at determining the concentrations of trace elements in food have been performed. The objective of this paper was to review the studies carried out in Catalonia on the concentrations of As and toxic metals (including Cd, Hg and Pb) in food, as well as their estimated dietary intakes (EDIs). The results of total diet studies (TDSs) and duplicate diet (DD) studies have been included. For most toxic elements, a continued reduction in the EDI has been observed. This reduction is associated with a decrease in their concentrations in food, and with certain changes in dietary habits. Fish and seafood is the food group showing the highest content of toxic elements. However, none of the adult groups exceeded-in general-the safety thresholds for As, Cd, Hg and Pb established by the European Food Safety Agency (EFSA).
{"title":"Human Exposure through the Diet to Arsenic and Other Toxic Elements: A Literature Review of Scientific Studies Conducted in Catalonia, Spain, in the Current Century.","authors":"Jose L Domingo","doi":"10.3390/toxics12100749","DOIUrl":"https://doi.org/10.3390/toxics12100749","url":null,"abstract":"<p><p>Human exposure to arsenic and other toxic elements such as cadmium, lead and mercury may lead to a wide range of adverse health effects. In relation to this, it is well established that the diet is the main route of exposure to both essential and toxic trace elements. In recent years, the levels of toxic elements in foodstuffs have been measured in numerous studies conducted all over the world. Scientific databases show that, in the current century, China and Spain have been the countries where the most surveys on this topic have been carried out. Regarding Spain, Catalonia is the region where most studies aimed at determining the concentrations of trace elements in food have been performed. The objective of this paper was to review the studies carried out in Catalonia on the concentrations of As and toxic metals (including Cd, Hg and Pb) in food, as well as their estimated dietary intakes (EDIs). The results of total diet studies (TDSs) and duplicate diet (DD) studies have been included. For most toxic elements, a continued reduction in the EDI has been observed. This reduction is associated with a decrease in their concentrations in food, and with certain changes in dietary habits. Fish and seafood is the food group showing the highest content of toxic elements. However, none of the adult groups exceeded-in general-the safety thresholds for As, Cd, Hg and Pb established by the European Food Safety Agency (EFSA).</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11510889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yuting Wang, Jia Xu, Liujie Yang, Nan Zhang, Liwen Zhang, Bin Han
<p><p>Urinary polycyclic aromatic hydrocarbon (PAH) metabolites are associated with oxidative stress; however, epidemiological studies have not reported the impacts of these urinary PAH metabolites on blood lipid levels. This study investigated the relationship between urinary PAH metabolites, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), and blood lipid profiles. A total of 109 elderly volunteers were recruited with complete datasets for analysis. Blood and morning urine samples were collected in the winter of 2011. The PAH metabolites, creatinine, and 8-OHdG levels in urine samples were analyzed using Gas Chromatography-Mass Spectrometry, spectrophotometry, and an ELISA kit, respectively. The blood lipid profiles were analyzed using an automatic biochemical analyzer. The relationship between lipid profiles and 8-OHdG was assessed using a two-independent sample nonparametric test, categorized by gender, smoking, and alcohol consumption status. After normalizing the concentration values, a general linear regression model was employed to examine the correlations between PAH metabolites, 8-OHdG, and lipid profiles. A mediation model was developed to investigate the mediating effect of 8-OHdG on the relationship between PAH metabolites and lipid profiles. The median of eight PAH metabolite concentrations in urine samples ranged from 1 to 10 μmol/mol creatinine (Cr). Significant differences in lipid profiles were observed across genders. However, no significant differences were found in smoking or alcohol consumption status for both genders. Linear regression analysis revealed that an increase in the logarithmic concentration of 2-hydroxynaphthalene (2-OHNap), 9-hydroxyfluorene (9-OHFlu), 3-hydroxyfluorene (3-OHFlu), 2-hydroxyfluorene (2-OHFlu), 1-hydroxypyrene (1-OHPyr), and 6-hydroxychrysene (6-OHChr) was associated with an increase in urinary 8-OHdG levels, after adjusting for BMI and age. Specifically, 1-hydroxynaphthalene (1-OHNap) and 1-OHPyr correlated negatively with apolipoprotein A1 (Apo A1). Conversely, 1-OHPyr was positively correlated with low-density lipoprotein cholesterol (LDL-C). In addition, b,c-dihydroxyphenanthrene (2-OHBcPhe) was positively associated with apolipoprotein B (Apo B). Notably, 8-OHdG did not exhibit a significant correlation with lipid profiles. The mediating effect of 8-OHdG on the relationship between hydroxylated PAHs and lipid profiles was not statistically significant. However, the indirect effects of hydroxylated PAHs on blood lipids were statistically substantial, specifically for 1-OHNap to Apo A1 (-0.025, 95% CI: -0.041, -0.009), 1-OHPyr to LDL-C (0.107, 95% CI: 0.011, 0.203), and 2-OHBcPhe to Apo B (0.070, 95% CI: 0.005, 0.135). This study suggests that an increase in urinary PAH metabolites may elevate the levels of urinary 8-OHdG and influence blood lipid profiles. However, no direct relationship was found between 8-OHdG and lipid profiles. The mediation analysis indicated that the effects of PAH metabol
{"title":"The Effect of Urinary Polycyclic Aromatic Hydrocarbon Metabolites on Lipid Profiles: Does Oxidative Stress Play a Crucial Mediation Role?","authors":"Yuting Wang, Jia Xu, Liujie Yang, Nan Zhang, Liwen Zhang, Bin Han","doi":"10.3390/toxics12100748","DOIUrl":"https://doi.org/10.3390/toxics12100748","url":null,"abstract":"<p><p>Urinary polycyclic aromatic hydrocarbon (PAH) metabolites are associated with oxidative stress; however, epidemiological studies have not reported the impacts of these urinary PAH metabolites on blood lipid levels. This study investigated the relationship between urinary PAH metabolites, urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), and blood lipid profiles. A total of 109 elderly volunteers were recruited with complete datasets for analysis. Blood and morning urine samples were collected in the winter of 2011. The PAH metabolites, creatinine, and 8-OHdG levels in urine samples were analyzed using Gas Chromatography-Mass Spectrometry, spectrophotometry, and an ELISA kit, respectively. The blood lipid profiles were analyzed using an automatic biochemical analyzer. The relationship between lipid profiles and 8-OHdG was assessed using a two-independent sample nonparametric test, categorized by gender, smoking, and alcohol consumption status. After normalizing the concentration values, a general linear regression model was employed to examine the correlations between PAH metabolites, 8-OHdG, and lipid profiles. A mediation model was developed to investigate the mediating effect of 8-OHdG on the relationship between PAH metabolites and lipid profiles. The median of eight PAH metabolite concentrations in urine samples ranged from 1 to 10 μmol/mol creatinine (Cr). Significant differences in lipid profiles were observed across genders. However, no significant differences were found in smoking or alcohol consumption status for both genders. Linear regression analysis revealed that an increase in the logarithmic concentration of 2-hydroxynaphthalene (2-OHNap), 9-hydroxyfluorene (9-OHFlu), 3-hydroxyfluorene (3-OHFlu), 2-hydroxyfluorene (2-OHFlu), 1-hydroxypyrene (1-OHPyr), and 6-hydroxychrysene (6-OHChr) was associated with an increase in urinary 8-OHdG levels, after adjusting for BMI and age. Specifically, 1-hydroxynaphthalene (1-OHNap) and 1-OHPyr correlated negatively with apolipoprotein A1 (Apo A1). Conversely, 1-OHPyr was positively correlated with low-density lipoprotein cholesterol (LDL-C). In addition, b,c-dihydroxyphenanthrene (2-OHBcPhe) was positively associated with apolipoprotein B (Apo B). Notably, 8-OHdG did not exhibit a significant correlation with lipid profiles. The mediating effect of 8-OHdG on the relationship between hydroxylated PAHs and lipid profiles was not statistically significant. However, the indirect effects of hydroxylated PAHs on blood lipids were statistically substantial, specifically for 1-OHNap to Apo A1 (-0.025, 95% CI: -0.041, -0.009), 1-OHPyr to LDL-C (0.107, 95% CI: 0.011, 0.203), and 2-OHBcPhe to Apo B (0.070, 95% CI: 0.005, 0.135). This study suggests that an increase in urinary PAH metabolites may elevate the levels of urinary 8-OHdG and influence blood lipid profiles. However, no direct relationship was found between 8-OHdG and lipid profiles. The mediation analysis indicated that the effects of PAH metabol","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Boyang Li, Yun Shao, Chen Liu, Jie Wang, Yanzhong Zhu, Xiaoqian Li
2,2',4,4'-tetrabromodiphenyl ether (BDE-47) is a widely used brominated flame retardant belonging to persistent organic pollutants (POPs). After being released into the marine environment, BDE-47 can cause a range of toxic effects on marine organisms through bioaccumulation, biomagnification, and intergenerational transmission. These effects include lethality, impaired motility, photosynthetic toxicity, immune damage, liver toxicity, developmental impairments, and reproductive toxicity. This article reviews the latest research progress on the toxic effects and molecular mechanisms of BDE-47 mentioned above. The primary mechanisms underlying its toxicity include oxidative stress, DNA damage, cellular apoptosis, impaired metabolism, and activation of the MAPK signaling cascade.
{"title":"Toxicological Effects and Mechanisms of 2,2',4,4'-Tetrabromodiphenyl Ether (BDE-47) on Marine Organisms.","authors":"Boyang Li, Yun Shao, Chen Liu, Jie Wang, Yanzhong Zhu, Xiaoqian Li","doi":"10.3390/toxics12100747","DOIUrl":"https://doi.org/10.3390/toxics12100747","url":null,"abstract":"<p><p>2,2',4,4'-tetrabromodiphenyl ether (BDE-47) is a widely used brominated flame retardant belonging to persistent organic pollutants (POPs). After being released into the marine environment, BDE-47 can cause a range of toxic effects on marine organisms through bioaccumulation, biomagnification, and intergenerational transmission. These effects include lethality, impaired motility, photosynthetic toxicity, immune damage, liver toxicity, developmental impairments, and reproductive toxicity. This article reviews the latest research progress on the toxic effects and molecular mechanisms of BDE-47 mentioned above. The primary mechanisms underlying its toxicity include oxidative stress, DNA damage, cellular apoptosis, impaired metabolism, and activation of the MAPK signaling cascade.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11510862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chia-Chen Wu, Danielle N Meyer, Alex Haimbaugh, Tracie R Baker
Lead (Pb) is a well-known neurotoxin with established adverse effects on the neurological functions of children and younger adults, including motor, learning, and memory abilities. However, its potential impact on older adults has received less attention. Using the zebrafish model, our study aims to characterize the dose-response relationship between environmentally relevant Pb exposure levels and their effects on changes in behavior and transcriptomics during the geriatric periods. We exposed two-year-old zebrafish to waterborne lead acetate (1, 10, 100, 1000, or 10,000 µg/L) or a vehicle (DMSO) for 5 days. While lower concentrations (1-100 µg/L) reflect environmentally relevant Pb levels, higher concentrations (1000-10,000 µg/L) were included to assess acute toxicity under extreme exposure scenarios. We conducted adult behavior assessment to evaluate the locomotor activity following exposure. The same individual fish were subsequently sacrificed for brain dissection after a day of recovery in the aquatic system. RNA extraction and sequencing were then performed to evaluate the Pb-induced transcriptomic changes. Higher (1000-10,000 ug/L) Pb levels induced hyperactive locomotor patterns in aged zebrafish, while lower (10-100 ug/L) Pb levels resulted in the lowest locomotor activity compared to the control group. Exposure to 100 µg/L led to the highest number of differentially expressed genes (DEGs), while 10,000 µg/L induced larger fold changes in both directions. The neurological pathways impacted by Pb exposure include functions related to neurotransmission, such as cytoskeletal regulation and synaptogenesis, and oxidative stress response, such as mitochondrial dysfunction and downregulation of heat shock protein genes. These findings emphasize a U-shape dose-response relationship with Pb concentrations in locomotor activity and transcriptomic changes in the aging brain.
{"title":"Implications of Lead (Pb)-Induced Transcriptomic and Phenotypic Alterations in the Aged Zebrafish (<i>Danio rerio</i>).","authors":"Chia-Chen Wu, Danielle N Meyer, Alex Haimbaugh, Tracie R Baker","doi":"10.3390/toxics12100745","DOIUrl":"https://doi.org/10.3390/toxics12100745","url":null,"abstract":"<p><p>Lead (Pb) is a well-known neurotoxin with established adverse effects on the neurological functions of children and younger adults, including motor, learning, and memory abilities. However, its potential impact on older adults has received less attention. Using the zebrafish model, our study aims to characterize the dose-response relationship between environmentally relevant Pb exposure levels and their effects on changes in behavior and transcriptomics during the geriatric periods. We exposed two-year-old zebrafish to waterborne lead acetate (1, 10, 100, 1000, or 10,000 µg/L) or a vehicle (DMSO) for 5 days. While lower concentrations (1-100 µg/L) reflect environmentally relevant Pb levels, higher concentrations (1000-10,000 µg/L) were included to assess acute toxicity under extreme exposure scenarios. We conducted adult behavior assessment to evaluate the locomotor activity following exposure. The same individual fish were subsequently sacrificed for brain dissection after a day of recovery in the aquatic system. RNA extraction and sequencing were then performed to evaluate the Pb-induced transcriptomic changes. Higher (1000-10,000 ug/L) Pb levels induced hyperactive locomotor patterns in aged zebrafish, while lower (10-100 ug/L) Pb levels resulted in the lowest locomotor activity compared to the control group. Exposure to 100 µg/L led to the highest number of differentially expressed genes (DEGs), while 10,000 µg/L induced larger fold changes in both directions. The neurological pathways impacted by Pb exposure include functions related to neurotransmission, such as cytoskeletal regulation and synaptogenesis, and oxidative stress response, such as mitochondrial dysfunction and downregulation of heat shock protein genes. These findings emphasize a U-shape dose-response relationship with Pb concentrations in locomotor activity and transcriptomic changes in the aging brain.</p>","PeriodicalId":23195,"journal":{"name":"Toxics","volume":"12 10","pages":""},"PeriodicalIF":3.9,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11511149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142508609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}