Synaptic plasticity plays an important role in learning and memory in the developing hippocampus. However, the precise molecular mechanism in lead exposure models remains to be studied. UCP2, an inner mitochondrial anion carrier, regulates synaptic plasticity through uncoupling neurons. And hnRNP K, an RNA binding protein, plays a role in modulating the expression of transcripts coding synaptic plasticity. We aim to investigate whether lead exposure affects UCP2 and hnRNP K expression levels. The Sprague-Dawley rats were exposed to different lead acetate concentrations (0 g/l, 0.5 g/l, 2.0 g/l) during gestational and lactational periods. PC12 cells were also exposed to different lead acetate concentrations (0 μM, 1 μM and 100 μM). We found that the expression levels of UCP2 and hnRNP K had significant declines in the lead exposure rat hippocampus and PC12 cells. Furthermore, the up-regulation of hnRNP K expression level could reverse the expression level of UCP2 in lead exposure models. In conclusion, these results suggest that lead exposure can reduce the expression level of UCP2 which is mediated by decreasing the expression level of hnRNP K.
{"title":"Mitochondrial uncoupling protein 2 is regulated through heterogeneous nuclear ribonucleoprotein K in lead exposure models.","authors":"Gaochun Zhu, Qian Zhu, Wei Zhang, Chen Hui, Yuwen Li, Meiyuan Yang, Shimin Pang, Yaobing Li, Guoyong Xue, Hongping Chen","doi":"10.1080/26896583.2020.1854596","DOIUrl":"https://doi.org/10.1080/26896583.2020.1854596","url":null,"abstract":"<p><p>Synaptic plasticity plays an important role in learning and memory in the developing hippocampus. However, the precise molecular mechanism in lead exposure models remains to be studied. UCP2, an inner mitochondrial anion carrier, regulates synaptic plasticity through uncoupling neurons. And hnRNP K, an RNA binding protein, plays a role in modulating the expression of transcripts coding synaptic plasticity. We aim to investigate whether lead exposure affects UCP2 and hnRNP K expression levels. The Sprague-Dawley rats were exposed to different lead acetate concentrations (0 g/l, 0.5 g/l, 2.0 g/l) during gestational and lactational periods. PC12 cells were also exposed to different lead acetate concentrations (0 μM, 1 μM and 100 μM). We found that the expression levels of UCP2 and hnRNP K had significant declines in the lead exposure rat hippocampus and PC12 cells. Furthermore, the up-regulation of hnRNP K expression level could reverse the expression level of UCP2 in lead exposure models. In conclusion, these results suggest that lead exposure can reduce the expression level of UCP2 which is mediated by decreasing the expression level of hnRNP K.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/26896583.2020.1854596","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25361481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01Epub Date: 2021-07-13DOI: 10.1080/26896583.2021.1943270
Linda S Von Tungeln, Cristina C Jacob, Greg R Olson, Gonçalo Gamboa da Costa, Frederick A Beland
In 2007, dietary exposure to "scrap melamine' resulted in the death of a large number of cats and dogs, which was attributed to the formation of melamine cyanurate crystals in their kidneys. In this study, we investigated if changes in urinary pH could diminish the renal toxicity associated with exposure to combinations of melamine and cyanuric acid. Female Sprague-Dawley rats were treated for three days with suspensions of melamine and cyanuric acid at doses that were expected to induce renal toxicity. Dosing was then discontinued and the rats were treated for seven days with drinking water solutions (i.e., ammonium chloride and sodium bicarbonate) that would alter urinary pH. The urinary pH of rats administered ammonium chloride drinking water decreased from pH 6.0-6.2 to pH 5.1-5.2. This was accompanied by a decrease in the incidence of melamine cyanurate crystals in the kidneys and a decrease in the incidence of renal lesions. These data suggest that acidification of urine may help overcome the renal toxicities associated with the formation of melamine cyanurate crystals in the kidney.
{"title":"Effect of urinary pH upon the renal toxicity of melamine and cyanuric acid.","authors":"Linda S Von Tungeln, Cristina C Jacob, Greg R Olson, Gonçalo Gamboa da Costa, Frederick A Beland","doi":"10.1080/26896583.2021.1943270","DOIUrl":"https://doi.org/10.1080/26896583.2021.1943270","url":null,"abstract":"<p><p>In 2007, dietary exposure to \"scrap melamine' resulted in the death of a large number of cats and dogs, which was attributed to the formation of melamine cyanurate crystals in their kidneys. In this study, we investigated if changes in urinary pH could diminish the renal toxicity associated with exposure to combinations of melamine and cyanuric acid. Female Sprague-Dawley rats were treated for three days with suspensions of melamine and cyanuric acid at doses that were expected to induce renal toxicity. Dosing was then discontinued and the rats were treated for seven days with drinking water solutions (<i>i.e.</i>, ammonium chloride and sodium bicarbonate) that would alter urinary pH. The urinary pH of rats administered ammonium chloride drinking water decreased from pH 6.0-6.2 to pH 5.1-5.2. This was accompanied by a decrease in the incidence of melamine cyanurate crystals in the kidneys and a decrease in the incidence of renal lesions. These data suggest that acidification of urine may help overcome the renal toxicities associated with the formation of melamine cyanurate crystals in the kidney.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40661174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01DOI: 10.1080/26896583.2021.1885283
Jeffrey S Willey, Richard A Britten, Elizabeth Blaber, Candice G T Tahimic, Jeffrey Chancellor, Marie Mortreux, Larry D Sanford, Angela J Kubik, Michael D Delp, Xiao Wen Mao
Both microgravity and radiation exposure in the spaceflight environment have been identified as hazards to astronaut health and performance. Substantial study has been focused on understanding the biology and risks associated with prolonged exposure to microgravity, and the hazards presented by radiation from galactic cosmic rays (GCR) and solar particle events (SPEs) outside of low earth orbit (LEO). To date, the majority of the ground-based analogues (e.g., rodent or cell culture studies) that investigate the biology of and risks associated with spaceflight hazards will focus on an individual hazard in isolation. However, astronauts will face these challenges simultaneously Combined hazard studies are necessary for understanding the risks astronauts face as they travel outside of LEO, and are also critical for countermeasure development. The focus of this review is to describe biologic and functional outcomes from ground-based analogue models for microgravity and radiation, specifically highlighting the combined effects of radiation and reduced weight-bearing from rodent ground-based tail suspension via hind limb unloading (HLU) and partial weight-bearing (PWB) models, although in vitro and spaceflight results are discussed as appropriate. The review focuses on the skeletal, ocular, central nervous system (CNS), cardiovascular, and stem cells responses.
{"title":"The individual and combined effects of spaceflight radiation and microgravity on biologic systems and functional outcomes.","authors":"Jeffrey S Willey, Richard A Britten, Elizabeth Blaber, Candice G T Tahimic, Jeffrey Chancellor, Marie Mortreux, Larry D Sanford, Angela J Kubik, Michael D Delp, Xiao Wen Mao","doi":"10.1080/26896583.2021.1885283","DOIUrl":"https://doi.org/10.1080/26896583.2021.1885283","url":null,"abstract":"<p><p>Both microgravity and radiation exposure in the spaceflight environment have been identified as hazards to astronaut health and performance. Substantial study has been focused on understanding the biology and risks associated with prolonged exposure to microgravity, and the hazards presented by radiation from galactic cosmic rays (GCR) and solar particle events (SPEs) outside of low earth orbit (LEO). To date, the majority of the ground-based analogues (e.g., rodent or cell culture studies) that investigate the biology of and risks associated with spaceflight hazards will focus on an individual hazard in isolation. However, astronauts will face these challenges simultaneously Combined hazard studies are necessary for understanding the risks astronauts face as they travel outside of LEO, and are also critical for countermeasure development. The focus of this review is to describe biologic and functional outcomes from ground-based analogue models for microgravity and radiation, specifically highlighting the combined effects of radiation and reduced weight-bearing from rodent ground-based tail suspension via hind limb unloading (HLU) and partial weight-bearing (PWB) models, although in vitro and spaceflight results are discussed as appropriate. The review focuses on the skeletal, ocular, central nervous system (CNS), cardiovascular, and stem cells responses.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/26896583.2021.1885283","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38910878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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}
Pub Date : 2021-01-01DOI: 10.1080/26896583.2021.1891825
Catherine M Davis, Antiño R Allen, Dawn E Bowles
Staying longer in outer space will inevitably increase the health risks of astronauts due to the exposures to galactic cosmic rays and solar particle events. Exposure may pose a significant hazard to space flight crews not only during the mission but also later, when slow-developing adverse effects could finally become apparent. The body of literature examining ground-based outcomes in response to high-energy charged-particle radiation suggests differential effects in response to different particles and energies. Numerous animal and cellular models have repeatedly demonstrated the negative effects of high-energy charged-particle on the brain and cognitive function. However, research on the role of space radiation in potentiating cardiovascular dysfunction is still in its early stages. This review summarizes the available data from studies using ground-based animal models to evaluate the response of the brain and heart to the high-energy charged particles of GCR and SPE, addresses potential sex differences in these effects, and aims to highlight gaps in the current literature for future study.
{"title":"Consequences of space radiation on the brain and cardiovascular system.","authors":"Catherine M Davis, Antiño R Allen, Dawn E Bowles","doi":"10.1080/26896583.2021.1891825","DOIUrl":"https://doi.org/10.1080/26896583.2021.1891825","url":null,"abstract":"<p><p>Staying longer in outer space will inevitably increase the health risks of astronauts due to the exposures to galactic cosmic rays and solar particle events. Exposure may pose a significant hazard to space flight crews not only during the mission but also later, when slow-developing adverse effects could finally become apparent. The body of literature examining ground-based outcomes in response to high-energy charged-particle radiation suggests differential effects in response to different particles and energies. Numerous animal and cellular models have repeatedly demonstrated the negative effects of high-energy charged-particle on the brain and cognitive function. However, research on the role of space radiation in potentiating cardiovascular dysfunction is still in its early stages. This review summarizes the available data from studies using ground-based animal models to evaluate the response of the brain and heart to the high-energy charged particles of GCR and SPE, addresses potential sex differences in these effects, and aims to highlight gaps in the current literature for future study.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/26896583.2021.1891825","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38910959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01Epub Date: 2021-02-07DOI: 10.1080/26896583.2020.1867449
Ruth Nabwire Wangia-Dixon, Kizito Nishimwe
Fumonisins, discovered in 1988 are a group of naturally occurring toxins produced by fusarium pathogenic fungi. Besides their presence in animal feeds, contamination of human foods such as corn, millet, oats, rye, barley, wheat and their products are widespread. Exposure to fumonisins results in species and organ specific toxicities including neurological disorders among equids, pulmonary edema in swine, esophageal cancer in humans and both kidney and liver related toxicities in rodents. This review seeks to consolidate groundbreaking research on the science of fumonisins toxicity, highlight recent progress on fumonisins research, and provide an overview of plausible mechanistic biomarkers for fumonisins exposure assessment.
{"title":"Molecular toxicology and carcinogenesis of fumonisins: a review.","authors":"Ruth Nabwire Wangia-Dixon, Kizito Nishimwe","doi":"10.1080/26896583.2020.1867449","DOIUrl":"https://doi.org/10.1080/26896583.2020.1867449","url":null,"abstract":"<p><p>Fumonisins, discovered in 1988 are a group of naturally occurring toxins produced by <i>fusarium</i> pathogenic fungi. Besides their presence in animal feeds, contamination of human foods such as corn, millet, oats, rye, barley, wheat and their products are widespread. Exposure to fumonisins results in species and organ specific toxicities including neurological disorders among equids, pulmonary edema in swine, esophageal cancer in humans and both kidney and liver related toxicities in rodents. This review seeks to consolidate groundbreaking research on the science of fumonisins toxicity, highlight recent progress on fumonisins research, and provide an overview of plausible mechanistic biomarkers for fumonisins exposure assessment.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/26896583.2020.1867449","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25343457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The space radiation environment is a complex combination of fast-moving ions derived from all atomic species found in the periodic table. The energy spectrum of each ion species varies widely but is prominently in the range of 400-600 MeV/n. The large dynamic range in ion energy is difficult to simulate in ground-based radiobiology experiments. Most ground-based irradiations with mono-energetic beams of a single one ion species are delivered at comparatively high dose rates. In some cases, sequences of such beams are delivered with various ion species and energies to crudely approximate the complex space radiation environment. This approximation may cause profound experimental bias in processes such as biologic repair of radiation damage, which are known to have strong temporal dependencies. It is possible that this experimental bias leads to an over-prediction of risks of radiation effects that have not been observed in the astronaut cohort. None of the primary health risks presumably attributed to space radiation exposure, such as radiation carcinogenesis, cardiovascular disease, cognitive deficits, etc., have been observed in astronaut or cosmonaut crews. This fundamentally and profoundly limits our understanding of the effects of GCR on humans and limits the development of effective radiation countermeasures.
{"title":"Everything you wanted to know about space radiation but were afraid to ask.","authors":"Jeffery Chancellor, Craig Nowadly, Jacqueline Williams, Serena Aunon-Chancellor, Megan Chesal, Jayme Looper, Wayne Newhauser","doi":"10.1080/26896583.2021.1897273","DOIUrl":"https://doi.org/10.1080/26896583.2021.1897273","url":null,"abstract":"<p><p>The space radiation environment is a complex combination of fast-moving ions derived from all atomic species found in the periodic table. The energy spectrum of each ion species varies widely but is prominently in the range of 400-600 MeV/n. The large dynamic range in ion energy is difficult to simulate in ground-based radiobiology experiments. Most ground-based irradiations with mono-energetic beams of a single one ion species are delivered at comparatively high dose rates. In some cases, sequences of such beams are delivered with various ion species and energies to crudely approximate the complex space radiation environment. This approximation may cause profound experimental bias in processes such as biologic repair of radiation damage, which are known to have strong temporal dependencies. It is possible that this experimental bias leads to an over-prediction of risks of radiation effects that have not been observed in the astronaut cohort. None of the primary health risks presumably attributed to space radiation exposure, such as radiation carcinogenesis, cardiovascular disease, cognitive deficits, etc., have been observed in astronaut or cosmonaut crews. This fundamentally and profoundly limits our understanding of the effects of GCR on humans and limits the development of effective radiation countermeasures.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/26896583.2021.1897273","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38910875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01Epub Date: 2021-08-23DOI: 10.1080/26896583.2021.1963606
Mercedes Lombarte, Brenda L Fina, Lucas R Brun, Stella Maris Roma, Alfredo Rigalli, Di Loreto V E
The use of fluoride (F) for therapeutic purposes is controversial and its toxicity is a health problem. The aim of this study was to evaluate the effect of F on endochondral ossification in growing rats. Twenty-four rats of 21 days were divided into 4 groups which received 0, 20, 40 or 80 μmol F/100 g body weight/day for 30 days, through an orogastric tube. Histological evaluation of growth plate cartilage (GPC) and primary and secondary bone were analyzed on sections of the metaphysis of tibias. Total thickness of the GPC (GPC.Th), thickness of resting zone (RZ.Th), proliferative zone (PZ.Th) and hypertrophic zone (HZ.Th); bone volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), trabecular separation (Tb.Sp), and apoptosis by the TUNEL were measured. A hyperplasia of the proliferative zone and a significant increase in PZ.Th with 40 and 80 μmol F without changes in GPC.Th were found. In the secondary trabecular bone, presence of immature trabeculae, peritrabecular inflammatory foci and sinusoidal dilatation were observed. A significant decrease in BV/TV was also found due to a decrease in Tb.Th and a progressive increase was observed in the number of apoptotic nuclei as the dose of F increased. In conclusion, results suggest that prolonged administration (30 days) of F negatively affect the endochondral ossification with increased chondrocyte proliferation and delayed maturity of new bone, causing inflammatory damage, edema, and increased apoptotic bone cells.
{"title":"Effect of fluoride on bone and growth plate cartilage.","authors":"Mercedes Lombarte, Brenda L Fina, Lucas R Brun, Stella Maris Roma, Alfredo Rigalli, Di Loreto V E","doi":"10.1080/26896583.2021.1963606","DOIUrl":"https://doi.org/10.1080/26896583.2021.1963606","url":null,"abstract":"<p><p>The use of fluoride (F) for therapeutic purposes is controversial and its toxicity is a health problem. The aim of this study was to evaluate the effect of F on endochondral ossification in growing rats. Twenty-four rats of 21 days were divided into 4 groups which received 0, 20, 40 or 80 μmol F/100 g body weight/day for 30 days, through an orogastric tube. Histological evaluation of growth plate cartilage (GPC) and primary and secondary bone were analyzed on sections of the metaphysis of tibias. Total thickness of the GPC (GPC.Th), thickness of resting zone (RZ.Th), proliferative zone (PZ.Th) and hypertrophic zone (HZ.Th); bone volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), trabecular separation (Tb.Sp), and apoptosis by the TUNEL were measured. A hyperplasia of the proliferative zone and a significant increase in PZ.Th with 40 and 80 μmol F without changes in GPC.Th were found. In the secondary trabecular bone, presence of immature trabeculae, peritrabecular inflammatory foci and sinusoidal dilatation were observed. A significant decrease in BV/TV was also found due to a decrease in Tb.Th and a progressive increase was observed in the number of apoptotic nuclei as the dose of F increased. In conclusion, results suggest that prolonged administration (30 days) of F negatively affect the endochondral ossification with increased chondrocyte proliferation and delayed maturity of new bone, causing inflammatory damage, edema, and increased apoptotic bone cells.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40550930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01Epub Date: 2021-08-23DOI: 10.1080/26896583.2021.1954460
Xiaobo He, Qingsu Xia, Qiang Shi, Peter P Fu
We recently established a genotoxic mechanism mediated by a set of (±)-6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (DHP)-DNA adducts, which lead to pyrrolizidine alkaloid (PA)-induced liver tumor initiation. This mechanism is involved in the metabolism of a series of carcinogenic PAs and PA N-oxides in rats in vivo and in vitro. There is a correlation between the order of liver tumor potency and the level of DHP-DNA adduct formation. Thus, these DHP-DNA adducts can be potential biomarkers of PA and PA N-oxide exposure and liver tumor initiation. To establish the generality of this mechanism, in the present study, we examined the metabolism of 13 potential carcinogenic PAs, 1 non-carcinogenic PA, and 5 PA N-oxides by male rat primary hepatocytes. With the exception of the nontoxic PA and vehicle control, all treated groups produced identical set of DHP-DNA adducts. These results support a general genotoxic mechanism mediated by the formation of characteristic DHP-DNA adducts leading to PA-induced liver tumor initiation.
我们最近建立了一套(±)-6,7-二氢-7-羟基-1-羟甲基- 5h -吡咯利嗪(DHP)-DNA加合物介导的基因毒性机制,导致吡咯利嗪生物碱(PA)诱导的肝脏肿瘤起始。该机制参与了大鼠体内和体外一系列致癌物质PAs和PA n -氧化物的代谢。肝肿瘤效力的强弱顺序与DHP-DNA加合物的形成水平有相关性。因此,这些DHP-DNA加合物可能是PA和PA n -氧化物暴露和肝脏肿瘤起始的潜在生物标志物。为了确定这一机制的普遍性,在本研究中,我们检测了13种潜在致癌PA, 1种非致癌PA和5种PA n-氧化物在雄性大鼠原代肝细胞中的代谢。除无毒PA和对照外,所有处理组均产生相同的DHP-DNA加合物。这些结果支持一般的遗传毒性机制介导的形成特征DHP-DNA加合物导致pa诱导的肝肿瘤起始。
{"title":"Metabolism of carcinogenic pyrrolizidine alkaloids and pyrrolizidine alkaloid <i>N</i>-oxides by rat primary hepatocytes generate the same characteristic DHP-DNA adducts.","authors":"Xiaobo He, Qingsu Xia, Qiang Shi, Peter P Fu","doi":"10.1080/26896583.2021.1954460","DOIUrl":"https://doi.org/10.1080/26896583.2021.1954460","url":null,"abstract":"<p><p>We recently established a genotoxic mechanism mediated by a set of (±)-6,7-dihydro-7-hydroxy-1-hydroxymethyl-5<i>H</i>-pyrrolizine (DHP)-DNA adducts, which lead to pyrrolizidine alkaloid (PA)-induced liver tumor initiation. This mechanism is involved in the metabolism of a series of carcinogenic PAs and PA <i>N</i>-oxides in rats <i>in vivo</i> and <i>in vitro</i>. There is a correlation between the order of liver tumor potency and the level of DHP-DNA adduct formation. Thus, these DHP-DNA adducts can be potential biomarkers of PA and PA <i>N</i>-oxide exposure and liver tumor initiation. To establish the generality of this mechanism, in the present study, we examined the metabolism of 13 potential carcinogenic PAs, 1 non-carcinogenic PA, and 5 PA <i>N</i>-oxides by male rat primary hepatocytes. With the exception of the nontoxic PA and vehicle control, all treated groups produced identical set of DHP-DNA adducts. These results support a general genotoxic mechanism mediated by the formation of characteristic DHP-DNA adducts leading to PA-induced liver tumor initiation.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40566689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Glyphosate is a toxic environmental pollutant that has the ability to induce biochemical and physiological alterations in living organisms. Several studies have focused on the research of protective techniques against the stress induced by this contaminant. In this context, we studied the protective effect of Spirulina against the disturbances induced by glyphosate. A biomarker approach was adopted to determine the impact of glyphosate, Spirulina and their mixture, during two time slots (4 and 7 days), on Mytilus galloprovincialis. Glyphosate treated mussels revealed significantly increased malondialdehyde and decreased acetylcholinesterase (AChE) levels. Spirulina normalized catalase (CAT), glutathione-S-transferase (GST), and AChE activities. Furthermore, it reduced glyphosate-induced malondialdehyde (MDA) levels. The current study suggests a protective effect of Spirulina against glyphosate-induced oxidative stress by strengthening the antioxidant system, sequestering ROS and inhibiting cellular damage.
草甘膦是一种有毒的环境污染物,具有诱导生物体内生化和生理变化的能力。一些研究集中在对这种污染物引起的应激的保护技术的研究上。在此背景下,我们研究了螺旋藻对草甘膦干扰的保护作用。采用生物标志物方法测定草甘膦、螺旋藻及其混合物在两个时间段(4天和7天)对褐贻贝的影响。草甘膦处理贻贝的丙二醛水平显著升高,乙酰胆碱酯酶(AChE)水平显著降低。螺旋藻过氧化氢酶(CAT)、谷胱甘肽- s -转移酶(GST)和乙酰胆碱酯酶(AChE)活性正常化。此外,它还降低了草甘膦诱导的丙二醛(MDA)水平。目前的研究表明,螺旋藻通过增强抗氧化系统、隔离活性氧和抑制细胞损伤,对草甘膦诱导的氧化应激具有保护作用。
{"title":"Protective role of <i>Spirulina platensis</i> against glyphosate induced toxicity in marine mussel <i>Mytilus galloprovincialis</i>.","authors":"Ouarghi Wided, Khazri Abdelhafidh, Mezni Ali, Samir Touaylia","doi":"10.1080/26896583.2021.1954833","DOIUrl":"https://doi.org/10.1080/26896583.2021.1954833","url":null,"abstract":"<p><p>Glyphosate is a toxic environmental pollutant that has the ability to induce biochemical and physiological alterations in living organisms. Several studies have focused on the research of protective techniques against the stress induced by this contaminant. In this context, we studied the protective effect of <i>Spirulina</i> against the disturbances induced by glyphosate. A biomarker approach was adopted to determine the impact of glyphosate, <i>Spirulina</i> and their mixture, during two time slots (4 and 7 days), on <i>Mytilus galloprovincialis</i>. Glyphosate treated mussels revealed significantly increased malondialdehyde and decreased acetylcholinesterase (AChE) levels. <i>Spirulina</i> normalized catalase (CAT), glutathione-S-transferase (GST), and AChE activities. Furthermore, it reduced glyphosate-induced malondialdehyde (MDA) levels. The current study suggests a protective effect of <i>Spirulina</i> against glyphosate-induced oxidative stress by strengthening the antioxidant system, sequestering ROS and inhibiting cellular damage.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40566688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-01-01Epub Date: 2021-09-01DOI: 10.1080/26896583.2021.1971477
Xiumei Jiang, Mary D Boudreau, Peter P Fu, Jun-Jie Yin
Nano-metals, nano-metal oxides, and carbon-based nanomaterials exhibit superior solar-to-chemical/photo-electron transfer properties and are potential candidates for environmental remediations and energy transfer. Recent research effort focuses on enhancing the efficiency of photoinduced electron-hole separation to improve energy transfer in catalytic reactions. Electron spin resonance (ESR) spectroscopy has been used to monitor the generation of electron/hole and reactive oxygen species (ROS) during nanomaterial-mediated photocatalysis. Using ESR coupled with spin trapping and spin labeling techniques, the underlying photocatalytic mechanism involved in the nanomaterial-mediated photocatalysis was investigated. In this review, we briefly introduced ESR principle and summarized recent advancements using ESR spectroscopy to characterize electron-hole separation and ROS production by different types of nanomaterials.
{"title":"Applications of electron spin resonance spectroscopy in photoinduced nanomaterial charge separation and reactive oxygen species generation.","authors":"Xiumei Jiang, Mary D Boudreau, Peter P Fu, Jun-Jie Yin","doi":"10.1080/26896583.2021.1971477","DOIUrl":"https://doi.org/10.1080/26896583.2021.1971477","url":null,"abstract":"<p><p>Nano-metals, nano-metal oxides, and carbon-based nanomaterials exhibit superior solar-to-chemical/photo-electron transfer properties and are potential candidates for environmental remediations and energy transfer. Recent research effort focuses on enhancing the efficiency of photoinduced electron-hole separation to improve energy transfer in catalytic reactions. Electron spin resonance (ESR) spectroscopy has been used to monitor the generation of electron/hole and reactive oxygen species (ROS) during nanomaterial-mediated photocatalysis. Using ESR coupled with spin trapping and spin labeling techniques, the underlying photocatalytic mechanism involved in the nanomaterial-mediated photocatalysis was investigated. In this review, we briefly introduced ESR principle and summarized recent advancements using ESR spectroscopy to characterize electron-hole separation and ROS production by different types of nanomaterials.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40566690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}