Bisphenol A (BPA), a prevalent environmental endocrine-disrupting chemical, has been well documented to be closely linked to the progression of type 2 diabetes; however, its underlying molecular mechanisms remain incompletely elucidated. In the present study, we exposed fertilized eggs of Tg(-1.2ins:EGFP) transgenic zebrafish to environmentally relevant concentrations of BPA and observed significant reductions in hatching and survival rates, severe impairment of pancreatic β-cell development, decreased insulin secretion, disrupted lysosomal activity and autophagic flux, increased cellular apoptosis, and elevated tissue glucose levels. Mechanistically, BPA exposure markedly upregulated the expression of miR-29a, accompanied by a significant downregulation of tfeb, a direct target gene of miR-29a. Additionally, the expression levels of the pancreatic β-cell developmental regulators pdx1 and mafa were decreased, coupled with reduced lysosomal acidity and accumulation of the autophagy substrate p62. Moreover, the pro-apoptotic genes bax and caspase3 were significantly upregulated, whereas the anti-apoptotic gene bcl-2 was downregulated. Furthermore, the transcript levels of core genes governing pancreatic β-cell development and endocrine function, including pdx1, mafa, and ins, were diminished, and the expression of glucose metabolism-related genes gck and glut2 was also suppressed. Notably, antisense RNA-mediated knockdown of miR-29a restored tfeb expression, reversed the aberrant expression of the above-mentioned genes, alleviated pancreatic β-cell injury, and rescued abnormal insulin secretion and glucose homeostasis. Collectively, these findings demonstrated that BPA induced aberrant glucose metabolism in pancreatic β-cells through the miR-29a/tfeb signaling axis, which represented a promising intervention target for BPA-triggered glucose metabolism disorders.

Lead is an important heavy metal material and also an omnipresent environmental pollutant, which poses extensive hazards to human health, including its nephrotoxicity. However, there are still many unknowns regarding its toxic mechanism and intervention strategy. Here, we revealed that lead exposure promoted the activation of PERK in HK - 2 cells (p - PERK and the ratio of p - PERK / PERK increased), enhanced the expression of its molecular chaperone binding immunoglobulin protein (BIP) and its downstream signaling molecule CCAAT / enhancer - binding protein homologous protein (CHOP). This indicated that lead exposure resulted in the occurrence of the unfolded protein response (UPR) in HK - 2 cells. Further, lead induced significant DNA damage, oxidative stress and apoptosis in HK-2 cells. Especially, when human umbilical cord mesenchymal stem cell - derived exosomes (hucMSC - exos) were ingested by HK-2 cells, all the levels of p - PERK, p - PERK / PERK ratio, BIP and CHOP were significantly down - regulated, which suggested that the UPR was significantly alleviated. Simultaneously, the above-mentioned toxic effects of lead were significantly reduced. Moreover, when GSK2606414 was employed to block the phosphorylation of PERK, the toxic effects of lead were also significantly alleviated. Hence, we conclude that hucMSC - exos can alleviate the toxicity of lead to HK-2 cells via interfering with the UPR, in which PERK plays a crucial role, and it may be a promising target for intervening in the toxicity of lead.

Lead is a ubiquitous environmental chemical with various toxic damage to human body. This investigation aimed to explore the intervention effect of human umbilical cord mesenchymal stem cells derived exosomes (HUC-MSC-exo) on the neurotoxicity of lead and the relevant mechanism. Differential gradient ultracentrifugation was adopted to isolate HUC-MSC-exo. Nanoparticle tracking assay (NTA), Transmission electron microscope (TEM) technology and exosomal specific biomarkers CD9, CD63 and CD81 were adopted for exosomal characterization. Human neuroblastoma cell (SH-SY5Y) was used as the recipient cell. Confocal laser scanning microscope analysis was conducted to confirm the intake of HUC-MSC-exo by SH-SY5Y cells. Cell migration ability, apoptosis, IL-6, IL-1β and TNF-α were analyzed. The role of miR-26a-5p/PTEN axis was assessed. The result showed that the exposure of SH-SY5Y cells to lead activated the miR-26a-5p/PTEN pathway by down-regulating miR-26a-5p and up-regulating PTEN expression, which was related to the significantly decreased cell migration and increased apoptosis, as well as significantly enhanced levels of inflammatory cytokine as compared with the control. While HUC-MSC-exo could significantly alleviate the cytotoxicity, apoptosis and inflammatory effects induced by lead on SH-SY5Y cells via partially restoring miR-26a-5p/PTEN pathway. Herein, we conclude that HUC-MSC-exo can alleviate lead-induced toxic effects on SH-SY5Y cells partially through miR-26a-5p/PTEN pathway.

The mechanistic target of rapamycin (RAPA) complex 1 (mTORC1) - transcription factor EB (TFEB) pathway plays a crucial role in response to nutritional status, energy and environmental stress for maintaining cellular homeostasis. But there is few reports on its role in the toxic effects of arsenic exposure and the related mechanisms. Here, we show that the exposure of bronchial epithelial cells (BEAS-2B) to sodium arsenite promoted the activation of mTORC1 (p-mTORC1) and the inactivation of TFEB (p-TFEB), the number and activity of lysosomes decreased, the content of reduced glutathione (GSH) and superoxide dismutase (SOD) decreased, the content of malondialdehyde (MDA) increased, the DNA and chromosome damage elevated. Further, when mTORC1 was inhibited with RAPA, p-mTORC1 and p-TFEB down-regulated, GSH and SOD increased, MDA decreased, the DNA and chromosome damage reduced significantly, as compared with the control group. Our data revealed for the first time that mTORC1 - TFEB pathway was involved in sodium arsenite induced lysosomal alteration, oxidative stress and genetic damage in BEAS-2B cells, and it may be a potential intervention target for the toxic effects of arsenic.

OBJECTIVE:To explore the correlation between polycystic ovary syndrome (PCOS) and periodontitis in light of cytokines levels, sex hormone levels and metabolism-related indicators and their changes during progression of the two diseases. METHODS:Twenty healthy subjects and 40 patients diagnosed with PCOS underwent full-mouth periodontal examinations to obtain full-mouth plaque score (FMPS), gingival bleeding index of probing (BOP), probing depth (PD), and clinical attachment level (CAL). The participants were divided into Group A without periodontitis or PCOS (n=15), Group B with PCOS but without periodontitis (n=28), Group C with periodontitis but without PCOS (n=5), and Group D with both diseases (n=12). Serum levels of luteinizing hormone/follicle stimulating hormone (LH/FSH), testosterone, prolactin, progesterone and estradiol, and the levels of interleukin 6 (IL-6), IL-17A, tumor necrosis factor α and matrix metalloproteinase 8 (MMP-8) in both serum and saliva samples were measured at the time of enrolment and at 3 and 6 months after enrolment and compared among the 4 groups. RESULTS:Serum MMP-8 level was significantly higher in Group B than in Group A (P<0.05). Salivary MMP-8 level was significantly higher in Group D than in Group B (P<0.05). Salivary MMP-8, LH, and LH/FSH levels and serum and salivary IL-6 and progesterone levels all tended to increase in the 6 months after enrollment (OR>1, P<0.05). During the follow-up period, serum IL-6 levels differed significantly between the non-PCOS groups (A and C) and PCOS groups (B and D)(P<0.05); serum IL-6 and salivary MMP-8 levels differed significantly between the non-periodontitis groups (A and B) and periodontitis groups (C and D)(P<0.05). Spearman correlation analysis indicated positive correlations of LH and LH/FSH with PD (P<0.05); testosterone and LH/FSH were positively correlated with serum MMP-8 levels (P<0.05), and PD, BOP and FMPS were positively correlated with salivary MMP-8 levels (P<0.01). CONCLUSION:There is a correlation between PCOS and periodontitis, and their progression is accompanied by changes in serum and salivary levels of pro-inflammatory cytokines and serum sex hormones.

OBJECTIVE:To investigate the impact of type 2 inflammation markers blood eosinophils (EOS) and fractional exhaled nitric oxide (FeNO) on bronchodilator responsiveness (BDR) in patients with chronic obstructive pulmonary disease (COPD).METHODS:This study was conducted among 389 patients with an established diagnosis of COPD in our hospital from October, 2019 to October, 2023, who all underwent bronchial dilation test (BDT) of the large and small airways. Based on smoking history, blood EOS, and FeNO, these patients were divided group A (blood EOS < 300/μL + FeNO < 35 ppb + smoking history < 20 pack-years), group B (blood EOS < 300/μL+FeNO < 35 ppb+smoking history ≥20 pack-years), group C (blood EOS ≥300/μL or FeNO≥35 ppb+smoking history ≥20 pack-years), and group D (blood EOS ≥300/μL or FeNO ≥35 ppb+smoking history < 20 pack-years) for analyzing the relationship between clinical indexes and BDR.RESULTS:BDR evaluation based on forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and maximum mid-expiratory flow (MMEF) yielded consistent results, all showing a younger mean age, higher FeNO levels, and higher blood EOS counts and percentages in patients positive for BDT (P < 0.05). The improvement value and improvement rate of FEV1 were significantly lower in group A than in group D. The improvement value and improvement rate of FEV1 as well as the improvement rate of MMEF were significantly lower in group B than in group D. In the overall patients, age and FeNO were significantly correlated with the improvement value and improvement rate of FEV1 and the improvement rate of MMEF (P < 0.05).CONCLUSION:Type 2 inflammation markers have different effects on BDR in the large and small airways of COPD patients, and their clinical significance needs further investigation.

Lead is a widespread environmental pollutant with serious adverse effects on human health, but the mechanism underlying its toxicity remains elusive. This study aimed to investigate the role of miR-584–5p / Ykt6 axis in the toxic effect of lead on HK-2 cells and the related mechanism. Our data suggested that lead exposure caused significant cytotoxicity, DNA and chromosome damage to HK-2 cells. Mechanistically, lead exposure down-regulated miR-584–5p and up-regulated Ykt6 expression, consequently, autophagosomal number and autophagic flux increased, lysosomal number and activity decreased, exosomal secretion increased. Interestingly, when miR-584–5p level was enhanced with mimic, autophagosomal number and autophagic flux decreased, lysosomal number and activity increased, ultimately, exosomal secretion was down-regulated, which resulted in significant aggravated toxic effects of lead. Further, directly blocking exosomal secretion with inhibitor GW4869 also resulted in exacerbated toxic effects of lead. Herein, we conclude that miR-584–5p / Ykt6 - mediated autophagy - lysosome - exosome pathway may be a critical route affecting the toxic effects of lead on HK-2 cells. We provide a novel insight into the mechanism underlying the toxicity of lead on human cells.

Mesenchymal stem cell - originated exosomes (MSC-exo) are promising non-cellular treatment agents for various diseases. The present study aimed to explore whether human umbilical cord MSC - originated exosomes (HUC-MSC-exo) have the function of protecting human cells (16HBE) against the damage caused by HQ and the related mechanism. HUC-MSC-exo was isolated with differential gradient ultracentrifugation method and characterized by using transmission electron microscope (TEM). 16HBE cells were used as the tool cells and co-cultured with HUC-MSC-exo. Confocal laser scanning microscope was employed to confirm the ingestion of HUC-MSC-exo by 16HBE. Cell proliferation, migration, oxidative stress, DNA and chromosome damages of 16HBE were analyzed under HQ stress, and the role of miR-221/PTEN axis was investigated. Our data showed that under HQ stress, different groups of cells exhibited significantly decreased proliferation and migration abilities, and significant oxidative stress, DNA and chromosome damage effects. HUC-MSC-exo could alleviate the cytotoxic, oxidative stress and genotoxic damage effects of HQ on 16HBE cells. Mechanistically, HQ exposure up-regulated the level of miR-221 and down-regulated PTEN, while HUC-MSC-exo could significantly reduce the level of miR-221 and promote PTEN expression, which was involved in alleviating the toxic effects of HQ on 16HBE cells. Our data indicates that HUC-MSC-exo can alleviate the oxidative stress, cytotoxic and genotoxic effects of HQ on 16HBE cells via miR-221/PTEN pathway, and it may be a promising agent for protecting against the toxicity of HQ.

Tributyltin chloride (TBTC) is a ubiquitous environmental pollutant with various adverse effects on human health. Exosomes are cell - derived signaling and substance transport vesicles. This investigation aimed to explore whether exosomes could impact the toxic effects caused by TBTC via their transport function. Cytotoxicity, DNA and chromosome damage caused by TBTC on MCF-7 cells were analyzed with CCK-8, flow cytometry, comet assay and micronucleus tests, respectively. Exosomal characterization and quantitative analysis were performed with ultracentrifugation, transmission electron microscope (TEM) and bicinchoninic acid (BCA) methods. TBTC content in exosomes was detected with Liquid Chromatography-Mass Spectrometry (LC-MS). The impacts of exosomal secretion on the toxic effects of TBTC were analyzed. Our data indicated that TBTC caused significant cytotoxicity, DNA and chromosome damage effects on MCF-7 cells, and a significantly increased exosomal secretion. Importantly, TBTC could be transported out of MCF-7 cells by exosomes. Further, when exosomal secretion was blocked with GW4869, the toxic effects of TBTC were significantly exacerbated. We concluded that TBTC promoted exosomal secretion, which in turn transported TBTC out of the source cells to alleviate its toxic effects. This investigation provided a novel insight into the role and mechanism of exosomal release under TBTC stress.

Bisphenol A (BPA), one of the typical environmental endocrine disruptors (EEDs), can promote the proliferation and migration of cancer cells, but the mechanism of which remains largely unclear. Exosome secretion plays an important role in the stress response of cells to environmental stimuli. This study was designed to explore whether exosome secretion was involved in the toxic effect of BPA on the proliferation and migration of MCF-7 cells, and the related mechanism. Our data shows that the IC50 value of MCF-7 exposure to BPA was about 65.82 mu M. The exposure of MCF-7 to 10 mu M BPA resulted in a decreased miR-26b expression and the activation of miR26b/Rab-31 pathway, consequently, the number and activity of lysosomes decreased, the secretion of exosomes increased, cell proliferation and migration were enhanced obviously. Interestingly, miR-26b mimic up-regulated the number and activity of lysosomes via miR-26b/miR-31 pathway, exosome secretion was down-regulated, cell proliferation and migration decreased. Further, when GW4869 was used to directly inhibit the exosome secretion of MCF-7 treated with BPA, their proliferation and migration were down-regulated. Herein, we concluded that the stimulating effect of BPA on the proliferation and migration of MCF-7 cells was associated with the lysosome related exosome secretion via miR-26b / Rab31 pathway.

OBJECTIVE:To investigate the impact of a history of atopy on the value of fractional exhaled nitric oxide (FENO) for predicting sputum eosinophils in patients with chronic cough.METHODS:A total of 868 patients with persistent cough lasting more than 3 weeks without pulmonary infection were enrolled, including 119 patients with subacute cough (defined as cough lasting 3-8 weeks) and 749 with chronic cough (longer than 8 weeks). The predictive value of FENO level for sputum eosinophilia was analyzed using receiver-operating characteristic (ROC) curve analysis, and the area under the curve (AUC) was calculated. The atopy status of the patients was determined by screening for history of allergy, hay fever, or animal or food allergies.RESULTS:Of the 868 patients enrolled, 173 patients (19.9%) had eosinophilic airway inflammation (EAI). In the overall patients, the median (Q1, Q3) FENO level was 18 (12, 35) ppb, ranging from 5 to 300 ppb. The patients with chronic cough and a positive history of atopy had a higher median FENO level than those without atopy (24 [13, 50] vs 18 [11, 34]; Z=2.25, P= 0.029), and FENO level was significantly correlated with EAI (r=0.281, P < 0.001). The AUCs of FENO for diagnosis of airway eosinophilia in patients with atopy and those without atopy were 0.677 (95% CI: 0.548-0.806) and 0.708 (95% CI: 0.660-0.756), respectively. The optimal cut-off value of FENO for diagnosing EAI was higher in patients with atopy than in those without atopy (72 vs 28.5 ppb).CONCLUSION:A history of atopy reduces the predictive value of FENO level for EAI in patients with chronic cough, suggesting the importance of examining the atopic status when interpreting test results of FENO.

The deficiency of effective biomarker for the toxic effects of water pollutants greatly limits the application of biological monitoring. This study aimed to investigate the possibility of circulating exosomes of indigenous fish acting as biomarker for the ecotoxicity effect of water environment. The Helong Reservoir in Guangzhou, China, was chosen as the investigating field, of which the water quality belongs to Class V (2013) (GB 3838-2002, China). The clean drinking water source of the upper reaches of the Liuxihe Reservoir was selected as the control. Indigenous fishes including Oreochromis niloticus (Nile tilapia), Labeo rohita (Rohu), Carassius auratus (Crucian carp) were sampled during the period from July 2020 to April 2021. Circulating exosomes of fish samples were isolated by using ultracentrifugation, characterized with transmission electron microscopy (TEM) and quantified by using bicinchoninic acid (BCA) assay. Oxidative stress, DNA and chromosome damage in liver, kidney, brain, gill and blood of fish samples were measured. The results showed that there were significant differences in superoxide dismutase (SOD) activity, glutathione (GSH) and malondialdehyde (MDA) contents, DNA and chromosome damage in fish samples between the Helong Reservoir and the control. Interestingly, there were also significant differences in circulating exosome levels of fish samples between them. Our data suggested that circulating exosome level of indigenous fish may be a novel biomarker for the ecotoxicity effects of water environment.

为探讨黄龙带水库浮游生物现状及水质情况,于2021年2—5月对黄龙带水库进行环境流行病学调查采样,分析其浮游生物的种类组成和丰度;通过Shannon-Wiener多样性指数和Pielou均匀度指数对水质进行综合评价.结果表明:本次调查共采集到黄龙带水库浮游植物6门30种,其优势藻类为绿藻门;浮游动物13属15种,以轮虫门为主.浮游植物和浮游动物丰度分别为10.00×105 ind./L和413 ind./L.黄龙带水库浮游生物Shannon-Wiener多样性指数大于3;浮游植物和浮游动物Pielou均匀度指数分别为0.67和0.94.黄龙带水库浮游生物多样性较高,水质综合评价结果为清洁贫营养型.

Methyl tert-butyl ether (MTBE), a widely used gasoline additive and a ubiquitous environmental pollutant in many countries and regions, can cause various kinds of toxic effects on human health. However, the molecular mechanism underlying its toxic effects remains elusive. The present study aimed to explore the cytotoxicity, DNA damage and oxidative damage effects of MTBE on human bronchial epithelial cells (16HBE) and the possible role of DNA polymerase β (pol-β) in this process. RNA interference (RNAi) was used to obtain pol-β gene knocked-down cells (pol-β-). CCK-8 assay was adopted to analyze the cell viability. Alkaline single-cell gel electrophoresis (SCGE) was performed to detect the DNA damage effects of MTBE. The enzyme activity of GSH-Px, SOD, CAT and the level of MDA were assessed. The data indicated that when treated with MTBE at the concentration exceeding 50 μmol/L and for the time exceeding 24 h, the pol-β- exhibited significantly decreased cell viability and increased DNA damage effects, as compared to the control (P < 0.05). Furthermore, there was significant difference in the levels of GSH-pX, SOD, CAT and MDA between the pol-β- and the control (P < 0.05). Our investigation suggests that MTBE can cause obvious cytotoxicity, DNA damage and oxidative damage effects on 16HBE cells. DNA polymerase β may be involved in protecting 16HBE cells from the toxic effects induced by MTBE exposure. These findings provide a novel insight into the molecular mechanism underlying the toxic effects of MTBE on human cells.

了解广州市典型水库水环境因子与浮游生物生态学现状及其水质情况,为水质安全的预防和控制工作提供基础资料.于2021年2月至5月,对该市典型水库进行了现场环境流行病学现况调查.根据水库水环境的历史资料,有针对性地对8种环境因子进行了检测;分析水环境中浮游动物及浮游植物的构成及丰度;运用Shannon-Weaver指数法分析水环境中浮游生物的多样性;运用Pielou指数法分析水环境中浮游生物的均匀度;基于浮游生物的生态学现状,对水环境质量进行了初步评价.参照《地表水环境质量标准》(GB 3838—2002),8种环境质量指标符合Ⅱ类水质限值.本次调查共采集到浮游植物6门40种,丰度为26.67×105 ind./L,优势藻类为绿藻(37.5％)和蓝藻(30％);浮游动物共采集到17属25种,丰度为488 ind./L,优势种类为轮虫(64％);浮游植物Shannon-Weaver多样性指数为1.35;浮游动物Shannon-Weaver多样性指数为1.22;浮游植物Pielou均匀度指数为0.25;浮游动物Pielou均匀度指数为0.26.虽然该水库理化指标符合Ⅱ类水质限值,但浮游生物多样性指数及均匀度指数较低.本次调查暴露了水质理化指标的局限性,理化指标无法全面反映水质的生态健康状况.水质理化监测与生物监测的联合运用,在水环境质量的全面和客观评价中具有重要意义.

外泌体是分泌的膜结合囊泡,其中包含大量可以改变受体细胞中基因表达的核酸、蛋白质和脂质.毒物可以改变外泌体的合成及其生物活性内含物的成分,因此外泌体可以作为暴露与效应的生物标志.尽管人体和动物研究已确认器官毒性的外泌体生物标志,而体外模型是研究外泌体功能生物学机制的理想选择,在此领域进一步使用体外模型对于探索外泌体生物学在毒理学中的潜在应用至关重要.本文对外泌体在毒理学研究中的重要性,外泌体体外模型的应用及其在暴露相关疾病中的作用综述如下.

目的 探讨某市典型水库水质的生态毒理学效应,为地方水质安全防护措施的合理实施提供基础资料.方法 自2020年7月～2021年4月,通过环境流行病学现场调查,采集在某市典型水库库区及清洁对照组水源生长的野生鲫鱼、泰国鲮鱼以及尼罗罗非鱼样本;运用微核实验分析鱼血细胞的染色体损伤效应;运用单细胞凝胶电泳技术(single cell gel electrophoresis,SCGE)分析鱼血细胞及肝细胞的DNA损伤效应;采用试剂盒法检测鱼肝组织超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)和丙二醛(MDA)含量;运用鱼卵黄蛋白原(vitellogenin,VTG)ELISA试剂盒法检测鱼血浆VTG水平,分析水质的环境雌激素效应.结果 某市典型水库库区3种鱼类血细胞彗星尾部DNA含量及血细胞微核形成率明显高于清洁对照组鱼类(P＜0.05);典型水库库区3种鱼类肝组织SOD活性明显低于对照组(P＜0.05),GSH及MDA含量明显高于对照组(P＜0.05);典型水库库区尼罗罗非鱼血浆VTG水平明显高于对照组(P＜0.05),而鲫鱼、泰国鲮鱼血浆VTG水平差异无统计学意义(P＞0.05).结论 某市典型水库水质对库区野生鱼类可能具有一定的生态毒性效应.

探讨广州市增塘水库浮游生物种群特征及水质现状,为水质安全监控提供基础资料.于2021年3—7月,运用环境流行病学现场调查采样方法,采集增塘水库浮游植物及浮游动物样本,分析其种群构成及丰度;采用Shannon-Weaver指数法分析水库浮游生物的多样性;采用Pielou指数法分析水库浮游生物的均匀度;基于上述指数对水库的水环境质量做出初步评价.本次调查共采集到浮游植物35种,隶属于5门27属.其中优势藻类为绿藻13种(37.15％),其次为蓝藻10种(28.57％);浮游植物丰度为29.00×105 ind./L,其中硅藻门的丰度最大,为13.05×105 ind./L.浮游动物共计14属19种,其中轮虫12种(63.16％),为优势种群,其次为桡足类5种(26.31％);浮游动物丰度为967 ind./L,其中轮虫丰度最大,为860 ind./L.浮游植物Shannon-Weaver H'为3.24,对应水质为清洁;浮游动物Shannon-Weaver H'为2.24,对应水质为轻度污染;浮游植物Pielou J'为0.63,对应水质为轻度污染;浮游动物Pielou J'值为0.53,对应水质为轻度污染.本次环境流行病学现场调查结果提示,广州市增塘水库水质目前处于轻度污染状态.

目的 探讨miR-148a-DNMT1对汽油添加剂甲基叔丁基醚(MTBE)所致人支气管上皮细胞(16HBE)DNA损伤的影响.方法 运用Lipofectamine 2000脂质体将miR-148a mimics转染至16HBE细胞;qRT-PCR分析miR-148a及DNMT1 mRNA的表达;Western Blot分析DNMT1蛋白的表达改变;以终浓度为8μmol/L的MTBE对正常16HBE,16HBE-mimics及16HBE-NC空载体组细胞分别染毒培养48 h;运用单细胞凝胶电泳(SCGE)实验分析各组细胞的DNA损伤程度.结果 转染miR-148a mimics的16HBE细胞中miR-148a表达增强(P＜0.05),DNMT1 mRNA及蛋白表达降低(均P＜0.05),MTBE对各组细胞DNA有损伤,损伤程度无明显差异(P＞0.05).结论 尚未发现miR-148a-DNMT1的表达变化对汽油添加剂MTBE所致DNA损伤的明显影响.

The present study was conducted to assess the genotoxic potential of water from the Helong Reservoir, which was designated as a strategic drinking water source by the Guangdong Provincial Government of China in October 2016. Four kinds of common indigenous fish samples (Labeo rohita, Cirrhinus molitorella, red tilapia, and Oreochromis niloticus) were collected at 6 sampling sites during the period from July to November 2020. Fish from the clean drinking water source of the upper reaches of the Liuxihe Reservoir in Guangzhou were collected as the control. Both the alkaline single cell gel electrophoresis assay and the micronucleus test were used to detect DNA damage and the micronucleus rate in erythrocytes of fish samples, respectively. The results indicated that there was a significant increase in comet tail length, Olive tail moment, and micronucleus rates of all fish samples compared with those of the control (p < 0.05). The order of sensitivity to DNA damage and micronucleus formation was Labeo rohita > Cirrhinus molitorella > red tilapia > Oreochromis niloticus. The results of the 2 kinds of experiments were in perfect agreement with each other. We conclude that there are obvious genotoxic effects from the water in the Helong Reservoir. As a strategic drinking water source, the safety of the Reservoir water quality should be considered. The local government should put the restoration of the Helong Reservoir water quality on the agenda as soon as possible. Environ Toxicol Chem 2021;40:1919-1927. © 2021 SETAC.