联苯胺对锦鲤肝脏酶活性的影响

以锦鲤(Cyprinus carprio)为试验生物,经不同浓度(6.0,3.0,2.0,1.2,0.6mg/L)联苯胺暴露14d,研究其对肝脏谷胱甘肽过氧化物酶(GSH-Px),过氧化氢酶(CAT),超氧化物歧化酶(SOD)和谷胱甘肽硫转移酶(GST)以及谷丙转氨酶(GPT)活性的影响.结果表明,锦鲤经联苯胺暴露,肝脏GSH-Px活性几乎持续受抑制;暴露第4d出现CAT的诱导,但随着暴露的延续,在第7,14d出现酶活性抑制;对SOD的影响多表现为诱导作用,但在高浓度(6.0,3.0mg/L)暴露第14d则出现酶活性抑制;对GST和GPT的影响一般表现为在低浓度暴露下的酶诱导,高浓度暴露下酶活性受抑制.GSH-Px对联苯胺暴露最为敏感,有可能成为评价水环境联苯胺污染的生物标志物.     

二氯乙酰胺对斑马鱼不同组织的毒性效应

新兴的氯胺消毒方式会产生一些新型含氮消毒副产物。了解卤代乙酰胺的毒性效应对于准确认识氯胺消毒方法具有重要的重要意义。该研究以1 000μg/L二氯乙酰胺为实验材料,通过斑马鱼急性暴露7 d后,分析1 000μg/L二氯乙酰胺对斑马鱼肝脏、肠、鳃、脑和肌肉组织的毒性效应。研究结果发现,成年斑马鱼在暴露于1 000μg/L二氯乙酰胺溶液7 d后,肝脏和肌肉组织内SOD的活性显著提高,此外肝脏、脑和肌肉组织中的MDA含量也显著增加。表明1 000μg/L二氯乙酰胺能引起不同组织间SOD活性和MDA含量发生变化,可能与不同组织内含有不同的脂类相关。     

氧氟沙星对锦鲤抗氧化系统和DNA损伤的影响

由于抗生素对人体健康和生态环境潜在的威胁,其大量使用已引起人们广泛关注。该研究通过毒性暴露试验,研究了氟喹诺酮类抗生素氧氟沙星(OFLX)对锦鲤抗氧化酶活性和DNA损伤的影响。结果表明,随着暴露浓度和时间的增加,OFLX对锦鲤鱼肝SOD活性、MDA和GST含量呈现显著的诱导效应。当OFLX浓度200 mg/L,暴露13 d时,锦鲤肝脏各项抗氧化酶活性指标均出现显著降低,表明OFLX对锦鲤的抗氧化系统的累积毒性超出了鱼体的自身调节能力,导致鱼体的抗氧化系统的损伤。鱼鳃组蛋白H2AX(γ-H2AX)磷酸化结果表明,OFLX可造成鱼体DNA损伤,诱导鱼鳃γ-H2AX产生和簇集,且呈现明显的剂量-效应关系。OFLX浓度200 mg/L,暴露4 d时鱼鳃γ-H2AX浓度达到最大值(110.49 ng/L)。随着暴露时间继续增加,各浓度组γ-H2AX含量均有所下降,表明OFLX可能导致造成DNA双链的断裂,导致γ-H2AX浓度下降。该结果为评估OFLX对锦鲤的抗氧化系统和DNA毒性影响提供了较为可靠的依据。     

鲫鱼对水中有机防晒剂的富集及代谢酶响应

采用半静态水体暴露方法研究了有机防晒剂对二甲氨基苯甲酸异辛酯(OD-PABA)在鲫鱼不同组织的分布、累积及生态毒理效应.结果表明,OD-PABA在不同组织中的含量随着水体暴露浓度的升高而持续升高,并在14或28d达到最大.不同浓度的OD-PABA在不同组织的生物富集因子(BCF)存在明显差异,基于暴露14d和28d计算得到的BCF值,肝脏为123~186,皮肤为117~163,肾脏为90.2~147.OD-PABA对鲫鱼肝脏EROD、PROD、BFCOD和GST活性都产生了诱导效应,其中EROD和GST的响应更为显著,最大诱导倍数分别为0.97和0.53倍.结果表明,水中的OD-PABA可在鲫鱼体内富集,并通过I相和II相代谢酶进行生物转化.     

栉孔扇贝对8:2FTCA的代谢转化与氧化应激响应

以栉孔扇贝（Chlamys farreri）为受试生物,研究了栉孔扇贝对8：2氟调聚羧酸（8：2FTCA）的代谢转化特征以及代谢过程中靶器官的氧化应激响应.结果发现,栉孔扇贝可将8：2FTCA转化为8：2氟调聚不饱和酸（8：2FTUCA）、7：3氟调聚羧酸（7：3FTCA）、全氟辛酸（PFOA）、全氟壬酸（PFNA）和全氟庚酸（PFHpA）等代谢产物.栉孔扇贝鳃和肝脏中代谢产物总量最高,为8：2FTCA的主要代谢靶器官.与本课题组前期虾夷扇贝的相关研究相比,8：2FTCA在栉孔扇贝与虾夷扇贝体内的生物转化行为主要有3方面相似之处：检测到的代谢产物相同、代谢靶器官相同以及鳃是最终代谢产物PFOA生成和蓄积的主要场所;不同之处主要体现在栉孔扇贝中代谢产物以7：3FTCA占比较高,虾夷扇贝中则是PFOA占比较高.同时在8：2FTCA暴露过程中,栉孔扇贝靶器官的关键抗氧化酶出现了一定的应激效应.丙二醛（MDA）和谷胱甘肽（GSH）等氧化应激指标以及谷胱甘肽过氧化物酶（GSH-Px）,超氧化物歧化酶（SOD）和过氧化氢酶（CAT）等抗氧化酶系出现不同程度变化：GSH-Px在整个代谢转化过程中呈现抑制效应;SOD,CAT活性在鳃中呈诱导效应,而在肝脏中呈现明显的剂量-效应关系,低剂量组中均呈抑制效应,高剂量组中大部分时间呈诱导效应.GSH和MDA含量不仅表现出剂量-效应关系,组织间也存在差异.暴露实验结束后,生理指标均有不同程度恢复.     

2,2',4,4'-四溴联苯醚对赤子爱胜蚓的抗氧化酶、代谢酶及其基因表达的影响

多溴联苯醚(PBDEs)是广泛存在于环境中的一种新型持久性有机污染物.四溴联苯醚同分异构体中的BDE-47是多溴联苯醚中最重要的单体之一.试验采用人工土壤培养法,通过亚急性试验,研究了在不同暴露时间阶段下,不同BDE-47剂量对赤子爱胜蚓(Eisenia fetida)抗氧化酶(过氧化氢酶CAT)、代谢酶(谷胱甘肽转移酶GST)以及二者基因表达的影响.结果表明,在暴露14 d和28 d时,CAT活性被诱导上升并且差异显著;GST活性变化差异不显著;CAT基因表达水平在第14 d时呈现抑制效应,在后续的第28 d和第42 d基因表达水平上调;GST基因表达水平整体呈现诱导效应,并且差异显著,随着暴露时间的增加,低毒处理组(10、50 mg·kg-1)的基因表达水平逐渐下调至低于对照组的水平,高毒处理组(100、200 mg·kg-1)的基因表达量仍高于对照组水平;在BDE-47的暴露试验中,CAT与GST活性及其基因表达水平两项指标对低毒处理组较高毒处理组更为敏感.     

噪声对脑、心脏、肝脏元素影响的研究

采用原子吸收法,试图从元素方面探讨强噪声暴露对机体重要器官的元素代谢的影响。结果发现与对照组相比经强噪声暴露后,脑、心脏、肝脏的元素锌、脑的元素钙及心肌的元素镁均呈极显著减少;而脑、心脏、肝脏的元素铜及心、肝脏的元素钙则呈极显著增加。在停止强噪声暴露后第5d,上述4种元素代谢仍没有恢复正常。结果表明：强噪声使机体重要器官的元素代谢严重障碍。提示强噪声环境是引起心脏病的原因之一,可能与强噪声使心肌元素代谢严重失调有关。     

联苯代谢对微生物的生长胁迫及分裂抑制

以联苯/多氯联苯降解菌株R04（Rhodococcus sp.R04）和几种模式微生物为研究对象，利用高效液相色谱、荧光显微镜、扫描电子显微镜等分析微生物在联苯及其代谢物培养条件下细胞分裂和形态的变化.结果表明联苯及其代谢产物对红球菌R04和几种模式微生物细胞的分裂有抑制作用，并对部分微生物形态有影响.与前体-联苯及其代谢产物2-羟基-6-酮基-6-苯基-2，4-己二烯酸相比，2，3-二羟基联苯对G⁺、G^-细菌，或是酵母细胞分裂都有较强的抑制和形态的改变.2，3-二羟基联苯导致R.R04和缺陷型R.R04细胞形成不完整隔膜的比例增加；造成96.4%的大肠杆菌BL21细胞表面凹陷，胞质内容物流失，菌体体积缩小；导致枯草芽孢杆菌89.6%的细胞体积明显缩小；导致金黄色葡萄球菌基本没有细胞能形成完整的分裂隔膜；导致红酵母细胞能进行出芽生殖的比例从64.2%降低到19.3%，但对其细胞形态无明显改变.联苯代谢物2，3-二羟基联苯对红球菌R04及其它微生物细胞分裂和增殖的抑制作用比其前体-联苯强，建议在研究环境化合物与微生物互作时，应考虑环境化合物代谢的毒性效应.     

鞘氨醇单胞菌完整细胞对溴氨酸的好氧降解

文章考察了鞘氨醇单胞菌QYY完整细胞对溴氨酸的好氧降解条件,并对其降解途径进行了分析。研究表明,该完整细胞在最佳条件为:温度30℃、初始pH7.0～8.0、摇床转速150r/min,磷酸缓冲溶液浓度为0.01～0.04mol/L时将溴氨酸完全脱色后产生3种产物:2-氨基-3-羟基-5-溴苯磺酸、2-氨基-4-羟基-5-溴苯磺酸为终产物;邻苯二甲酸为中间产物。其脱色过程中,大部分溴氨酸直接降解为终产物,仅有一小部分溴氨酸在降解过程中形成邻苯二甲酸。邻苯二甲酸则通过苯甲酸代谢途径开环。     

苯并(a)芘和芘暴露对梭鱼肝脏超氧化物歧化酶活性的影响

在实验生态条件下，浓度范围0．1－0．5ug/L的苯并（a)芘和芘的短期暴露（7d),50ug/L浓度组造成梭鱼肝脏SOD活性先抑制后诱导的效应，5ug/L浓度在7d的暴露中，SOD活性未出现诱导而是抑制。同样在50ug/L浓度下，苯并（a)芘暴露4d后SOD活性出现诱导，而芘在暴露7d后才出现诱导，这间接反映了苯并（a)芘和芘的毒性大小。这些结果说明梭鱼肝脏SOD活性与苯并（a)芘和芘暴露有一定的相关性，可以作为海洋环境多环芳烃污染监测的一种生物标志物。     

基于代谢组学指标的土壤亚致死剂量汞对蚯蚓的毒性研究

将赤子爱胜蚓(Eisenia fetida)暴露于亚致死剂量(1.0、5.0、25.0 mg·kg~(-1))汞污染土壤中4周,以蚯蚓个体(致死率、体重增长率)及小分子代谢物(代谢组)为指标研究其对汞的动态毒性响应,并采用最小二乘判别分析(OPLSA-DA)对暴露组及对照组的代谢物进行分类,进而识别潜在的标记物.结果表明,蚯蚓对汞的吸收尚未达到稳态,蚯蚓体内代谢物的响应依赖于暴露剂量及暴露时间.暴露1周时,蚯蚓体重略有增长但不显著;最低暴露剂量(1.0 mg·kg~(-1))导致蚯蚓体内亮氨酸、异亮氨酸、色氨酸、组氨酸、酪氨酸、5-氧脯氨酸、2-脱氧肌苷显著低于对照水平,柠檬酸、肌苷酸与腺苷在5.0、25.0 mg·kg~(-1)剂量下显著高于对照水平;暴露4周时,最高暴露剂量(25 mg·kg~(-1))显著抑制了蚯蚓的生长;汞添加组的蚯蚓体内谷氨酸、酪氨酸、马来酸、2-脱氧肌苷水平显著低于对照.上述代谢物对汞的动态变化表明它们可作为潜在生物标记物,用于诊断土壤汞污染.对代谢途径分析发现,1.0～25.0 mg·kg~(-1)汞即可破坏蚯蚓正常氨基酸代谢、三羧酸循环,扰乱能量代谢,对蚯蚓产生氧化损伤.本研究结果表明,相比个体水平的受试终点,代谢组学指标比个体水平指标能更敏感地响应较低剂量汞,是土壤汞污染生态毒性效应诊断的有效指标.另外,本研究结果可为土壤汞污染的风险评估及相关环境标准的修订提供大量基础数据.     

4-氯-3-甲基苯酚(PCMC)暴露对成年斑马鱼内源性物质的影响

建立了4-氯-3-甲基苯酚（PCMC）的水生生物斑马鱼暴露毒理学模型,研究了斑马鱼PCMC暴露后内源性代谢物的变化.同时,在斑马鱼PCMC半数致死浓度LC₅₀的基础上,以1/10 LC₅₀为暴露浓度进行代谢组学分析.最后,经超高效液相色谱串联三重四级杆飞行时间质谱（UHPLC-Triple-TOF-MS）检测,结合主成分分析（PCA）和正交偏最小二乘法判别分析（OPLS-DA）进行代谢谱分析.结果发现,空白对照组和暴露组在代谢水平上有明显差异.进一步分析后筛选出9种上调物质和11种下调物质作为潜在生物标志物,主要包括氨基酸、嘌呤、糖类和脂质.根据差异代谢物生理功能分析发现,PCMC主要通过影响嘌呤代谢、甘油磷脂代谢、淀粉和蔗糖代谢、组氨酸代谢、丙酮酸代谢及苯丙氨酸、酪氨酸和色氨酸的生物合成,对斑马鱼的心血管系统、神经系统、蛋白代谢和能量代谢等方面产生毒性效应.本研究建立的代谢组学方法能全面评价氯酚类消毒剂对水生生物的毒性效应,为进一步阐明氯酚类消毒剂的毒性机制提供了理论基础.     

Metabolism of benzo[a]pyrene in peroxynitrite/Fe(III) porphyrin system

The peroxynitrite/porphyrin biomimetic system was established to investigate the effects of peroxynitrite on benzo[a]pyrene (B[a]P) metabolism. Three model systems consisting of different iron porphyrins were compared, and the results showed that the peroxynitrite/T(p-Cl)PPFeCl system was the highest catalytic efficiency in the metabolism of B[a]P. We analyzed the B[a]P metabolites produced from this system by RP-HPLC method and firstly identified the formation of nitrobenzo[a]pyrenes which are the special metabolites of B[a]P induced by peroxynitrite.     

Metabolism of benzo[a]pyrene in peroxynitrite/Fe(Ⅲ) porphyrin system

The peroxynitrite/porphyrin biomimetic system was established to investigate the effects of peroxynitrite on benzo[a]pyrene (B[a]P) metabolism. Through the comparison of three model systems consisting of different iron porphyrins, we found that the peroxynitrite/T(p-Cl)PPFeCl system showed the highest catalytic efficiency in the metabolism of B[a]P. We analyzed the B[a]P metabolites produced from this system by RP-HPLC method and firstly identified the formation of nitrobenzo[a]pyrenes which are the special metabolites of B[a]P induced by peroxynitrite.     

Metabolism of benzo[a]pyrene in peroxynitrite/Fe（Ⅲ） porphyrin system

The peroxynitrite/porphyrin biomimetic system was established to investigate the effects of peroxynitrite on benzo[a]pyrene （B[a]P） metabolism. Three model systems consisting of different iron porphyrins were compared, and the results showed that the peroxynitdte/T（p-Cl）PPFeCl system was the highest catalytic efficiency in the metabolism of B [a]P. We analyzed the B [a]P metabolites produced from this system by RP-HPLC method and firstly identified the formation of nitrobenzo[a]pyrenes which are the special metabolites of B [a]P induced by peroxynitrite.     

单甲脒农药的微生物降解代谢研究

研究了门多萨假单胞菌ＤＲ－８菌株对单甲脒农药的降解代谢。该菌利用率甲脒作为生长的唯一氮源，其对单甲脒的呼吸作用试验确证了该农药的生物可降解性。单甲脒对细菌生物氧化代谢关联酶活性的影响研究表明，脱氢酶对单甲脒较敏感，而ＮＡＤＨ氧化酶则耐受性较强。     

Alterations of endogenous metabolites in urine of rats exposed to decabromodiphenyl ether using metabonomic approaches

There is large usage of polybrominated diphenyl ethers （PBDEs） especially for decabromodiphenyl ether （BDE-209, Deca-BDE） in controlling the risks of fire. The toxicological effects of PBDEs are worth being concerned about. Female SD rats were daily gavaged with BDE-209 ether at the dose of 100 mg/kg for 20 days. Histological observation was performed for the screening of the target organs for BDE-209 exposure. The distribution and metabolism of PBDEs in the exposed main organs were evidenced by HRGC-HRMS. Alterations of the endogenous metabolite concentrations in urine were investigated using metabonomic approaches based on IH NMR spectrum. Histopathological changes including serious edema in kidney, hepatocellular spotty necrosis and perivasculitis in liver indicated that BDE-209 caused potential influences on endogenous metabolism in the exposed liver and the kidney. BDE-209 was found to be highly accumulated in lipid, ovary, kidney and liver after 20 days＇ exposure. Occurrence of other lower brominated PBDEs in the rats demonstrated that reductive debromination process happened in vivo. Hydroxylated and methoxylated-BDEs, as metabolism products, were also detected in the rat tissues. A total of 12 different endogenous metabolites showed obvious alterations in urine from the exposed rats, indicating the disturbance of the corresponding internal biochemical processes induced by BDE-209 exposure. These findings in vivo suggested the potential health risk might be of concern due to the toxicological effects of BDE-209 as a ubiquitous compound in the environment.     

白腐菌对氯丹的降解性能及降解途径研究

 研究了2株多氯代二苯并二噁英高效降解白腐菌Phlebia lindtneri及Phlebia brevispora对氯丹的降解能力.在2个不同的液体培养体系中,2菌株对于高浓度(25μmol/L)的反式氯丹展现了较高的代谢能力,经6周培养后其降解率均达到50%以上.用GC/MS对其降解产物分析表明,氯丹的降解存在脱氢,脱氯化氢,羟基化以及氯原子的羟基置换4条不同的初始降解途径,除七氯,环氧七氯及氧化氯丹等常见初始代谢产物外,还发现3-羟基氯丹,氯代六氯醇,七氯二醇,羟基六氯,二羟基六氯等大量的羟基化代谢产物.尤其是P. lindtneri可以将曾被认为是终端代谢产物的氧化氯丹进行降解,并通过氯原子的羟基置换作用将其转化成羟基化代谢产物.     

Thiolated arsenicals in arsenic metabolism: Occurrence, formation, and biological implications

Arsenic (As) is a notoriously toxic pollutant of health concern worldwide with potential risk of cancer induction, but meanwhile it is used as medicines for the treatment of different conditions including hematological cancers. Arsenic can undergo extensive metabolism in biological systems, and both toxicological and therapeutic effects of arsenic compounds are closely related to their metabolism. Recent studies have identified methylated thioarsenicals as a new class of arsenic metabolites in biological systems after exposure of inorganic and organic arsenicals, including arsenite, dimethylarsinic acid (DMAV), dimethylarsinous glutathione (DMAIIIGS), and arsenosugars. The increasing detection of thiolated arsenicals, including monomethylmonothioarsonic acid (MMMTAV), dimethylmonothioarsinic acid (DMMTAV) and its glutathione conjugate (DMMTAVGS), and dimethyldithioarsinic acid (DMDTAV) suggests that thioarsenicals may be important metabolites and play important roles in arsenic toxicity and therapeutic effects. Here we summarized the reported occurrence of thioarsenicals in biological systems, the possible formation pathways of thioarsenicals, and their toxicity, and discussed the biological implications of thioarsenicals on arsenic metabolism, toxicity, and therapeutic effects.     

Leaf metabolic influence of glyphosate and nanotubes on the Arabidopsis thaliana phyllosphere

Chemical exposure can indirectly affect leaf microbiota communities, but the mechanism driving this phenomenon remains largely unknown. Results revealed that the co-exposure of glyphosate and multi-carbon nanotubes (CNTs) caused a synergistic inhibitory effect on the growth and metabolism of Arabidopsis thaliana shoots. However, only a slight inhibitory effect was induced by nanotubes or glyphosate alone at the tested concentrations. Several intermediate metabolites of nitrogen metabolism and fatty acid synthesis pathways were upregulated under the combined treatment, which increased the amount of energy required to alleviate the disruption caused by the combined treatment. Additionally, compared with the two individual treatments, the glyphosate/nanotube combination treatment induced greater fluctuations in the phyllosphere bacterial community members with low abundance (relative abundance (RA) <1%) at both the family and genus levels, and among these bacteria some plant growth promotion and nutrient supplement related bacteria were markable increased. Strikingly, strong correlations between phyllosphere bacterial diversity and metabolites suggested a potential role of leaf metabolism, particularly nitrogen and carbohydrate metabolism, in restricting the range of leaf microbial taxa. These correlations between phyllosphere bacterial diversity and leaf metabolism will improve our understanding of plant-microbe interactions and the extent of their drivers of variation and the underlying causes of variability in bacterial community composition.