Alpha-tocopherol supplementation on chromium toxicity: a study on rat liver and kidney cell membrane

Membrane damage is one of the important consequence of chromium,an environmental toxicant,to produce cytotoxicity.α-tocopherol,a membrane protectant can be used to reduce the chromium-induced membrane damage.In the present study,the impact of chromium in presence and absence of α-tocopherol was studied on plasma membrane of live and kidney in male Wistar rats(80-100g body weight).Significant increase in membrane cholesterol level as well as significant decrease in membrane phospholipid level in chromium exposed(0.8mg/100g body weight/d,i.p.,for 4 weeks)animals suggest structural alteration of both liver and kidney plasma memebrane.The alkaline phosphatase,total ATPase and Na^ -K^ -ATPase activities of plasma membrane were significantly decreased in both liver and kidney after chromium treatment.However,α-tocopherol (30mg/100g diet)supplementation can restrict the changes in these membrane-bound enzyme activities.Thus,the usefulness of dietary supplementation of α-tocopherol to restrain the chromium-induced membrane damage is suggested.     

邻苯二甲酸二异壬酯单独暴露及与褪黑素联合作用对小鼠脑组织损伤研究

人类神经系统成熟的海马神经元细胞不能进行复制与自我修复,导致了神经系统易受到环境污染物损伤的风险.邻苯二甲酸二异壬酯(Diisonyl phthalate,DINP)是一种增塑剂替代产品,类雌激素作用较弱,正受到欧盟的推广使用.虽然目前已有一些研究表明了DINP的毒性,但有关其神经毒性的体内研究国内还较少.因此,本研究探讨了DINP单独暴露及与褪黑素联合作用对小鼠脑组织的影响.行为学分析显示,经灌胃200 mg·kg~(-1)·d~(-1)的DINP会导致小鼠行为学出现明显变化;脑组织病理学观察、免疫组化分析(半胱氨酸蛋白酶3(Caspase-3)、胶质纤维酸性蛋白(GFAP))、氧化应激水平检测(活性氧簇(ROS)、还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)活性、8-羟基脱氧鸟苷(8-OH-d G)、DNA-蛋白质交联(DPC))、炎症水平检测(肿瘤坏死因子ɑ(TNF-ɑ)、白介素1β(IL-1β))结果显示,小鼠脑组织海马区出现了病理学损伤,氧化应激和炎症水平上升(p0.01).DINP处理后予以50 mg·kg-1·d-1的褪黑素可以降低氧化应激水平,对小鼠脑组织海马区起到保护作用.以上数据表明,实验剂量(200 mg·kg~(-1)·d~(-1))DINP处理后可以导致小鼠脑组织损伤,同时予以褪黑素可以在一定程度上缓解这种损伤.     

Detection and occurrence of pentachlorophenol residues in chicken liver and fat

Abstract

A method for the detection of pentachlorophenol (PCP) residues in chicken liver and fat is presented. A detection limit of 0.002 mg/kg was achieved. Recoveries from liver and fat were in the range 82–88% and 95–97%, respectively.

Low level residues of PCP were found in all 1072 liver and 723 fat samples. These levels were <0.010 mg/kg in 92.7% of the fat and 75.6% of the livers. Only 0.75% of the liver samples had PCP levels>0.1 mg/kg. None of the more toxic impurities of PCP were detected in the chicken tissues.     

Characterisation of early responses to cadmium in roots of Salix matsudana Koidz

This study deals with the characterisation of early responses of roots of Salix matsudana in respect to oxidative stress, subcellular distribution, and chemical forms when exposed to 50 μmol/L Cd. Within 12 h, the root length is reduced and the contents of O₂^??, H₂O₂, and malondialdehyde are increased by 49%, 43%, and 35%. Cd is mainly retained in the cell walls; small amounts are distributed into other cell organelles. The largest proportion of Cd is found in the NaCl extractable, pectate-, and protein-integrated fraction.     

Distribution of bisphenol-A, triclosan and n-nonylphenol in human adipose tissue, liver and brain

In this study, an analytical method was optimized for the determination of bisphenol-A (BPA), triclosan (TCS) and 4-n-nonylphenol (4n-NP), environmental contaminants with potential endocrine disruptive activities, in human tissues. The method consisted of a liquid extraction step, derivatization with pentafluorobenzoylchloride followed by a clean-up on acidified silica and detection with gas chromatography coupled with mass spectrometry (GC-ECNI/MS). Recoveries ranged between 92% and 102% with a precision below 5%. Limits of quantification ranged between 0.3-0.4 ng g⁻¹, 0.045-0.06 ng g⁻¹ and 0.003-0.004 ng g⁻¹ for BPA, TCS and 4n-NP in different tissues, respectively. The method was applied for the determination of BPA, TCS and 4n-NP in paired adipose tissue, liver and brain samples from 11 individuals. BPA could be detected in almost all tissues, with the highest concentrations found in adipose tissue (mean 3.78 ng g⁻¹), followed by liver (1.48 ng g⁻¹) and brain (0.91 ng g⁻¹). TCS showed the highest concentrations in liver (3.14 ng g⁻¹), followed by adipose tissue (0.61 ng g⁻¹), while it could be detected in only one brain sample. Levels of 4n-NP were much lower, mostly undetected, and therefore 4n-NP is considered of minor importance for human exposure. Despite the measurable concentrations in adipose tissue, these compounds seem to have a low bioaccumulation potential. The reported concentrations of free BPA in the various tissues are slight disagreement with pharmacokinetic models in humans and rats and therefore the possibility of external contamination with BPA during sample collection/storage cannot be ruled out.     

Triclosan in Fresh Water Fish Gibelion Catla from the Kaveri River,India, and Its Consumption Risk Assessment

Triclosan is a common antimicrobial agent that is found in significant levels in the aquatic environment and may elicit effects on aquatic organisms through unexpected modes of action. In this study, triclosan was quantified in fish from the Kaveri River, India, by using the gas chromatography and mass spectrometry technique and it was found in the range of 0.73–50 ng/g wet weight (ww). The mean bioaccumulation factor based on water (BAF_w 820) and sediment (BAF_s 2.12) in the Kaveri River showed that triclosan is accumulative in fish, and reflects its feeding behavior. The bioaccumulation indicates triclosan's persistence or prevalence throughout the river stretch. Human risk assessment through dietary intake demonstrated that the triclosan exposure is five orders of magnitude lower than the acceptable daily intake (50 μg/kg bw) and US EPA reference dose (300 μg/kg bw/day). This investigation is the first to report the bioaccumulation of triclosan in freshwater fish from India. Further, the results indicate that this fish acts as a biomarker of exposure for triclosan and thus shall be used to report triclosan pollution in the future.     

Assessment of thyroid hormone activity of halogenated bisphenol A using a yeast two-hybrid assay

The thyroid hormone agonist/antagonist activities of halogenated derivatives of bisphenol A (BPA) were assessed using a yeast two-hybrid assay incorporating the human thyroid hormone α (TRα), both with and without possible metabolic activation by rat liver S9 preparation. In the absence of the rat liver S9 preparation, 3,3′,5,5′-tetrabromobisphenol A (TBBPA), 3,3′,5,5′-tetrachlorobisphenol A (TCBPA), and 3,3′,5-trichlorobisphenol A (3,3′,5-triClBPA) exhibited agonist activity, whereas 3-chlorobisphenol A (3-ClBPA), 3,5-dichlorobisphenol A (3,5-diClBPA), 3,3′-dichlorobisphenol A (3,3′-diClBPA), and BPA did not. The activities of TBBPA and TCBPA increased markedly (7.6-fold and 3.1-fold, respectively) after their metabolic activation with the rat liver S9 preparation. TBBPA, TCBPA, and 3,3′,5-triClBPA inhibited the binding of triiodothyronine (T3) to TRα at 2 × 10⁻⁵ M without rat liver S9 treatment and 4 × 10⁻⁶ M with rat liver S9 treatment, demonstrating their T3 antagonist activity. These results revealed that metabolic activation by rat liver S9 significantly increased the agonist/antagonist potential of some halogenated BPAs.     

甲醛暴露时间延长加剧小鼠哮喘模型肺氧化损伤并促进IL-17表达

为了探究不同暴露时间甲醛对小鼠哮喘模型肺氧化应激及IL-17表达的影响,用浓度为3.0 mg·m~(-3)的甲醛气体吸入染毒,同时将48只雄性Balb/c小鼠随机分为6组:(1)对照组(生理盐水组);(2)ovalbumin(OVA)致敏组;(3)0.5 h甲醛+OVA组;(4)1h甲醛+OVA组;(5)1.5 h甲醛+OVA组;(6)2 h甲醛+OVA组,以不同时间长度进行甲醛暴露,连续35 d。OVA致敏组、0.5 h甲醛+OVA组、1 h甲醛+OVA组、1.5 h甲醛+OVA组、2 h甲醛+OVA组均在第11、18及25天腹腔注射OVA致敏液(5 mg OVA+175 mg Al(OH)_3+30 mL生理盐水),第29~35天(共计1周)进行1%OVA雾化(30 min·d~(-1)),每日1次,诱发哮喘。第36天进行以下操作:取肺组织测定肺系数并制作肺匀浆,检测肺组织中活性氧自由基(ROS)、丙二醛(MDA)和还原型谷胱甘肽(GSH)的含量,并采用ELISA法检测肺组织中IL-17的水平。同时,采用HE染色法观察小鼠肺部气道的病理学变化。结果显示,在浓度为3.0 mg·m~(-3)的甲醛气体吸入染毒条件下,与对照组相比,1.5 h甲醛+OVA染毒组、2 h甲醛+OVA染毒组ROS、MDA、IL-17含量上升,具有统计学意义(P0.01)。同时,随着暴露时间长度的增加,小鼠肺部气道出现明显病理学变化。综上所述,每天2 h甲醛+OVA染毒能对小鼠肺造成损伤并恶化OVA对小鼠肺的损伤,产生炎症反应,并通过氧化应激反应介导。     

DDTs对水生哺乳动物的组织残留基准初步研究

作为一种曾经广泛使用的氯化烃杀虫剂,DDT及其主要代谢产物DDE和DDD(合称为DDTs)是一类典型的具有持久性和生物累积性的有毒污染物。亲脂性和持久性使得DDTs可以通过食物链进行生物放大,从而对处于高营养级的水生哺乳动物造成严重的毒害作用。在综述DDTs对哺乳动物的毒性研究基础上,采用物种敏感度分布(species sensitivity distribution,SSD)和毒性百分数排序法(toxicity percentile rank method,TPRM)推导DDTs保护水生哺乳动物的组织残留基准(Tissue Residue Guideline,TRG)。使用SSD和TPRM得到的TRG分别为23.9和22.7 ng·g-1食物(湿重)。相应的,DDTs保护水生哺乳动物的水质基准分别为188.2和178.7 pg·L-1。依据研究得到的DDTs的组织残留基准及其在鱼类体内的含量评估对水生哺乳动物的风险。研究结果可用于评估DDTs对水生哺乳动物的生态风险,并为DDTs的风险管理提供理论依据。     

组织残留法在水生生物基准中的应用概述

水生生物基准已成为生态风险评价和水环境管理的主要参考依据,在水污染治理、控制和管理以及水生生物保护方面发挥着重要作用。环境和生物学参数对基于水体或沉积物等外暴露浓度的毒性阈值和环境基准存在影响,使其具有变异性和不确定性。而基于组织残留的毒性剂量指标可以减少毒性值的变异性以及不确定性,特别是对于生物累积性物质而言,在毒性效应及环境基准研究中存在显著优势。针对组织残留法在水生生物基准研究中的应用,对组织残留法的概念、优势、应用,以及组织残留基准的推导方法等几个方面进行了综述,并提出了组织残留法在应用中存在的关键问题及建议,旨在推动环境基准、生态风险评价理论和方法的研究,以及为水环境管理和污染防治提供技术支持。