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.     

Arsenic toxicity in mice and its possible amelioration

Oral administration of arsenic trioxide(3 and 6 mg/kg body weight/d) for 30 d caused, as compared with vehicle control, dose-dependent significant reductions in body weight, absolute weight, protein, glycogen, as well as, total, dehydro and reduced ascorbic acid contents both in the liver and kidney of arsenic-treated mice. Succinic dehydrogenase(SDH) and phosphorylase only in the liver activities were significantly reduced in a dose-dependent manner. Acid phosphatase activity was significantly decreased in the liver of low dose arsenic-treated animals;however, significant rise in its activity was observed in high dose group. As compared with vehicle control, treatment also caused significant dose-dependent reductions in SDH, alkaline phosphatase and acid phosphatase activities in the kidney of mice. Vitamin E cotreatment as well as, 30 d withdrawal of arsenic trioxide treatment with or without vitamin E caused significant amelioration in arsenic-induced toxicity in mice. Administration of vitamin E during withdrawal of treatment also caused significant amelioration as compared from only withdrawal of the treatment. It is concluded that vitamin E ameliorates arsenic-induced toxicities in the liver and kidney of mice.     

Debrominated and methoxylated polybrominated diphenyl ether metabolites in rainbow trout (Oncorhynchus mykiss) after exposure to decabromodiphenyl ether

Decabromodiphenyl ether (BDE209) is the primary component in a commonly used flame retardant. Previous studies had proved that BDE209 itself was not toxic, while its metabolites including debrominated diphenyl ethers (De-BDEs) and methoxylated brominated diphenyl ethers (MeO-BDEs) posed a potential threat to organisms. Many studies had indicated that BDE209 could metabolize quickly in mammals, but lacking in the basic data about the metabolism of BDE209 in fish. In the present study, two replicate treatment groups of rainbow trout (Oncorhynchus mykiss) were exposed to BDE209 via a single intraperitoneal injection approximately 100 and 500 ng/g, respectively. Muscle, liver and blood samples were collected to analyze the specific metabolites on day 1 and day 28 post injection. The highest concentration of BDE209 was detected in muscle tissues, from 796.1 ng/g wet weight (day 1) to 687.1 ng/g wet weight (day 28) in high dose group, suggesting that BDE209 could accumulate slightly in muscle tissues. However, BDE209 was not detected in the blood for all treatments. Most congeners of De-BDEs were found in muscle and liver tissues, with the highest concentration in the liver. The main De-BDEs were nona-, octa-, hepta- and penta-De-BDEs. A total of seven MeO-BDE metabolites were observed among di erent fish tissues. Blood had the highest contribution of the MeO-BDE metabolites. Each MeO-BDE congener increased over the 28 days. These results in contrast to other studies suggested possible species-specific di erences in metabolic abilities.     

Analysis of PFAAs in American alligators part 2: Potential dietary exposure of South Carolina hunters from recreationally harvested alligator meat

Exposure to perfluorinated alkyl acids (PFAAs) has been linked to many harmful health effects including reproductive disorders, developmental delays, and altered liver and kidney function. Most human exposure to environmental contaminants, including PFAAs, occurs through consumption of contaminated food or drinking water. This study uses PFAA data from meat samples collected from recreationally harvested American alligators (Alligator mississippiensis) in South Carolina to assess potential dietary exposure of hunters and their families to PFAAs. Consumption patterns were investigated using intercept surveys of 23 hunters at a wild game meat processor. An exposure scenario using the average consumption frequency, portion size, and median perfluorooctane sulfonic acid (PFOS) concentration in alligator meat from all hunt units found the daily dietary exposure to be 2.11 ng/kg body weight per day for an adult human. Dietary PFOS exposure scenarios based on location of harvest suggested the highest daily exposure occurs with alligator meat from the Middle Coastal hunt unit in South Carolina. Although no samples were found to exceed the recommended threshold for no consumption of PFOS found in Minnesota state guidelines, exposure to a mixture of PFAAs found in alligator meat and site-specific exposures based on harvest location should be considered in determining an appropriate guideline for vulnerable populations potentially exposed to PFAAs through consumption of wild alligator meat.     

酸和铝胁迫对锦鲤不同组织SOD活性的影响

该实验目的是研究酸(pH=5,Al=0μg/L)、铝(pH=7,Al=800μg/L)单独及联合(pH=5,Al=800μg/L)作用下,锦鲤鱼脑、肾、肝超氧化物歧化酶(SOD)活性的反应变化情况。结果表明,与对照组(pH=7,Al=0μg/L)相比,锦鲤鱼脑无论在酸、铝单独作用还是联合作用下,SOD活性在染毒第1天均显著降低(p<0.01),但随后酸铝联合组、单独作用组分别在3 d、9 d恢复正常;肾SOD则只有在酸铝联合作用下,且只有在染毒第1天产生显著抑制(p<0.01),随后也恢复正常;肝SOD则无论在何种情况下,均无抑制现象发生。     

壬基酚对大鼠5-羟色胺分解代谢通路的影响

为探讨壬基酚对5-羟色胺(5-HT)代谢网络分解代谢通路的毒性作用机制,将24只SD雄性大鼠分为阴性对照组和壬基酚低、中、高剂量组[30,90,270mg/(kg·bw)],隔日玉米油灌胃染毒28d后检测大鼠血浆及肝匀浆中单胺氧化酶(MAO)活性和血浆中5-HT含量,并称量肝、肾和睾丸重量.结果显示,壬基酚暴露高剂量组大鼠体质量增量极显著低于对照组(P<0.01);染毒至第3周起,各组大鼠平均食物利用率有统计学意义(P<0.05);与对照组相比,高剂量组肝脏、肾脏脏器系数均有统计学意义(P<0.01),中、高剂量组睾丸脏器系数均有统计学意义(P<0.05);中、高剂量组血浆MAO酶活性极显著低于对照组(P<0.01),中、高剂量组肝匀浆MAO酶活性显著低于对照组(P<0.05);中、高剂量组血浆5-HT含量极显著高于对照组(P<0.01).壬基酚暴露剂量与大鼠体内MAO酶活性及5-HT水平均呈剂量-效应关系,壬基酚可通过分解代谢通路影响5-HT的代谢网络.     

多溴联苯醚在桂花鱼体内的分布

使用 GC-MS-NCI检测方法对持久性有机污染物多溴联苯醚(PBDEs)的同系物BDE28,47,66,85,99,100,138,153,154,183,209 在桂花鱼体内的含量及分布进行了研究．结果表明,Σ₁₀ PBDEs（不包括BDE209）在肾脏中含量最高,肌肉中含量最低,其干重平均值分别为5.71 ng·g^-1 和0.95 ng·g^-1．Σ₁₀ PBDEs在肾脏、鱼鳔、肝脏、鱼鳃、生殖腺、鱼皮、肠胃和肌肉中的干重含量分别为3.04～12.8、0.81～6.90、1.28～8.87、0.09～6.36、1.05～5.73、0.022～5.06、0.69～5.98和0.14～2.61 ng·g^-1．Σ₁₀ PBDEs在各组织和器官的含量顺序为: 肾脏、鱼鳔、肝脏> 鱼鳃、生殖腺> 肠胃、肌肉、鱼皮．桂花鱼体所含低溴取代 PBDEs 以 BDE47 为主要同系物,所占丰度为35.7%～65.6%．十溴取代物 BDE209 在所有样品中检出率为 45.2%,其中在肾脏和生殖腺中含量较高．研究表明,PBDEs 由摄食、呼吸2种主要途径进入桂花鱼体内,易富集在肝脏、鱼鳔、鱼鳃等脂肪含量较高的组织和器官中．     

家用洗涤剂对鱼生物标志物的影响

 将鱼暴露在家用洗涤剂中1周和2周后,通过测定腺苷三磷酸(ATP)酶、谷胱甘肽硫转移 酶(GST)和脱氧核糖核酸(DNA)加合物等几种生物标志物,来评价家用洗涤剂对鲫鱼(Carassiu s auratus)的毒性影响.结果表明,暴露1周后,各指标无明显变化;暴露2周后,鳃ATP酶活性降 低,肝GST活性升高,DNA加合物相对标记水平增大;而肾ATP酶活性没有明显改变.两种家用洗 涤剂的暴露结果是一致的.研究结果表明了家用洗涤剂对鱼的毒性和潜在致癌性.     

Study on the sensitivity to cadmium of marine fish Salaria basilisca（Pisces： Blennidae）

The present study tested the sensitivity of Salaria basilisca to water-cadmium (Cd) contamination. For this purpose, liver somatic index (LSI), Cd concentrations and the activities of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured in the liver of S. basilisca exposed to Cd-contaminated water (2 mg Cd/L as CdCl2) for 14 and 28 d. The results showed that the LSI decreased significantly after 14 and 28 d of Cd-exposure. Cd bioaccumulation in the liver resulted in an increasing uptake up to 42 g/g dry weight after 28 d of exposure. Activities of CAT and SOD were significantly increased with increasing exposure time. A significant increase in GSH-Px activity, under Cd influence, was observed during 14-day exposure period (p < 0.0001). However, a significant decrease (p < 0.05) in this activity with respect to control fish was registered after 28 d of Cd-exposure. These results showed that Cd accumulation in the liver of S. basilisca could induce oxidative stress as demonstrated by changes in the antioxidant enzyme activities. Results also emphasized that S. basilisca may considered as a sensitive species to Cd exposure.     

Se-Ca联合膳食干预缓解Cd诱导小鼠肝肾毒性

为探究Se-Ca联合膳食干预对生物Cd中毒的缓解效果,选取88只BALB/c小鼠,随机划分为19组,在相同饲料Cd暴露浓度下(2mg/kg)分别设置低、中、高浓度的Se和Ca单独和联合膳食干预处理,并观察30d后小鼠的生长发育、肝肾功能、氧化应激状态和组织病理变化.结果显示,Se-Ca联合干预可有效缓解Cd蓄积所致小鼠生长发育迟缓现象,且进一步促进小鼠生长;肝肾功能及氧化应激指标测定结果表明,Se-Ca联合干预对Cd暴露下小鼠肝脏AST、GSH、SOD、GSH-Px和肾脏BUN、MDA、SOD的保护效果优于单一元素干预;联合干预仅需较小剂量即可达到单独Se或Ca干预对肝肾病理损伤的最佳缓解效果.Se-Ca联合膳食干预可有效缓解Cd摄入导致的生长发育缓慢和肝肾毒性,且较之单一元素的干预效果更佳.     

土壤铬(Ⅵ)对赤子爱胜蚓的生态毒性效应

为研究土壤中Cr(Ⅵ)对赤子爱胜蚓(Eisenia fetida)的毒性效应,以人工土壤为测试介质,按照OECD指南中的方法,测定了Cr(Ⅵ)对赤子爱胜蚓的LC₅₀(半数致死浓度),并考察了w〔Cr(Ⅵ)〕为10~160mg/kg(以干质量计,下同)时Cr(Ⅵ)对赤子爱胜蚓的生长和生殖的影响. 结果表明:①Cr(Ⅵ)在人工土壤中14d的LC₅₀为245.06mg/kg,95%置信限为208.31~288.29mg/kg;②与对照组相比,暴露28d时,w〔Cr(Ⅵ)〕为10~20mg/kg试验组的赤子爱胜蚓体质量显著增加(P<0.01);w〔Cr(Ⅵ)〕为80~160mg/kg试验组的赤子爱胜蚓体质量则受到显著抑制(P<0.01);③赤子爱胜蚓的产茧量和幼蚓孵化量均随着w〔Cr(Ⅵ)〕的升高而降低,其中,Cr(Ⅵ)抑制赤子爱胜蚓产茧量和幼蚓孵化量的EC₅₀(半数有效浓度)分别为62.32和49.92mg/kg. 赤子爱胜蚓的体质量、产茧量和幼蚓孵化量均对土壤中w〔Cr(Ⅵ)〕比较敏感,尤其幼蚓孵化量是赤子爱胜蚓毒性效应的几项测试终点中最为敏感的一种,可以作为生态风险评估的指标.      

苯处理SD大鼠器官和血中DNA加合物的形成与分布

以Ｐ１核酸酶提高灵敏度的＾３２Ｐ后标记法系统研究活体条件下腹腔注射苯处理的ＳＤ大鼠脏器和血细胞中ＤＮＡ加合物的形成与分布。结果表明，苯诱导或Ａｒｏｃｌｏｒ诱导对苯处理的ＳＤ大鼠体内ＤＮＡ加合物的形成有明显的促进作用，苯诱导的促进作用大于Ａｒｏｃｌｏｒ诱导。采用共价加合物标记指数对＾３２Ｐ后标记法数据进行计算的结果表明，此指数能反映出同一处理不同器官及不同处理相同器官中的ＤＮＡ加合物的形成与分布情况     

离子液体[C14mim]Br对大鼠亚慢性毒性的初步研究

研究了离子液体溴化-1-十四烷基-3-甲基咪唑盐([C_(14)mim]Br)对大鼠的亚慢性毒性.实验设立3个染毒组(2.5、5、10 mg·kg~(-1))和1个对照组,对大鼠经口染毒90 d后,分别考察大鼠的体重、血清生化指标、脏体指数、组织形态学的变化.结果表明,与对照组相比,染毒组大鼠的体重增长随着染毒剂量的增加而降低,肝脏/体重系数增大,其血清中碱性磷酸酶(ALP)、丙氨酸氨基转移酶(ALT)、天门冬氨酸转氨酶(AST)、直接胆红素(DBIL)和和球蛋白(GLB)水平均明显升高,A/G(ALB/GLB)、血清总蛋白(TP)值则明显下降.病理检查结果显示,染毒组大鼠的肝脏、肾脏及肺均有不同程度的损伤及病变.研究表明,[C_(14)mim]Br亚慢性染毒对大鼠的肝肾均有损伤,且其毒性呈一定的剂量依赖性.     

Tissue distribution of perfluoroalkyl acids and health status in wild Mozambique tilapia (Oreochromis mossambicus) from Loskop Dam, Mpumalanga, South Africa

This study examined concentrations of 15 perfluoroalkyl acids (PFAAs) in tissues from male Mozambique tilapia (Oreochromis mossambicus) collected at Loskop Dam, Mpumalanga, South Africa in 2014 and 2016. Nine of the 15 PFAAs were detected frequently and were included in statistical analysis and included two of the most commonly known PFAAs, perfluorooctanesulfonic acid (PFOS) (median, 41.6 ng/g) and perfluorooctanoic acid (PFOA) (median, 0.0825 ng/g). Of the tissues measured, plasma (2016 and 2014 median, 22.2 ng/g) contained the highest PFAA burden followed by (in descending order): liver (median, 11.6 ng/g), kidney (median, 9.04 ng/g), spleen (median, 5.92 ng/g), adipose (median, 2.54 ng/g), and muscle (median, 1.11 ng/g). Loskop Dam tilapia have been affected by an inflammatory disease of the adipose tissue known as pansteatitis, so this study also aimed to investigate relationships between PFAA tissue concentrations and incidence of pansteatitis or fish health status. Results revealed that healthy tilapia exhibited an overall higher (p-value < 0.05) PFAA burden than pansteatitis-affected tilapia across all tissues. Further analysis showed that organs previously noted in the literature to contain the highest PFAA concentrations, such as kidney, liver, and plasma, were the organs driving the difference in PFAA burden between the two tilapia groups. Care must be taken in the interpretations we draw from not only the results of our study, but also other PFAA measurements made on populations (human and wildlife alike) under differing health status.     

典型工业源下风向居民住宅区PM2.5暴露评价

采用便携式PM_2.5采样仪于2010年10—11月对典型工业源——某钢铁厂下风向某住宅区室内、外的ρ(PM_2.5)进行同步监测,同时对该区域居民每日时间-活动模式进行问卷调查,以评价居民住宅区内PM_2.5潜在暴露剂量和暴露浓度(以ρ计)及探讨其影响因素. 结果表明:该钢铁厂下风向居民单位体质量、个体的住宅区内PM_2.5潜在暴露剂量分别为36.1 μg/(kg·d)、960.8 μg/d,日均暴露浓度为120.1 μg/m3. 影响居民个体住宅区内PM_2.5潜在暴露剂量的因素依次为工作日/周末>暴露浓度>文化程度;影响居民单位体质量住宅区内PM_2.5潜在暴露剂量的因素依次为体质量>年龄>文化程度>工作日/周末>暴露浓度;性别与二者均没有显著相关关系.      

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.     

大连沿海常见海产品PFOS和PFOA的暴露水平调查

文章应用液相色谱-质谱分析方法,对2009年春季大连沿海常见海产品体内PFOS和PFOA的暴露水平进行了调查。鱼、蟹、乌贼和海胆肌肉中PFOS的平均暴露水平分别为0.40 ng/g,0.07 ng/g,0.09 ng/g及0.12 ng/g(湿重),而PFOA的平均暴露水平分别为0.06ng/g,0.01 ng/g,0.06 ng/g及0.10 ng/g(湿重)。鱼类肝脏中PFOS和PFOA的平均暴露水平分别为0.90 ng/g和0.24 ng/g。调查结果表明,大连沿岸常见海产品体内普遍检测到PFOS和PFOA,并且肝脏中PFOS和PFOA暴露水平均高于肌肉组织。通过比较发现,大连沿岸鱼类样品中PFOS的暴露水平低于美、日等国家的沿岸海域鱼类的暴露水平。     

Elimination of a pollution associated with chromic acid during the electro-deposition of Cr(III) using appropriate anodic and membrane materials in a double film bath

A method using trivalent chromium has been used to replace hexavalent chromium for the electro-deposition of chromium. Using a tri-chamber bath system various anodic materials and membranes were evaluated to minimize the production of environmentally and health damaging chromic acid. By measuring the absorbance of Cr(VI) at 640 nm, the results indicate that the use of a titanium plated ruthenium (Ti-Ru) anode produces the least amount of chromic acid byproduct compared to lead-gold alloy and graphite anodes. The concentration of Cr(VI) in the immediate vicinity of the Ti-Ru anode decreased from 0.389 mg/L to 0 during a 40-min deposition period. The use of a Nafion^TM quaternary cation exchange membrane portioning the buffer and anode selectively prevented Cr(III) from entering the anode compartment whilst allowing the migration of H⁺ to maintain overall voltaic continuity. It has been demonstrated that the use of a Ti-Ru anode with a Nafion^TM membrane can eliminate the production of chromic acid associated with the electro-deposition of chromium plate thereby preventing its health damaging exposure to plant operators and preventing discharge of Cr(VI) into the environment. Addition of a surfactant improved current efficiency by 34.7%.     

粉煤灰处理Cr6+废水的试验研究

利用电厂粉煤灰进行了处理含铬(VI)废水试验,探讨了粉煤灰投加量、pH值、接触时间、温度和含铬浓度等因素对除铬效果的影响。结果表明,在废水pH=10左右、Cr6+浓度<100mg/L,粉煤灰的用量140g/L时,在常温下吸附处理2h,对铬的去除率可达到72%以上。粉煤灰吸附处理含铬废水符合Freundlich等温式,以物理吸附为主。对于低浓度含铬(VI)的废水,处理后可达标排放。     

饮水型砷暴露对小鼠多系统脏器的毒性作用

为揭示饮水型砷暴露对机体的毒性,系统研究了砷摄入对实验动物基础生理和多系统脏器的毒性损伤作用.选雄性ICR小鼠为受试动物,以自由饮用含砷10 mg·L^-1的水溶液进行染毒,连续染毒60 d后检测发现,饮水砷暴露对小鼠一般体征和体重无显著影响,肝脏脏器系数显著降低,心脏、肺脏、肾脏和睾丸脏器系数降低,但无统计学意义.砷染毒组血清谷丙转氨酶（ALT）和谷草转氨酶（AST）活性显著升高,总胆固醇（TC）和甘油三酯（TG）含量显著升高,高密度脂蛋白胆固醇（HDL-C）含量显著降低,低密度脂蛋白胆固醇（LDL-C）含量显著升高;肝脏、小肠、心脏、肺脏、肾脏和睾丸组织中还原型谷胱甘肽（GSH）含量和超氧化物歧化酶（T-SOD）活性显著降低,过氧化氢（H₂O₂）和丙二醛（MDA）含量显著升高,并出现程度不同的组织形态结构损伤.研究结果表明,饮水砷暴露可诱发实验小鼠肝脏功能异常、生理代谢紊乱,导致消化系统、循环系统、呼吸系统、泌尿系统与生殖系统等多系统脏器组织的氧化损伤和结构病变,砷暴露对机体的毒性作用存在组织器官差异性,对肝脏的损伤较严重.