Gender-based comparative toxicity of di-ethyl phthalate in Wistar rats

In recent years, the exposure of humans to phthalate esters through environmental contamination has increased. One among them is di-ethyl phthalate (DEP), which is used as a plastisizer for cellulose ester plastic films and sheets, solid rocket propellants, molded and extruded articles, as a component in insecticide sprays and various other substances, as well as in industrial applications. Release into the environment occurs primarily as a result of production and manufacturing of DEP and during the use and disposal of products containing DEP. Therefore, a study was undertaken to evaluate gender-specific toxicity of DEP in Wistar rats. Rats of both sexes, weighing 125–130?g, were administered 50?ppm (w/v) DEP in water ad libitum for a period of 180 days and were given normal diet. Control animals received normal diet and water ad libitum. During the treatment, rats were weighed every week and water consumption per day was measured. After the completion of treatment, liver weight?:?body weight^?1 ratio, liver weight, body weight^?1, liver and serum enzymes, and other biochemical parameters of liver and serum were assessed. It was observed that there was no significant change in body weight^?1, liver weight, liver weight?: body weight^?1 ratio, and water consumption in both sexes. There were significant increases in liver acid phosphatase (ACP) activity and kidney glutathione levels, and nonsignificant changes in liver alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), succinate dehydrogenase (SDH), and lactate dehydrogenase (LDH) activities in DEP-treated male rats, whereas in DEP-treated female rats the liver showed significant decrease in ALP and SDH and nonsignificant changes in AST, ALT, and LDH activities. Serum ACP and LDH levels in DEP-treated male rats were significantly decreased, and in the case of DEP-treated female rats, only serum LDH levels were significantly decreased. There was no significant change in serum ALP, AST, and SDH levels in DEP-treated male and female rats as compared to control rats. Histology of the livers of both male and female rats showed loss of hepatic architecture, degenerative changes in hepatocytes, and vacuolation in hepatocytes in both the centrilobular and periportal areas. It can be concluded from this study that prolonged exposure to DEP at 50?ppm levels can be harmful to animals and humans. This is evident from the present study as certain significant changes in enzyme activities in the liver, serum, and histological alterations in liver were observed.     

火箭推进剂单推-Ⅲ对大鼠肺的毒性效应

为探讨新型火箭推进剂单推-Ⅲ(主成分为肼)对大鼠肺的毒性效应及其作用机制,将24只雄性Wistar大鼠随机分为4组:生理盐水对照组、低剂量组、中剂量组和高剂量组,采用气管滴注法染毒,染毒剂量分别为每次0、5.50、13.75、27.50mg·kg-(1以每kg大鼠滴注的肼(mg)计算),每天1次,连续染毒14d,腹主动脉放血处死,检测肺组织病理学改变、氧化损伤、炎性因子和肺组织细胞DNA损伤.结果表明,1)单推-Ⅲ染毒可导致大鼠肺组织炎症:低剂量组表现为轻度肺间质性炎症,中、高剂量组表现为中度肺间质性炎症;2)单推-Ⅲ染毒可导致大鼠肺组织氧化损伤:随着染毒剂量的增加,大鼠支气管肺泡灌洗液中乳酸脱氢酶(LDH)逐渐升高,而总抗氧化能力(T-AOC)逐渐降低,高剂量组与对照组差异显著(p<0.05);3)单推-Ⅲ可导致大鼠肺组织炎性免疫损伤:随着染毒剂量的增加,肺组织匀浆液中肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)均逐渐升高,高剂量组与对照组差异显著(p<0.05);4)单推-Ⅲ可导致大鼠肺组织细胞DNA损伤:随着染毒剂量的增加,尾部DNA含量、尾长、尾矩、Olive尾矩均逐渐升高,其中高剂量组尾长、Olive尾矩与对照组差异显著(p<0.05).综合以上实验结果可以看出火箭推进剂单推-Ⅲ对大鼠肺组织可产生一定的毒性效应.     

ZnO纳米粒子通过线粒体通路抑制小鼠光感受器细胞Na~+/K~+-ATP酶表达和活性的作用研究

氧化锌(ZnO)纳米粒子已被发现具有生物毒性,氧化应激被认为是最重要的因素之一。前期实验证实,ZnO纳米粒子能显著减少锰超氧化物歧化酶(Mn SOD)蛋白的表达,降低Mn SOD活性。本文通过检测乳酸脱氢酶(LDH)释放、线粒体活性氧(ROS)水平和膜电位(Δφm)、延迟整流钾电流变化和Na~+/K~+-ATP酶的表达及活性等变化,检测ZnO纳米粒子对小鼠光感受器细胞的细胞毒作用。结果表明,ZnO纳米粒子可显著增强小鼠光感受器细胞中LDH的释放、增加线粒体内ROS水平并下调Δφm、阻断延迟整流钾电流,同时降低Na~+/K~+-ATP酶的表达及活性,从而对小鼠视网膜光感受器细胞产生细胞毒作用,提示ZnO纳米粒子可通过线粒体通路引起氧化应激,从而抑制小鼠光感受器细胞Na~+/K~+-ATP酶表达和活性,产生细胞毒性,导致细胞死亡。本文的研究结果有助于理解ZnO纳米粒子引起细胞毒性的作用机理。     

Lead-induced alterations in protein-deficient rat liver–role of zinc

This study was designed to determine the protective effects of zinc (Zn) using liver marker enzymes in the serum and liver along with hepatic elemental profile in lead (Pb)-treated protein-deficient (PD) Sprague–Dawley male rats. Zn in the form of zinc sulfate at a dose of 227?mg?L^?1 in drinking water was administrated to control, PD as well as Pb-treated PD rats for 8 weeks. Pb treatment was given orally as lead acetate at a dose level of 100?mg?kg^?1 body weight to control and PD rats. The effects of different treatments were studied on the activities of enzymes that included alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum. The status of different elements (Cl, K, Mn, Fe, Cu, Zn, Se, Rb, Pb) in liver was also studied. Rats given PD diet and Pb showed significant inhibition in serum ALP activity associated with significant elevation in both AST and ALT activities. Serum ALP activity showed a significant inhibition week 1 until week 8 in Pb-treated PD rats. In contrast, serum AST activity was elevated both at 3 and 8 weeks while serum ALT activity was elevated at 8 weeks in Pb-treated PD rats. Pb treatment to PD rats elevated hepatic ALP, AST and ALT activities but depressed hepatic AST. Zn supplementation to Pb-treated PD rats restored the altered enzyme activities. The levels of K, Fe, Cu, Zn, Se and Rb were altered in protein deficiency. Furthermore, treatment with Pb to these animals depressed the Cu levels. Zn treatment to Pb-treated PD animals tended to restore the levels of altered elements. Hence, the present study clearly suggests that Zn plays an important role in regulating the liver marker enzymes and essential elements under conditions of Pb toxicity and protein deficiency.     

非暴露式气管滴注3种典型纳米材料对大鼠肝、肾的毒性效应

为探讨纳米二氧化硅(Nano-SiO2)、纳米四氧化三铁(Nano-Fe3O4)和单壁碳纳米管(SWCNTs)对大鼠肝、肾的毒性效应,将49只雄性Wistar大鼠随机分为7组,包括生理盐水对照组,以及3种纳米材料的低剂量组(2mg·mL-1)和高剂量组(10mg·mL-1),采用非暴露式气管滴注法染毒,每2d染毒1次,每次每只0.2mL,共染毒5周,眼眶取血后处死大鼠,称肝、肾重量计算脏器系数,测定大鼠血清中反映肝、肾功能的生化指标,并对肝、肾进行病理学观察.结果表明,1)3种纳米材料均可导致大鼠体重明显降低,但对肝、肾脏器系数无明显影响;2)病理学观察发现,3种纳米材料均可导致大鼠肝细胞轻度脂肪变性,肾脏则无明显改变;3)3种纳米材料均可导致大鼠肝功能异常,部分肝功能指标如谷草转氨酶(AST)、碱性磷酸酶(ALP)、谷丙转氨酶(ALT)等出现显著降低;4)3种纳米材料均可导致大鼠肾功能异常,部分肾功能指标如尿酸(UA)、肌酐(CREA)、尿素氮(BUN)等出现显著升高或降低.以上结果提示,经呼吸道染毒的Nano-SiO2、Nano-Fe3O4和SWCNTs均可对大鼠肝、肾产生一定的毒性效应.     

载带苯并[a]芘的纳米碳／二氧化硅颗粒引起大鼠氧化应激作用的研究

通过人工制备载带B[a]P的纳米碳(C)和纳米二氧化硅(SiO2)颗粒,采用气管滴注染毒方式,以7.5mg·kg-1(以体重计)的染毒剂量急性染毒大鼠,观察染毒24小时后载带B[a]P的纳米C/SiO2颗粒对机体产生氧化应激损伤的联合毒性效应.结果表明,在急性染毒后大鼠外周血中反映机体脂质过氧化损伤程度指标的丙二醛(MDA)含量表现为染毒组较对照组显著增加(p<0.05),表明纳米颗粒诱发机体发生了氧化应激反应.在急性染毒后各组大鼠肺泡灌洗液中谷胱苷肽过氧化物酶(GSH-PX)和超氧化物岐化酶(T-SOD)活力与对照组相比显著增加(p<0.05)(载带B[a]P的纳米SiO2组除外);载带B[a]P的纳米SiO2组肺泡灌洗液中GSH-PX活力与对照组相比无显著差异,而与单纯纳米SiO2组和B[a]P组比较显著降低,推测与抗氧化酶的一过性增高有关;载带B[a]P的纳米C组肺泡灌洗液T-SOD活力与其单纯纳米C组和单纯B[a]P组比较显著增加(p<0.05),由此表明载带B[a]P的复合纳米C/SiO2颗粒在致机体氧化损伤效应方面二者存在一定的协同作用.     

In vitro cytotoxicity of multi-wall carbon nanotubes on human cell lines

The aim of this study was to evaluate the in vitro toxicity of two multi-wall carbon nanotubes on four different cell lines: human alveolar epithelial (A549) cells, hepatocytes (Hep 3B cells), human embryonic kidney cells, and intestinal (P407 cells) cells. The adverse effects of carbon nanoparticles were analyzed after 24 h incubation with different cell lines using the trypan blue dye exclusion method. Incubation of carbon nanotubes with different cells produced a concentration-dependent inhibition of growth of the cells. The TC₅₀ or IC₅₀ values (toxic concentration 50, i.e., concentration of particles inducing 50% cell mortality) of two nanoparticles were (1) found to be in the range 23.5–30.5 µg mL^?1, and (2) less than that of quartz (known toxic agent, 28.8–66.9 µg mL^?1), indicating the greater cytotoxic effect of carbon nanoparticles than quartz particles.     

Comparative effects of five chelating agents on testicular toxicity in mice induced by acute exposure to cadmium

The aim of this study was to develop new antidotes for cadmium (Cd) since this metal is known to produce mammalian toxicity. N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), N-benzyl-D-glucamine dithiocarbamate (BGD), diethyldithiocarbamate (DDTC), 2,3-dimercaptopropanol (BAL), and ethylenediamine-tetraacetic acid (EDTA) were studied for their ability to inhibit the adverse effects induced by Cd on mouse testes. The parameters examined included concentrations of Cd, calcium (Ca), iron (Fe), and zinc (Zn) in testes, lipid peroxidation (LPO) levels in testes, lactate dehydrogenase (LDH) activity in serum and reproductive ability of male mice. Mice injected intraperitoneally (ip) with CdCl₂ (2.5?mgCd?kg^?1) after 30?min or 24?h, were then injected ip with chelating agents (400?µmol?kg^?1). Cd increased the concentrations of testicular Ca, Cd, Fe, Zn, and LPO levels as well as the activity of LDH in serum. HBGD and BGD effectively prevented the increase in above indices, and improved the reproductive ability weakened by exposure to Cd. The results suggested that HBGD and BGD are more effective detoxificants in the case of testicular toxicity in mice induced by acute exposure to Cd.     

内质网应激在PFOS致大鼠肝损伤中的作用

通过全氟辛烷磺酸(PFOS)28 d大鼠经口染毒评价PFOS肝损伤效应,探讨内质网应激在PFOS毒效应中的作用。Wistar大鼠随机分组,分别以0 mg·kg~(-1)、5 mg·kg~(-1)和10 mg·kg~(-1)PFOS灌胃染毒28 d。HE染色观察大鼠肝脏形态改变。ELISA法测定各组丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)和淀粉酶(AMY)含量变化。紫外分光光度法测定肝组织匀浆中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性变化。RT-PCR检测肝脏内质网应激标志蛋白表达水平。结果表明,PFOS造成大鼠体重降低、肝重增高(P0.05),组织切片显示肝细胞出现脂质沉积。PFOS不同剂量组大鼠ALT随暴露浓度增加,分别为(50.96±10.02)U·L~(-1)、(71.73±11.55)U·L~(-1),显著高于对照组(P0.05),AST、ALP含量与对照组相比显著上升(P0.05),高剂量组AMY水平为(833.46±63.05)U·L~(-1),与对照组相比显著降低(P0.05)。GSH-Px和SOD水平随PFOS浓度增加出现了显著降低(P0.05),而MDA水平显著升高(P0.05)。内质网应激标志蛋白表达均较对照组显著上升(P0.05)。以上结果说明PFOS可导致大鼠肝细胞损伤,其机制可能与内质网应激调控有关。     

4种典型纳米材料对小鼠胚胎成纤维细胞毒性的初步研究

为探讨不同种类纳米材料对原代培养小鼠胚胎成纤维细胞(Mouse embryo fibroblasts,MEF)的毒性效应及作用机制,选择4种典型的纳米材料(纳米碳、单壁碳纳米管、纳米氧化锌、纳米二氧化硅)制备颗粒悬液,设立5个剂量组(5、10、20、50、100μg·mL-1)对BALB/c小鼠MEF细胞进行24、48、72h染毒培养,利用细胞形态学观察和噻唑蓝实验(MTT比色法)检测上述4种纳米材料对MEF细胞活性的影响,同时,测定染毒24h后细胞培养液上清中乳酸脱氢酶(LDH)活性以探讨纳米颗粒对细胞膜完整性的影响.结果显示:1)4种纳米材料均能明显影响MEF细胞的生长形态.染毒24h后,MEF细胞发生不同程度的回缩变形,细胞间隙增大,排列稀疏,胞内颗粒物增多,细胞透明度下降.2)纳米碳、纳米氧化锌、纳米二氧化硅对MEF细胞增殖的抑制作用和对细胞膜完整性的损伤作用均随染毒剂量的升高而增强,具有明显的剂量-效应关系,其半数致死浓度(24h-IC50)分别为21.85、21.94、461.10μg·mL-1;碳纳米管组的剂量-效应之间不呈对数线性关系,未能得出其24h-IC50.3)在不同染毒剂量水平上,4种纳米材料的毒性对比差异显著:低剂量水平上纳米碳与碳纳米管的毒性强于纳米氧化锌和纳米二氧化硅,随着剂量的升高纳米氧化锌的细胞毒性升高最为显著.结果提示,纳米材料能够对MEF细胞造成毒性损伤,破坏细胞膜的完整性可能只是作用途径之一;纳米材料的毒性可能受粒径、形状、化学组成等许多因素的影响.     

Comparative changes in absorption,distribution and toxicity of copper and cadmium chloride in toads during the hibernation and the role of vitamin C against their toxicity

The aim of this study was to determine the bioavailability and adverse effects of cadmium (Cd) and copper (Cu) on hibernating Egyptian toads and whether ascorbic acid (vitamin C) blocked Cd- and Cu-induced effects during hibernation. The oxidative status of liver, kidney, and intestine of Bufo regularis to Cd, Cu, and/or a combination of both metals administered orally for 2 weeks was determined. In the protection studies, vitamin C was given for 1?h prior to administration of Cu, Cd, and/or metal combination for 2 weeks. Treatment with Cu, Cd, and a combination of both metals produced a reduction in red blood count cells and hemoglobin content, while white blood count cells showed an increase in numbers during these treatments. After 2 weeks exposure, Cd and Cu increased significantly in all the tissues studied. Cu storage presented the following sequence: liver?>?intestine?>?kidney. Cd storage presented the following sequence: intestine?>?kidney?>?liver. When exposed to both metals, Cu and Cd storage presented the following sequence: liver?>?intestine?>?kidney. Histopathological examination of the liver revealed marked alterations including loss of hepatic cell architecture, and some cells exhibited distinct cytoplasmic vacuoles. The majority of blood vessels exhibited a marked dilatation and congestion with infiltration of blood cells, prominent hyperemia of hepatic veins, and significant proliferation of bile ductules. Histopathological changes in the kidney showed destruction and degeneration of both renal tubule cells and glomerular with infiltration of leukocytes and inflammatory cells. Histopathological alterations in the intestine were restricted to the innermost mucosal epithelium with marked degeneration of the villi and submucosa and an extensive fragmentation of mucosal epithelium as well as atrophy of goblet cells. The administration of vitamin C 1?h prior to administration of Cd, Cu, and metal combination did not protect against hepatic, renal, and intestinal damage. However, parental vitamin C given alone increased tissue toxicity.     

多壁碳纳米管引起白鼠肺部毒性的评价(Comparative Pulmonary Toxic Assessment of Mutil-Wall Carbon Nanotubes in Rats)

以雄性Wistar大白鼠为研究对象,观察了多壁碳纳米管(MWNTs)体内暴露后肺部的病理学变化.采用气管注入方式将直径为40～60nm多壁碳纳米管(40～60MWNTs)和直径小于10nm的多壁碳纳米管(10MWNTs)暴露于大白鼠的体内,同时分别采用纳米二氧化硅(SiO2)和乙炔碳黑(Cb)作为阳性和阴性对照.实验结果表明:实验中采用的纳米颗粒均不同程度地引起了肺部的损伤,同剂量下损伤严重程度顺序为:Cb>10MWNTs>40～60MWNTs>SiO2.多壁碳纳米管对肺部损伤的程度与剂量呈依赖关系,当在低剂量(1mg·kg-1)时,40～60MWNTs仅仅对肺部引起了轻微的炎症损伤,随着剂量的增大,多壁碳纳米管对肺部的损伤越来越严重,出现明显的病理损伤.     

纳米铜颗粒的种间毒性关系

纳米颗粒的种间毒性关系尚无明确结论,因此很难判断纳米颗粒对未进行毒性测试的物种的风险如何。本文作者将5种水蚤(Daphnia magna, Daphnia pulex, Daphnia galeata, Ceriodaphnia dubia, Chydorus sphaericus)暴露于4种不同粒径的纳米铜颗粒(CuNPs)和1种亚微米铜颗粒的悬浊液中,考察物种的形态特征与CuNPs急性毒性的关系。结果显示,杆状的CuNPs比球状的CuNPs毒性更低。纳米铜颗粒与溶出铜离子均对CuNPs的毒性有贡献,其中,当新生蚤的体长、体表面积和身体体积更小时,5种悬浊液中颗粒的毒性更大。5种蚤的身体体积与5种CuNPs的毒性显著相关(r_adj²>0.51, p < 0.001),78-nm CuNPs与蚤身体体积的相关性最好 (r_adj²?=?0.95, p < 0.001)。这个研究可以为纳米颗粒对有相似外形特征的物种进行毒性种间外推提供线索。
精选自Lan Song, Martina G. Vijver, Geert R. de Snoo and Willie J.G.M. Peijnenburg. Assessing toxicity of copper nanoparticles across five cladoceran species. Environmental Toxicology and Chemistry: Volume 34, Issue 8, pages 1744–1750, August 2015. DOI: 10.1002/etc.3000
详情请见http://onlinelibrary.wiley.com/doi/10.1002/etc.3000/full     

纳米铜颗粒的种间毒性关系

纳米颗粒的种间毒性关系尚无明确结论,因此很难判断纳米颗粒对未进行毒性测试的物种的风险如何。本文作者将5种水蚤(Daphnia magna, Daphnia pulex, Daphnia galeata, Ceriodaphnia dubia, Chydorus sphaericus)暴露于4种不同粒径的纳米铜颗粒(CuNPs)和1种亚微米铜颗粒的悬浊液中,考察物种的形态特征与CuNPs急性毒性的关系。结果显示,杆状的CuNPs比球状的CuNPs毒性更低。纳米铜颗粒与溶出铜离子均对CuNPs的毒性有贡献,其中,当新生蚤的体长、体表面积和身体体积更小时,5种悬浊液中颗粒的毒性更大。5种蚤的身体体积与5种CuNPs的毒性显著相关(r_adj²>0.51, p < 0.001),78-nm CuNPs与蚤身体体积的相关性最好 (r_adj²?=?0.95, p < 0.001)。这个研究可以为纳米颗粒对有相似外形特征的物种进行毒性种间外推提供线索。
精选自Lan Song, Martina G. Vijver, Geert R. de Snoo and Willie J.G.M. Peijnenburg. Assessing toxicity of copper nanoparticles across five cladoceran species. Environmental Toxicology and Chemistry: Volume 34, Issue 8, pages 1744–1750, August 2015. DOI: 10.1002/etc.3000
详情请见http://onlinelibrary.wiley.com/doi/10.1002/etc.3000/full     

纳米铜颗粒的种间毒性关系

纳米颗粒的种间毒性关系尚无明确结论,因此很难判断纳米颗粒对未进行毒性测试的物种的风险如何。本文作者将5种水蚤(Daphnia magna, Daphnia pulex, Daphnia galeata, Ceriodaphnia dubia, Chydorus sphaericus)暴露于4种不同粒径的纳米铜颗粒(CuNPs)和1种亚微米铜颗粒的悬浊液中,考察物种的形态特征与CuNPs急性毒性的关系。结果显示,杆状的CuNPs比球状的CuNPs毒性更低。纳米铜颗粒与溶出铜离子均对CuNPs的毒性有贡献,其中,当新生蚤的体长、体表面积和身体体积更小时,5种悬浊液中颗粒的毒性更大。5种蚤的身体体积与5种CuNPs的毒性显著相关(r_adj²>0.51, p < 0.001),78-nm CuNPs与蚤身体体积的相关性最好 (r_adj²?=?0.95, p < 0.001)。这个研究可以为纳米颗粒对有相似外形特征的物种进行毒性种间外推提供线索。
精选自Lan Song, Martina G. Vijver, Geert R. de Snoo and Willie J.G.M. Peijnenburg. Assessing toxicity of copper nanoparticles across five cladoceran species. Environmental Toxicology and Chemistry: Volume 34, Issue 8, pages 1744–1750, August 2015. DOI: 10.1002/etc.3000
详情请见http://onlinelibrary.wiley.com/doi/10.1002/etc.3000/full     

Acute toxicity and histopathology study of a galactose-specific lectin from the seeds of Tetracarpidium conophorum (African walnut) (Hutch and Dalz)

A lactose-binding lectin (TCL) was purified from the seeds of African walnut, Tetracarpidium conophorum, and acute toxicity studies of the lectin were carried out with Swiss albino male mice. Animals were administered doses of TCL from 500 to 2500?mg?kg^?1 body weight (b.wt.) orally while intraperitoneally the dose ranged from 10 to 600?mg?kg^?1 b.wt. Animals were then assessed for organ and body weight changes, mortality, and histopathology. TCL did not cause any observable toxicity via the oral route; however, when administered intraperitoneally, TCL elicited toxicity with an LD₅₀ of 50?mg?kg^?1 b.wt. Death from intoxication was preceded by convulsion, hypoactivity, salivation, ataxia, and weakness. The animals given lethal doses of the lectin showed profound respiratory depression which was judged to be the primary cause of death. Histopathological analysis indicated that the lungs, liver, and spleen were adversely affected while the kidney and other organs were essentially normal. In all the affected organs, the severity of toxicity was dose-dependent as the effect of the lectin became more pronounced with increase of the dose administered.     

Comparison of in vitro characteristics of and experimental lesions produced by a clinical and an environmental isolate of Aspergillus flavus

In the present study, two strains of Aspergillus flavus (one from a human corneal ulcer and one from the environment) were found to be strikingly similar in vitro in terms of thermotolerance, inability to grow in an anaerobic environment and in secreting proteinases; however, one obvious difference was that the clinical isolate produced 120 ppb of aflatoxin B1 in glucose salt medium while the environmental isolate did not produce this toxic metabolite. Alterations in the activities of acid phosphatase (ACP), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and glutathione-S-transferase were observed in the liver, kidney and serum in an experimental rat model, irrespective of whether the animal had been challenged with the clinical isolate or the environmental isolate of A. flavus. In rats that had been challenged with the clinical isolate, a significant decrease in the activity of kidney ALP was noted, whereas in rats that had been challenged with the environmental isolate, the reverse was observed. While these differential alterations may have occurred due to differences in the toxin-producing ability of the two isolates, further investigation is warranted to clarify whether other phenotypic, or genotypic, differences are also involved.     

Monitoring of cellular enzymes in the serum of electroplating workers at Coimbatore

Chromium compounds are potent toxic and carcinogenic substances. With respect to toxicity, hepatic and renal toxicity have been reported both in workers and in animals exposed to chromium (VI). Chromium (VI) compounds induces DNA damage in vivo and in cultured cells as well as the cytotoxicity evaluated by the leakage of lactate dehydrogenase. The present study reports the cytotoxicity of chrome platers who are employed from 8 to 25 years in electroplating industries at Coimbatore, Tamilnadu. Blood samples were collected and estimated for glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and total protein in the serum. The study revealed that there is a significant elevation in the level of LDH, ALP, CPK and transaminases and a decrease in total protein in serum. The results of the study suggests that chromium (VI), a hepatotoxic chemical may perhaps damage the plasma membrane resulting in leakage of enzymes in to the serum of chromeplaters.     

Chronic mixture toxicity study of Clophen A60 and diethyl phthalate in male rats

Chemical mixtures are an important area of research as individuals are exposed to low doses of persistent chemical agents known as environmental pollutants throughout their life time. Polychlorinated biphenyls (PCBs) and diethyl phthalate (DEP) are ubiquitous environmental pollutants that could be present in the same environmental compartment; hence organisms may get simultaneously exposed to both. Therefore, a study was undertaken to see whether PCB and DEP together show interactive chronic mixture toxicity in male Wistar rats. Healthy male Wistar rats weighing 70–100?g were randomly assigned to four groups of six each. Control rats were fed on normal diet and water ad libitum. Oil control rats were maintained on a normal diet mixed with corn oil. Rats were given Clophen A60 (PCB) and DEP dissolved individually in corn oil mixed with the diet at 50?mg?kg^?1 of the diet/day, as well as a mixture in corn oil mixed with the diet both at 50?mg?kg^?1 of the diet/day. After 150 days of treatment animals were sacrificed and enzymes and other biochemical parameters in the serum and liver were assessed. Liver weight to body weight ratio showed a significant increase in Clophen A60 and in Clophen A60?+?DEP treated rats. In the DEP, Clophen A60 and Clophen A60?+?DEP treated groups there was significant increase in liver and serum alanine aminotransferase (ALT) and acid phosphatase (ACP) activity. Aspartate aminotransferase (AST) was significantly increased in the liver and serum of DEP treated rats only. Cholesterol levels were significantly increased only in the serum and the liver of DEP treated rats. Triglyceride levels were significantly increased in the serum of treated rats and only in the liver of Clophen A60 and Clophen A60?+?DEP treated rats. Liver glycogen levels were significantly increased in DEP and Clophen A60?+?DEP treated rats. In all treated animals, there was a significant decrease in liver glutathione reductase (GR). Histology of liver showed severe vacuolations, fatty degeneration and loss of hepatic architecture in Clophen A60 and Clophen A60?+?DEP treated rats, whereas in DEP treated rats only loss of hepatic architecture and granular deposits in the hepatocytes was predominant with mild vacuolations of centrilobular and periportal area. It is evident from this study of mixture toxicity of Clophen A60 and DEP that there is no significantly enhanced toxicity due to the interaction of these two compounds. On the other hand, to some extent there is alleviation in toxicity as evidenced by enzyme ACP and AST levels in the liver. The hepatocellular damage and biliary congestion caused by these two compounds, which can be confirmed by significantly increased liver weights and elevated serum and liver enzyme levels as well as histology, was almost the same between individual and mixture treated group.     

Pulmonary inflammation induced by office dust and the relation to 1 → 3-β-glucan using different extraction techniques

It is observed that 1?→?3-β-glucan, a major cell wall component of fungi, induces pulmonary inflammation. There is inconsistency in determining the correlation between the levels of glucan measured by current extraction methods and the respiratory inflammation observed in individuals or lab animals exposed to environmental dust samples. The glucan-specific limulus amebocyte lysate (G-LAL) method was used after extraction with dimethyl sulfoxide (DMSO) or sodium hydroxide (NaOH) to analyze the glucan content of office dust samples collected from a water-damaged building. C3HeB/FeJ mice, an endotoxin-sensitive strain, were treated with different dust samples (2.5?mg?kg^?1 body weight) or saline (vehicle control) by pharyngeal aspiration. At 1?day after aspiration, bronchoalveolar lavage (BAL) was performed, and lung inflammation and injury were assessed by measuring: (1) neutrophil (PMN) infiltration, (2) inflammatory cytokine (IL-6, IL-10, MCP-1, IFN-γ, TNF-α, and IL12-p70) levels, and (3) albumin and lactate dehydrogenase in recovered BAL fluid. Both DMSO and NaOH extraction increased the detection of glucan by approximately 20-fold compared to water extraction. However, only the DMSO extraction method showed a statistically significant positive correlation between 1?→?3-β-glucan and albumin levels, total numbers of BAL, polymorphonuclear leukocytes (PMNs) cells recovered, levels of TNF-α, MCP-1, and IL-6. In conclusion, 1?→?3-β-glucan is a potent inflammatory agent in dust samples and DMSO extraction for glucan analysis may prove useful in understanding the impact of environmental contamination by glucans on lung disease.