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.     

Time-dependent effects of pentabrominated diphenyl ether (PBDE) on thyroid hormones and histology in rats

In order to examine the time-dependent effects of pentabrominated diphenyl ether (BDE-99) on thyroid hormones levels and histological structure in rats, 4-week-old SD rats were divided into 10 groups randomly, according to their body weight. Rats in treatment groups were orally gavaged with BDE-99 at the dose of 60 mg kg^?1 for 10, 15, 20, 30 or 40 days, while rats in control group received equal volume of corn oil. Serum levels of thyroxine (FT4), triiodothyronine (FT3), and thyroid stimulating hormone (TSH) were measured by radioimmunoassay. Sections of thyroids were dyed with hematoxylin-eosin (HE) to detect any pathologically alterations. In BDE-99 treated groups, on day 10, changes in serum levels of FT4, FT3 and TSH were not found. On days 15 and 20, serum levels of FT4 and FT3 decreased, accompanied by increased levels of TSH. On days 30 and 40, serum levels of these hormones returned to control values. As for alterations in histology, on day 15, follicular epithelium of the thyroid were found to proliferate into two layers in BDE-99 treated rats. On day 20, in focal areas the two-layer follicular epithelia were observed to continuously proliferate into 3–4 layers of follicular epithelium, called hyperplasia plaques. On days 30 and 40, solid buds and secondary follicles to solid buds were detected. The earliest alteration of thyroid hormones in treated SD rats occurred at the duration of 10–15 days, with corresponding histopathologic changes. As the exposure time increased, the serum level of hormones and histopathology altered accordingly in a time-dependent manner.     

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.     

Dietary selenium fortification: a potential solution to chronic arsenic toxicity

Selenium (Se), an important micronutrient and antioxidant, also acts as an antagonist of arsenic (As). Se supplementation of diet was investigated in mitigating chronic As toxicity in mammals. Experiments were conducted to determine whether Se supplementation in As-exposed rats might (i) decrease As-induced lipid peroxidation in liver, (ii) increase blood antioxidant status, and (iii) reverse suppression of the secondary antibody response. Male Wistar rats were exposed to As (40 and 80?ppm) in drinking water and received challenge diets with three different levels of Se (deficient: <0.01?ppm, adequate: 0.15 ppm, and fortified: 0.6?ppm) for 16 weeks. Clinical variables including behavior, body weight, and food and water consumption were recorded weekly, and blood sample was collected monthly. Antioxidant status was assessed through glutathione sulfhydryl (GSH) levels in whole blood. Lipid peroxidation in the liver was evaluated using the malondialdehyde (MDA) assay. The antibody response was measured using keyhole limpet hemocyanin as an immunogen. Se deficiency significantly increased hepatic lipid peroxidation and suppressed antibody production relative to the Se-adequate and -fortified groups, confirming that Se deficiency exacerbates the damage produced by As exposure. Se fortification markedly elevated the blood GSH level in both As-exposed groups, indicating protective effects. At adequate Se levels, rats showed signs of counteracting As-mediated toxicity. However, Se fortification produced more pronounced benefits against As-induced toxicity, a pattern that was particularly notable in the 40?ppm As group.     

Combined effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin and polychlorinated biphenyl congeners in rats

The objective of this work was to evaluate potential interactions between 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls congeners (PCBs) in rats. Groups of five adult female rats were given 0, 2.5, 25, 250, or 1000?ng TCDD/kg body weight/day or TCDD in combination with a mixture of PCB congeners at a concentration of 2 or 20?µg?kg^?1 body weight/day by gavage for 28 days. After the 28-day treatment period, the rats were killed for the analysis of biochemical, liver enzyme activities, and hematological and pathological end points. Growth suppression, increased absolute and relative liver weights, and decreased thymic weight were observed in the 1000?ng TCDD group alone, or the groups receiving a mixture of 1000?ng TCDD and 2 and 20?µg PCBs. TCDD-increased liver and thymic weights were not altered by PCBs; however, growth suppression was more pronounced in animals receiving 1000?ng TCDD and 2?µg PCBs. Increased hepatic microsomal methoxy resorufin-O-demethylase and ethoxy resorufin-O-deethylase activities occurred in 250 and 1000?ng?kg^?1 TCDD-treated animals, which were antagonized by PCBs. Effects of 250?ng TCDD on serum cholesterol and liver uridine diphosphate glucuronosyl transferase activity were reduced by 20?µg PCBs. Treatment with 1000?ng TCDD increased serum albumin, decreased liver vitamin A, increased kidney vitamin A, and liver microsomal glutathione-S-transferase activity, which were not affected by PCBs. Decreased hemoglobin, platelet, packet cell volume, and red cell indices were observed in TCDD-treated rats, but no interactive effects were seen. Histopathological evaluation revealed that liver, thyroid, and thymus were the target organs, but the effects of co-exposure to PCBs and TCDD were variable. These results indicate that the mixture effects of PCBs and TCDD may be additive, synergistic, or antagonistic depending on the dose level and end points measured.     

三(1,3-二氯-2-丙基)磷酸酯诱发肝脏损害及病理改变研究

本研究观测有机磷酯阻燃剂(OPFRs)污染是否可以诱发肝脏损害,考察其发生及发展程度,并探讨其发生机理,为有机磷阻燃剂污染的防治和相关疾病的有效治疗提供基础数据和科学依据。实验以大鼠为动物模型,将60只SPF级SD雄性大鼠分为5组,每组12只,选取典型的氯代有机磷阻燃剂三(1,3-二氯-2-丙基)磷酸酯(TDCPP)对大鼠进行染毒,空白对照组不做任何处理,溶剂对照组以相同体积的橄榄油灌胃,染毒组以不同剂量的TDCPP进行灌胃(125 mg·kg~(-1)·d~(-1)、250 mg·kg~(-1)·d~(-1)和500 mg·kg~(-1)·d~(-1)),每周测量体重,于第4周和第8周取血检测肝功及其他生化指标,在第8周每组抽取3只大鼠取肝脏组织做HE染色,并用透射电镜观察分析肝组织病理学改变。TDCPP对大鼠染毒8周后,结果表明:(1)体重指标在灌胃1周后开始发生差异,TDCPP处理组大鼠的体重有下降的趋势,染毒组与空白对照组和溶剂对照组相比较,差异显著(*P0.05,**P0.01),其中高剂量灌胃组的体重下降最为明显(**P0.01);(2)血清肝功指标表现出显著变化,血清谷丙转氨酶、谷草转氨酶、胆固醇和甘油三脂水平在第8周呈现明显下降趋势,染毒组与空白对照组和溶剂对照组比较,差异明显(*P0.05,**P0.01);(3) TDCPP暴露组生理生化指标变化明显,血清乙酰胆碱酯酶活性显著降低,MDA含量显著升高,SOD活力显著性降低,造成氧化损伤,与空白对照组和溶剂对照组比较,差异显著(*P0.05,**P0.01);(4)病理切片结果显示染毒组与对照组比较,细胞坏死现象明显,且高剂量组坏死更为严重。研究结果显示:TDCPP可引起大鼠体重明显下降,大鼠肝脏细胞损伤、合成功能下降,造成肝脏代谢功能紊乱,造成较为严重的肝损伤。     

PCB disposition and different biological effects in rats following direct soil exposure vs. PCBs off-gassed from the soil

A comparison of PCB congener profiles and limited biological effects was made between direct exposure to PCB-contaminated soil and vapor phase PCBs from that soil to determine congener patterns useful for identifying exposure sources in humans and wildlife. Weanling female Sprague–Dawley rats were exposed to either control or PCB-contaminated soil (from a landfill in Southern Illinois) for 1 and 2 weeks. The exposures were via direct contact with the soil or via airborne exposure with the rats isolated from the soil by a wire screen. Total PCB of 25% contaminated soil used in the study was 13?500?ppm. No PCBs were detectable in control rats. In direct-exposed rats, total PCB residues in fat pad, ear skin, serum, liver, and inguinal lymph nodes after the 1-week exposure were 6256, 185, 3.2, 149, and 41?ppm, respectively, but decreased to 465, 72, 1.7, 106, and 32.4?ppm after the 2-week exposure. In airborne-exposed rats, total PCB residues were 7.8, 1.6, 0.03, 0.2, and 0.6 in the same manner and slightly increased in fat pad and ear skin to 11.6 and 2.14, respectively. Decreases in both the concentrations and percentages of “episodic” PCBs (those congeners rapidly metabolized) in the fat pad were apparent following the 2-week exposure compared to the 1-week exposure by both routes. Both EROD and BROD activities were significantly increased in the direct-exposed rats, whereas only BROD activity increased in airborne-exposed rats. Serum T ₄ levels were depleted in the direct-exposed rats regardless of time of exposure but were increased insignificantly after 1-week and significantly after 2 weeks in the airborne-exposed rats. No significant changes in serum insulin levels were apparent in any of the treated groups. The results suggested that exposure of animals to PCBs via different routes could result in different PCB profiles, which could cause different biological effects.     

Manganese toxicity in Drosophila melanogaster: extension of the life span by resveratrol

The effect of resveratrol was studied on the life span and motor activity of Drosophila melanogaster treated with manganese (Mn). Two days after emerging from the pupa, male wild type D. melanogaster were fed for 13 days with corn media containing 15?mM Mn. Thereafter, Drosophila were divided into six groups of 300 flies each: (1) the flies remained treated with Mn; (2) began treatment with 0.43?mM resveratrol (Mn-resveratrol group); (3) received no additional treatment (Mn-no treatment group); (4) simultaneously fed with Mn and resveratrol (Mn?+?resveratrol group). In addition, a control (5) with no treatment and another group (6) fed only with resveratrol after emerging from the pupa were included. All Mn-treated flies (group 1) were dead on the 25th day. The life span in the resveratrol group was 91?±?0.33 days (mean?±?S.E.M.) and in Mn-resveratrol flies was 83?±?2 days. These two values were significantly higher than those detected in the control (5) and Mn-no treatment (group 3) flies whose life span were 68?±?0.33 and 67?±?2.31 days, respectively. The Mn?+?resveratrol-fed flies had a markedly higher life span (31?±?1.53 days) than Mn-fed flies (23?±?0.88 days). In the flies that received Mn (Mn and Mn?+?resveratrol groups), the motor activity decreased significantly with respect to control (groups 5) and the Mn–resveratrol and resveratrol groups. In conclusion, resveratrol increased significantly the life span of Mn-treated D. melanogaster.     

The relations of antioxidant vitamins A,E, and C with MDA levels in serum and liver of rats treated with nitrosamines

In this study, we investigated the levels of vitamins A, E, and C in serum and liver, and malondialdehyde (MDA) were followed by long-term administration of some nitrosamines. Sprague-Dawley rats were divided into four groups. N-Nitrosodiethylamine (NDEA), 1-Nitrosopiperidine (NPip), and N-Nitrosopyrrolidine (NPyr) were administered 200 ppb, orally with water for 30 consecutive days to experimental groups. Animals were decapitated at 3rd, 7th, 15th, and 30th days of the administrations. Significant increases were observed in MDA levels treated with nitrosamines at all times. Serum MDA levels were found to be significantly higher in NDEA-treated animals than in control and other groups at 30th day. Liver MDA levels were highly increased in NPyr-treated group. Significant decreases were observed in the levels of vitamins A, E, and C in rats treated with nitrosamines at all times. There were also significantly negative correlations at present changes among the serum or liver MDA levels and vitamin A, E, and C levels in all nitrosamines-treated groups. These findings demonstrate that exposure at low levels of nitrosamines decreased vitamin A, E, and C levels while it attributed lipid peroxidation. Therefore, maintaining an adequate level of antioxidant vitamins in serum and liver may be necessary for the prevention or protection of long-term nitrosamine exposures.     

新型阻燃剂TCPP对斑马鱼的毒性研究

为了明确新型阻燃剂磷酸三(2-氯丙基)酯(TCPP)的生态风险,本研究采用斑马鱼为模式生物,评价了TCPP对成鱼和胚胎的毒性效应。急性毒性研究结果表明,TCPP对斑马鱼成鱼的96 h致死中浓度(LC50)为47.06 mg·L~(-1),而对胚胎96 h-LC50为26.01 mg·L~(-1),且会影响胚胎的正常发育,导致孵化出的仔鱼产生畸形。成鱼14 d延长毒性试验结果表明,TCPP对斑马鱼成鱼的无可观察效应浓度(NOEC)为1.00 mg·L~(-1),染毒暴露后肝脏和性腺指数随TCPP浓度增加轻微下降,但肝脏中卵黄蛋白原(VTG)的含量和性腺中芳香化酶的活性随TCPP浓度增加普遍升高。此外,TCPP的暴露还会导致斑马鱼脑垂体中合成促性腺激素的相关基因表达量增加。因此,TCPP对斑马鱼成鱼和胚胎的急性毒性均为低毒级,但长期暴露会干扰内分泌系统的调控功能,影响斑马鱼的正常发育。     

全氟辛烷基磺酸钾(PFOS)和纳米氧化锌(Nano-ZnO)复合暴露对斑马鱼下丘脑-垂体-甲状腺轴功能的影响

全氟辛烷基磺酸钾(PFOS)和纳米氧化锌(Nano-Zn O)广泛存在于环境中,但是它们复合暴露对水生生物的潜在毒性机制尚未明确。本文探讨PFOS和Nano-Zn O复合暴露对斑马鱼下丘脑-垂体-甲状腺轴(HPT轴)毒性的影响。将斑马鱼胚胎从孵化开始暴露于PFOS(0.2、0.4、0.8 mg·L~(-1))、Nano-Zn O(6.75、12.5、25 mg·L~(-1))、PFOS+Nano-Zn O(0.2+6.75、0.4+12.5、0.8+25 mg·L~(-1))溶液中15 d后,分析幼鱼的发育毒性,体内的甲状腺激素(甲状腺素(T4)和三碘甲状腺氨酸(T3)含量和与甲状腺有关基因(CRF、TSH、NIS、TG和TPO)的表达情况。结果发现复合暴露组与单独暴露组相比,前者显著诱导了幼鱼的畸形率,降低了幼鱼的存活率,并抑制了幼鱼的体长。复合暴露组显著增加了幼鱼体内T3含量,同时抑制体内T4的含量。与单独暴露组相比,复合暴露组显著诱导了CRF和NIS基因的表达,同时抑制了TSHβ和TG基因的表达。而TPO基因的表达水平在单独和复合暴露组中没有显著差异。本研究首次证明了PFOS和Nano-Zn O复合暴露对斑马鱼幼鱼甲状腺轴的干扰效果并对其进行了机制探讨。     

Hepatoprotective effects of taurine against mercury induced toxicity in rats

An attempt has been made to study the influence of taurine on mercury intoxicated rats. The animals were treated with sublethal dose of mercuric chloride (2 mg/kg body wt.) for 30 days. During the mercury treatment, the level ofAspartate transaminase(AST), Alanine transaminase (ALT) and Alkaline phosphatase(ALP) in serum and lipid peroxidation (LPO) in liver tissue significantly increased whereas Glutathione (GSH), Glutathione peroxidase(GPx), Catalase (CAT) and Superoxide dismutase (SOD) were simultaneously decreased in the liver tissue. Present results indicate that the liver tissue was completely damaged, after mercury treatment. In another group of animals, taurine (5 mg/kg body wt.) was administrated for another 15 days. Taurine administration was observed to improve the liver function in mercury intoxicated animal as indicated by the decline in increased levels of AST, ALT and ALP in serum and LPO content in liver tissue. The decreased level of antioxidant system (GSH, GPx, CATand SOD) has been promoted Results suggested that taurine played a vital role in reducing the mercury toxicity in intoxicated animals.     

Effects of the level of dietary protein on the toxicity of hexachlorocyclohexane in rats

Male albino rats were fed for 28 days from weaning on diets containing 5% (group 1), 10% (group 2) and 21% (group 3, normal protein) protein as casein. At the end of dietary period, HCH was administered daily for 30 days to investigate the interaction between protein deficiency and pesticide toxicity. The results indicated that rats fed a lower protein diet and HCH had a higher mortality, lower rate of growth, increased liver weight and deposition of the pesticide in blood and tissues in larger amounts. Blood pressure (systolic and diastolic) was significantly increased and the heart rate showed tachycardia in low protein exposed animals. A significant increase of total lipids, cholesterol, triglycirides, free fatty acids in serum and tissues of animals exposed to low protein was observed. A close correlation existed between lipid accumulation and storage of HCH in tissues and dietary protein seemed to play an important role in detoxification.     

Time-dependent effects of chlordane on thyroid histological structure and function in rats

In order to study the time-dependent effects of chlordane on thyroid hormone levels and histological structure in rats, 120 healthy 4-week-old SD rats were divided randomly into 12 groups. Rats in treatment groups were treated orally by gavage with chlordane at a dose of 15 mg kg^?1 for 5, 10, 15, 20, 30, or 40 days, while rats in control group received an equal volume of corn oil. Serum levels of thyroxine (FT4), triiodothyronine (FT3), and thyroid stimulating hormone (TSH) were measured by radioimmunoassay. Sections of thyroids were dyed with hematoxylin–eosin to detect any pathological alterations. In chlordane treated groups, on day 5, changes in serum levels of FT4, FT3, and TSH were not found. On days 10 and 15, serum levels of FT4 and FT3 decreased, accompanied by increased levels of TSH. On days 20, 30 and 40, serum levels of these hormones returned to control values. As for alterations in histology, on day 10–15, follicular epithelium of the thyroid were found to proliferate into two layers in chlordane treated rats. On day 20, in focal areas the two-layer afollicular epithelia were observed to continuously proliferate into 3–4 layers of follicular epithelium, termed hyperplasia plaques. On days 30 and 40, solid buds and secondary follicles to solid buds were detected. The earliest alteration of thyroid hormones in treated SD rats occurred between 5 and 10 days with corresponding histopathologic changes. As the exposure time increased, the serum levels of hormones and histopathology altered in a time-dependent manner.     

塑料增塑剂对凡纳滨对虾存活、生长和免疫的影响(Effects of Plastic Plasticizers on Survival, Growth and Immune Factors of Litopenaeus vannamei)

研究了塑料增塑剂邻苯二甲酸二甲酯(DMP)、邻苯二甲酸二乙酯(DEP)、邻苯二甲酸二丁酯(DBP)和邻苯二甲酸二辛酯(DOP)对凡纳滨对虾(Litopenaeus vannamei)存活、生长和免疫的影响.96h急性毒性实验表明,在助溶剂Tween20的安全浓度范围内,随着DMP、DEP、DBP和DOP水平的升高,凡纳滨对虾存活率呈下降趋势,24h、48h、72h和96h的LC50分别为40.33、35.29、25.48、19.14mg·L-1,30.52、23.45、16.96、15.38mg·L-1,7.51、6.97、6.57、6.06mg·L-1和6.85、5.87、5.01、4.47mg·L-1;DMP、DEP、DBP和DOP对凡纳滨对虾的安全浓度随塑料增塑剂碳链的增加呈下降趋势,分别为8.11、4.15、1.80和1.29mg·L-1.90d慢性毒性实验表明,凡纳滨对虾存活率、特定生长率、血清蛋白含量、血清酚氧化酶和超氧化物歧化酶活性均以对照组和0.0400mg·L-1助溶剂Tween20处理组最高,而且显著高于1/100倍DMP、DEP、DBP和DOP安全浓度处理组(p<0.05).     

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。     

Phytochemical screening and toxicological profile of methanolic extract of Picralima nitida fruit-rind (Apocynaceae)

The methanol (M) extract of the fruit-rinds of Picralima nitida (PN) was analyzed phytochemically and evaluated for its toxicity effect in Wistar rats. The rats were administered graded doses (0.75, 1.5, 3, and 6 g kg^?1 p.o) of the extract daily for 6 weeks and the toxicological effect of these varying levels of extract were examined on the serum, hepatic, and renal concentration of biochemical parameters as well as the histopathology of tissue section of these liver, kidney, and lungs. Clinical signs and hematology were also evaluated. Phytochemical analysis revealed that alkaloids and polyphenols were major compounds. Both biochemical and histopathological data presented demonstrate dose-dependent signs of toxicity. Our results show a significant elevation in serum concentration of aspartate amino-transferase, alanine amino-transferase, glucose, creatinine, total cholesterol, and protein with high-dose of PN treatment tested. PN also caused a significant reduction in hepatic malondialdehyde and a slight increase in glutathione concentration at the lowest dose tested. Renal urea level was reduced significantly in test groups. A significant change was observed in the relative weights of the spleen, heart, and kidneys. The total white blood cell count was reduced, whereas the hematocrit level was increased remarkably in animals that received high doses of the extract. The acute toxicity LD₅₀ was estimated at 14.5 and 12.5 g kg^?1 body weight for male and female, respectively. These results show that prolonged usage of this extract at 1.5–6 g kg^?1 dose could cause liver, kidney, and lung injury, while the effect was mild at small dose levels (0.75 g kg^?1). Thus, the extract should be taken with caution bearing in mind that higher doses could affect the liver, kidneys, and lungs.     

Protective properties of filamentous blue–green alga Spirulina against the oxidative stress induced by cadmium in freshwater mussel Unio ravoisieri

ABSTRACT

Cadmium (Cd) is a toxic-heavy metal that induces a wide range of behavioural, biochemical and physiological effects in aquatic organisms. Oxidative damage has been proposed as a possible mechanism involved in cadmium toxicity. The current study was carried out to evaluate the antioxidant activity of Spirulina as feed additive (1?mg/L) against the toxicity of cadmium (Cd) 0.5?mg/L in freshwater mussel Unio ravoisieri. At the end of the exposed period of 4 days, digestive gland antioxidant status Superoxide dismutase, Catalase, Glutathione-S-transferase and damage markers such as Malondialdehyde and Protein carbonyl were determined. Associations between biomarkers were assessed by a multivariate analysis technique, principal component analysis (PCA). The results of this study revealed that digestive gland antioxidant status showed a significant decrease when mussels were exposed to Cd. Superoxide dismutase, Catalase and Glutathione-S-transferase activities in the Cd?+?SP group were significantly higher than the Cd group (p P?相似文献   

17β3-雌二醇对西伯利亚鲟幼鱼的雌激素效应

为了研究以及评估在利用17β-雌二醇(estradiol-17β,E2)混饲投喂进行人工诱导西伯利亚鲟(Acipenser baerii)性别逆转过程中,外源雌激素处理对西伯利亚鲟幼鱼的雌激素效应以及激素残留风险.实验选取健康的2月龄西伯利亚鲟840尾,设置E2在饲料中的投喂剂量为1 mg·1kg-1(C组)和10 m...     

Protective effects of Manasamitra vatakam on aluminum-induced nephrotoxicity,oxidative stress,and histological damage

The aim of this study was to investigate the nephroprotective and antioxidant property of Manasamitra vatakam (MMV) against aluminum (Al)-induced toxicity in rats. The kidney function marker parameters such as serum urea, uric acid, and creatinine were significantly increased in Al-treated rats as compared with controls. Similarly, the antioxidant enzyme activities such as superoxide dismutase, glutathione S-transferase, Na⁺/K⁺-ATPase and Mg-ATPase, reduced glutathione were also found significantly increased in Al-treated rats. A significantly decreased level of these parameters was observed in the MMV (orally 100?mg?kg^?1 body weight)-treated group along with a reduced level of malonaldehyde, molecular chaperones of an antioxidative stress protein, and mRNA expression of HSP70. The biochemical observations were also supported by histopathological observations. Thus, this study supports the nephroprotective and antioxidant activities of MMV.