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.     

Role of GSH in the amelioration of chromium-induced membrane damage

Membrane damage is one of the important consequences of chromium (Cr), an environmental toxicant, induced cytotoxicity. Reduced glutathione (GSH), a membrane protectant may be used to reduce the Cr-induced membrane damage. In the present study, the impact of Cr in presence and absence of GSH was studied on plasma membrane of the liver and kidneys in male Wistar rats. Significant increases in membrane cholesterol levels as well as significant decreases in membrane phospholipid levels in Cr exposed (0.8 mg per 100 g body weight, i.p., for 28 days) animals suggest structural alterations in both the liver and kidney plasma membranes. Alkaline phosphatase (ALP), total ATPase, and Na⁺–K⁺–ATPase activities of plasma membrane were significantly decreased in both the liver and kidneys after Cr treatment. This treatment also produced significant weight loss and increased Cr content in the liver and kidneys. However, GSH (8 mg per 100g body weight, i.p., daily at an interval of 6 h after injection of Cr for a period of 28 days) supplementation restored alterations induced by Cr in plasma membrane of both the liver and kidneys but was not able to eliminate the deposited Cr from the liver and kidney tissues.     

Protective effects of curcumin on antioxidant status,body weight gain,and reproductive parameters in male rats exposed to subchronic 2,3,7,8-tetrachlorodibenzo-p-dioxin

The aim of this study was to investigate the effects of curcumin (CUR) on antioxidant status, body weight (BW) gains, and some reproductive parameters in male rats exposed to subchronic doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Thirty-two rats were divided into four groups. The first group was kept as control. The second group (TCDD group) was given TCDD at a dose of 50 ng·kg^?1 BW per day; the third group (CUR group) was treated with CUR at a dose of 80 mg·kg^?1 BW per day. The fourth group (TCDD + CUR group) was given TCDD and CUR at the same doses simultaneously. Malondialdehyde (MDA) levels were significantly increased in the TCDD group. In addition, TCDD exposure decreased liver superoxide dismutase (SOD) activity, catalase (CAT) activities of kidney and brain, glutathione peroxidase (GSH-Px) activities of liver, kidney, and brain, and glutathione levels of liver, kidney, and heart. However, CUR treatment with TCDD exposure decreased MDA levels in all tissues and increased SOD activities of liver, kidney, and brain, CAT activity of heart, and GSH-Px activities of heart and brain. TCDD caused a decrease in BW gain, and CUR partially eliminated this effect of TCDD. In addition, while reproductive organ weights, sperm concentration, and sperm motility tended to decrease with TCDD exposure, these effects tended to be close to normal levels by CUR treatment. In conclusion, CUR was seen to be effective in the treatment and prevention of toxicity induced by subchronic TCDD exposure.     

Antioxidant effect of L-cysteine on sodium-valproate-induced oxidative stress in rat liver: biochemical and ultrastructural approaches

L-Cysteine has protective efficacy in cases of oxidative tissue injury. Sodium valproate is widely used as an anticonvulsant and an antidepressant in spite of hepatotoxicity as side effect. The aim of this study was to evaluate the protective role of L-cysteine in liver toxicity induced by sodium valproate overdose. Release of the hepatic enzymes, aspartate aminotransferase and alanine aminotransferase, and levels of lipid profiles, as well as the oxidative, enzymatic, and non-enzymatic antioxidant were assessed. Liver damage was judged histologically. L-Cysteine decreased the activity of alanine aminotransferase and aspartate aminotransferase, as well as improved the level of lipid profile, increased the enzymatic antioxidant (catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase), and decreased the lipid peroxidation. L-Cysteine administration inhibited liver injury of sodium valproate.     

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.     

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.     

基于谷胱甘肽结合作用定量研究微囊藻毒素的解毒代谢机制

基于谷胱甘肽(GSH)解毒作用探讨了微囊藻毒素-RR(MCRR)在不同动物肝脏和肾脏合作下的代谢机制。通过人工合成MCRR的谷胱甘肽代谢物(MCRR-GSH),腹腔注射至鲫鱼和大鼠体内,利用液相色谱串联质谱技术(LC-MS/MS)定量检测MCRR-GSH及其下游半胱氨酸代谢物(MCRR-Cys)在组织内的代谢动力学变化。在72 h的暴露实验中,实验组鲫鱼和大鼠体内均定量检测到MCRR-GSH和MCRR-Cys。MCRR-GSH在肾脏中的浓度显著高于其他组织(P0.05),鲫鱼和大鼠体内累积浓度分别是(0.161±0.001)和(0.116±0.005)μg·g~(-1)DW。同样的,MCRR-Cys主要分布于鲫鱼和大鼠的肾脏组织。鲫鱼肾脏中MCRR-Cys的浓度出现明显的波动,而肝脏和胆汁内的MCRR-Cys浓度却呈现出上升的趋势;大鼠肾脏内MCRR-Cys的浓度呈缓慢下降的趋势,浓度范围为(8.899±0.817)μg·g~(-1)DW至(3.336±0.263)μg·g~(-1)DW。基于以上结果推测,微囊藻毒素在肝脏和肾脏合作下的解毒过程为:MC在肝脏内经GSH结合作用生成的代谢物MC-GSH随血液循环转运至肾脏,在肾脏内MCGSH快速地转化为下游代谢物MC-Cys以促进排泄。     

常用杀菌剂对啶虫脒中华蜜蜂毒性潜在增效作用研究

啶虫脒对蜜蜂急性毒性较低,且允许在作物花期施用,而杀菌剂也是蜜源植物花期常用药剂。本文采用点滴法和摄入法测定了10种常用杀菌剂对啶虫脒中华蜜蜂毒性的潜在增效作用。结果表明,点滴田间实际暴露剂量的杀菌剂使啶虫脒对中华蜜蜂的毒性不同程度的增加。点滴杀菌剂和啶虫脒24 h、48 h后,咪鲜胺、丙环唑、腈菌唑、戊唑醇、苯醚甲环唑、嘧菌酯、己唑醇、吡唑醚菌酯、三唑酮、氟硅唑使啶虫脒毒性分别增加14.02、10.74、8.50、7.92、4.77、4.28、4.19、4.07、2.74、2.67倍和8.01、10.14、4.80、7.09、2.66、2.56、3.62、2.69、2.24、1.49倍。摄入田间实际暴露剂量的杀菌剂和啶虫脒混剂24 h、48 h后,啶虫脒对中华蜜蜂的毒性增加。其中,丙环唑、氟硅唑、苯醚甲环唑、嘧菌酯、咪鲜胺使啶虫脒的毒性分别增加3.62、2.46、2.10、1.98、1.56倍和2.07、2.81、2.20、2.58、2.23倍。因此蜜源植物花期应避免丙环唑、咪鲜胺、戊唑醇、腈菌唑与啶虫脒先后喷施或混合喷施,慎用己唑醇等其他6种杀菌剂,以防啶虫脒残留导致中华蜜蜂采集蜂中毒。     

Protective effect of Tamarindus indica fruit pulp extract on collagen content and oxidative stress induced by sodium fluoride in the liver and kidney of rats

Fluorosis is a serious public health problem in many parts of the world. The generation of reactive oxygen species and lipid peroxidation has been considered to play an important role in the pathogenesis of chronic fluoride toxicity. The present study was undertaken to evaluate the protective effect of Tamarindus indica fruit pulp extract on the collagen content and oxidative stress in liver and kidney of fluoride-exposed rats. The first group served as control. The second group received 200 mg L^?1 of sodium fluoride through drinking water. The third and fourth groups received T. indica fruit pulp extract (200 mg kg^?1 body weight) alone and along with fluorinated drinking water respectively, daily by gavage for a period of 90 days. At the end of the experiment, blood samples were collected from all groups, and liver and kidney samples were taken concurrently. Levels of malondialdehyde and glutathione and the activities of superoxide dismutase and catalase were evaluated in the liver and kidney of experimental rats. Furthermore, level of hydroxyproline and histological examination of liver and kidney along with serum biochemical parameters were evaluated. In conclusion, fluoride was determined to cause adverse effects in rats, and the supplementation of tamarind to these animals alleviated the adverse effects of fluoride.     

Sub-chronic exposure to carbendazim induces biochemical and hematological alterations in male goats

The present investigation reports the effect of repeated (90 days) administration of carbendazim on the biochemical and hematological parameters in male goats. Carbendazim administered orally at a daily dose of 50 mg kg^?1 body weight for 90 consecutive days resulted in increased plasma concentration of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), gamma-glutamyl transferase (GGT), creatinine and albumin, while alkaline phosphatase (ALP) and glucose levels were decreased. Decrease in total leukocyte (TLC) and neutrophil count and increase in lymphocyte count was observed in the treatment group. The findings of the present investigation indicate that sub-chronic exposure to carbendazim in male goats causes hepatic and slight kidney dysfunctions.     

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.     

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.     

铬在小鼠体内的蓄积效应与毒性

铬的工业用途很广,主要用于金属加工、电镀、制革等行业,这些行业排放的三废导致了环境铬污染,对环境生态和人体健康造成危害。为探究铬对动物的毒性作用,选择昆明种纯系小白鼠作为受试生物,研究六价铬在小鼠体内的蓄积效应及毒性。结果显示,饮用水中一定浓度的六价铬(15~70 mg·L-1)可抑制小鼠体重的正常增长,染毒30 d后,小鼠肝脏和肾脏脏器系数下降,脾脏和脑的脏器系数提高;总铬含量在心脏和脾脏中增高,其他脏器中无明显蓄积效应;铬染毒组小鼠骨髓细胞活性氧水平提高,骨髓嗜多染红细胞微核率显著增高。结果表明,通过饮水摄入六价铬可造成小鼠肝肾损伤,心脏和脾脏内铬蓄积,并通过活性氧损伤效应破坏机体的遗传稳定性。     

Biomarkers of oxidative stress as indicators of water pollution in Nile tilapia (Oreochromis niloticus) from a water reservoir in Riyadh,Saudi Arabia

Antioxidant enzyme activities of fish (Oreochromis niloticus) were determined in order to assess the status of pollution in the Wadi Namar (WN), near Riyadh, Saudi Arabia. Activities of four antioxidant enzymes as superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), and concentrations of glutathione (GSH) and oxidant malondialdehyde (MDA) were selected as bioindicators. Fish (n = 14) were sampled in the month of April 2013 from WN and a control site (CS). SOD activity was increased by 37.9%, 47%, and 29% in kidney, liver, and heart, respectively, while a significant decrease (36.4%) was observed in gills of O. niloticus from WN as compared to fish from CS. CAT activity was reduced by 51%, 55%, 47%, and 35% in kidney, liver, heart, and gills of O. niloticus from WN. The GST activities in kidney, liver, and heart of O. niloticus from WN were elevated by 34%, 48%, and 32%, respectively. However, significant fall (49%) in gills of fish was noted from WN compared to fish from CS. GSH levels were increased by 44%, 36%, and 38% in kidney, liver, and heart, respectively, but decreased by 30% in gills. MDA levels of O. niloticus were significantly increased in kidney, liver, and heart in fish from WN. Data indicated that WN is polluted mainly by industrial and urban discharge of liquid waste products.     

Glutathione S-transferase activity in rats exposed to methyl parathion

Methyl parathion is an organophosphate insecticide that has been used in agriculture and the domestic sector for several years. This pesticide and others, arriving through different processes, exert significant effects on water quality with serious consequences for environmental and human health. The main objective of this study was to investigate the changes of Glutathione S-transferase enzyme activity in methyl parathion exposed rat tissues. For this purpose, wistar rats (Rattus norvegicus) were injected intraperitoneally with 7 mg kg^?1 dose of methyl parathion, while corn oil was applied to control groups in the same way. The liver, kidneys, brain and small intestine were quickly removed after 0, 2, 4, 8, 16, 32, 64, and 72 hours of injection of methyl parathion and the glutathione S-transferase activity was determined in these tissues. As a result it was seen that glutathione S-transferase activity increases in all tissues in the group of male and female rats to which methyl parathion was given. The increase of glutathione S-transferase activity may be a result of methyl parathion's toxic effect because it is one of the most important enzymes of detoxification metabolism.     

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.     

Changes in the level of transaminases in Indian major carp, Labeo rohita exposed to sublethal concentration of tannery and distillery effluents

The activity of alanine aminotransferase (ALAT) and aspartate aminotransferase (AAT) of different tissues of fingerlings of Labeo rohita under the influence of two effluents has been studied. The alanine aminotransferase activity was increased over the control in different exposed periods of tannery and distillery effluent treatments. The alanine aminotransferase in the liver showed increased activity at different periods than that of the muscle, kidney, gill and brain (p < 0.001) (60.09%) over the control during the 40 days exposure in both the effluents treatments. The increased activity of alanine aminotransferase was highly significant (p > 0.001) in all the tissue in tannery and distillery effluents treatments. Similarly aspartate aminotransferase activity was increased over the control in all the treated tissues from 10 to 40 days exposure. But this increase, was not significant in the muscle tissue in distillery and tannery treatements after 10 days exposure. From 10 to 40 days, the activity was increased but a maxmum elevation was observed during 40 days, where the elevation was more in the liver, which was followed by muscle, kidney, gill, brain (brain < gill < kidney < muscle < liver).     

双酚A对小鼠肝脏和肾脏细胞的氧化损伤

为探究双酚A(BPA)的氧化毒性,分别以剂量为20、40和80mg·kg~(-1)·d~(-1)的BPA对雄性昆明小鼠灌胃处理1周,并测定了小鼠体内活性氧自由基(ROS)水平、还原型谷胱甘肽(GSH)含量、丙二醛(MDA)含量和DNA-蛋白质交联系数(DPC)。与对照组相比,各BPA暴露组小鼠肝脏和肾脏细胞中的ROS生成量、MDA含量和DPC系数均升高,而GSH含量下降(P<0.05或P<0.01)。ROS生成量、GSH含量和DPC系数均显示出剂量-效应关系。研究表明,BPA可扰乱小鼠肝脏和肾脏细胞的氧化应激平衡,诱导细胞氧化损伤。     

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。     

Substitution of toxicologically critical solvents in the residue analysis of acetamiprid: Towards green chemistry

The article presents the reduced use of toxicologically critical solvents for the extraction and clean-up of a neo-nicotinoid pesticide, acetamiprid from vegetables. Acetamiprid was extracted from spiked vegetable samples of cabbage by the use of different techniques like microwave-assisted extraction (MWAE), sonication and by the conventional method of homogenization. The study revealed that though higher percent recoveries of 78–92 were obtained in the blending method, solvent use was high as compared to MWAE. In MWAE, the percent recoveries recorded were in the range of 46–89 depending upon the solvent used and power employed. A mixture of methanol–water and methanol–acetone at 400 W power levels gave percent recoveries of 72 and 82, respectively, as compared to solvent mixtures, namely, acetone–hexane and acetone–hexane–water, which recorded recoveries of 49 and 67%. The study indicates that the choice of solvent and power employed plays a significant role in MWAE for enhanced recoveries.