硫丹和狄氏剂对多刺裸腹的毒性效应

为了解亚致死浓度的有机氯农药硫丹和狄氏剂对枝角类的急性、慢性和联合毒性作用,采用急性毒性实验方法研究了硫丹和狄氏剂对多刺裸腹溞(Moina macrocopa)的48 h半效应浓度,应用生命表实验方法研究了亚致死浓度的硫丹(0、52和208 μg/L)和狄氏剂(0、12和48μg/L)对多刺裸腹溞生命表统计学参数的影响.结果表明,硫丹及狄氏剂对多刺裸腹溞的48 h半效应浓度是834.9和185.8 μg/L.硫丹对多刺裸腹溞出生时的生命期望(e0)、世代时间(T)和净生殖率(R0)有显著的影响(P<0.05),但对种群内禀增长率(rm)没有显著的影响(P>0.05);狄氏剂仅对种群内禀增长率有显著的影响(P<0.05);硫丹与狄氏剂的交互作用对所有生命表统计学参数均无显著影响(P>0.05).与硫丹浓度为0时相比,52和208μg/L的硫丹均使多刺裸腹溞的e0.和T显著缩短,R0显著降低;与狄氏剂浓度为0时相比,48μg/L的狄氏剂使多刺裸腹溞的rm显著升高.这说明硫丹与狄氏剂对多刺裸腹溞的联合作用形式是独立相加,没有产生协同作用.     

番茄碱对乙酰胆碱酯酶活性影响的研究

通过电化学方法分析了番茄碱对乙酰胆碱酯酶活性的影响.结果表明:(1)乙酰胆碱酯酶经盐析、凝胶过滤层析分离纯化,酶比活力达到685.3 U/mg,提纯倍数达到229.5倍;(2)低浓度(1 mmol/L)番茄碱对乙酰胆碱酯酶有明显的激活作用,阳极化扫描的氧化峰电流由1.4 μA升至2.8 μA;高浓度(10 mmol/L)番茄碱对乙酰胆碱酯酶有明显的抑制作用,阳极化扫描的氧化峰电流由1.4 μA降至0.5 μA.说明采用循环伏安法、线形扫描电化学手段,对碘化胆碱的电化学行为可分析番茄碱对乙酰胆碱酯酶的活性影响,此项研究为探讨番茄碱的作用机理奠定基础,为研制性能优良的生物传感器提供理论依据.     

溴氰菊酯连续暴露对罗非鱼血清乙酰胆碱酯酶活性的影响

以罗非鱼为受试生物,研究了不同水温(23℃～27 ℃)对罗非鱼血清中乙酰胆碱酯酶活性的影响,并在此基础上研究了不同浓度(1.0、2.0、3.0、5.0和10.0 μg·L-1)溴氰菊酯暴露下,罗非鱼血清中乙酰胆碱酯酶活性的动态变化.水温分别为23℃和27℃时,乙酰胆碱酯酶的活性分别为(2.75±0.21)和(2.73±0.26)U·ml-1,活性波动范围分别为-12.0%～13.1%和-11.0%～14.2%.水温为(25±1)℃,染毒10 d时,2.0μg·L-1以上浓度的溴氰菊酯对罗非鱼血清中乙酰胆碱酯酶具有明显的抑制作用;染毒20 d时,2.0μg·L-1以上浓度的溴氰菊酯对其抑制率均超过40%;染毒25 d时,5.0 μg·L-1的溴氰菊酯对其抑制率达到最大,为62.3%.实验结果表明:水温在23℃～27℃的波动不会对罗非鱼血清中乙酰胆碱酯酶的活性产生显著影响;水温为(25±1)℃时,高浓度溴氰菊酯(≥2.0 μg·L-1)会对罗非鱼血清中乙酰胆碱酯酶的活性产生抑制作用,而且抑制率随染毒时间的延长呈增加趋势.     

夹竹桃叶乙醇提取物对斑马鱼的毒性评价

研究表明, 夹竹桃(Nerium indicum Mill.)及其提取物对多种害虫具有较强的毒杀作用, 已在害虫生物防治中显示出较大作用。为了合理开发夹竹桃植物, 需要进一步评价夹竹桃植物对水生生物的安全性和对动物的毒理学。文章利用索氏提取法提取夹竹桃叶乙醇粗提物, 并进一步用氯仿萃取浓缩、硅胶柱层析方法提取分离乙醇精提物, 经鉴定为强心甙组分。在此基础上, 委托浙江省医学科学院评价了乙醇粗提物对实验动物的毒理学, 并采用静态法评价了这二种提取物对斑马鱼(Brachydanio rerio)的急性毒性和慢性效应。结果表明: 夹竹桃叶乙醇粗提物的提取率为45%, 乙醇精提物(主要成分为强心甙组分)的提取率为0.25%。乙醇粗取物对大鼠经口和经皮毒性为低毒级, 对家兔皮肤和眼无刺激, 对豚鼠的致敏反应属弱致敏性。这说明夹竹桃叶乙醇粗提物对哺乳动物十分安全。在急性毒性试验中, 发现斑马鱼的死亡率与提取物处理浓度和处理时间均呈明显的正相关。处理浓度越大, 斑马鱼的死亡率越高; 同一浓度处理时间越长, 死亡率越高。用24 mg/L 乙醇粗提物处理6、12、24 和48h 的死亡率分别为26.67%、60%、91.11%和95.56%; 用0.5 mg/L乙醇精提物处理12、24、48、72 和96h 的死亡率分别为6.25%、33.33%、52.08%、54.17%和60.42%; 用24 mg/L 乙醇粗提物处理96h 或32 mg/L 处理48h, 或者用1 mg/L 乙醇精提物处理24h, 斑马鱼全部死亡。在慢性毒性试验中, 用3.33-10.0 mg/L 乙醇粗提物处理斑马鱼28d, 其死亡率为12%-20%。乙醇粗提物处理斑马鱼后, 急性毒性LC50=12.52 mg/L(药后96h)10 mg/L, 慢性毒性LC50=199.51 mg/L(药后28d); 乙醇精提物处理斑马鱼后, 急性毒性LC50=0.46 mg/L(药后96h)1 mg/L, 根据《化学农药环境安全评价试验准则》(1990)中农药对鱼类的毒性分级标准, 说明夹竹桃叶乙醇粗提物对斑马鱼的毒性属于低毒, 比较安全; 乙醇精提物对斑马鱼的毒性则为高毒, 十分不安全。       

红霉素对大型溞生殖、生长和基因表达的生态毒理效应

红霉素（ERM）在水环境中广泛检出,并产生生态毒理风险。以大型溞为模式生物,研究了ERM在浮游动物繁殖、生长、抗氧化及神经系统方面的慢性毒理效应。结果表明ERM对大型溞的急性毒性为低毒（48 h-LC₅₀为315.41 mg/L,96 h-LC₅₀为163.08 mg/L）。在2 μg/L和200 μg/L浓度下暴露21 d,ERM会干扰大型溞的繁殖、生长、氧化应激防御及解毒相关基因的表达,诱导丙二醛含量上升,抑制抗氧化系统超氧化物歧化酶和谷胱甘肽转移酶及神经系统乙酰胆碱酯酶活性,引起细胞膜损伤和神经传导紊乱,造成大型溞前期产卵率升高,且对生长发育和游泳行为产生不利影响。解析了ERM在浮游动物繁殖、生长及在蛋白和基因水平上的毒理响应,为揭示抗生素对水生生物种群稳定和生态系统安全的影响提供基础数据支撑。     

雌性斑马鱼暴露于环境剂量三唑磷对亲代生殖和氧化应激及子代胚胎发育的影响

三唑磷作为一种广泛使用的有机磷杀虫剂,该药物在自然水体中的残留可对非靶标生物产生潜在威胁,文章旨在探究三唑磷对斑马鱼的毒性效应。研究将3月龄雌性斑马鱼(Danio rerio)持续暴露于环境相关浓度的三唑磷(10μg/L) 21d,然后与健康雄鱼自然受精产卵;通过测定雌鱼生殖力、亲代与子代的氧化应激及子代胚胎发育相关指标,评估三唑磷对亲代雌鱼及其子代的毒性效应。主要研究结果:亲代雌鱼经10μg/L三唑磷暴露后,产卵量显著提高(P<0.05),肝脏内乙酰胆碱酯酶(AChE)活性显著降低(P<0.05),丙二醛(MDA)含量显著增加(P<0.05),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽-S-转移酶(GST)和羧酸酯酶(CarE)活性均显著增强(P<0.05);所产子代胚胎受精率、受精卵直径、胚胎心率和初孵仔鱼体长均显著降低(P<0.05),仔鱼畸形率显著增加(P<0.05),孵化率无显著性差异;仔鱼AChE与SOD活性呈下降趋势但差异不显著, MDA含量显著增加(P<0.05), GPx与GST活性显著降低(P<0...     

锑胁迫对斑马鱼酶活性的影响研究

研究重金属锑胁迫下,分析生物体内各类酶活性的变化,了解生物对锑胁迫的响应机制。以斑马鱼为受体研究对象,探究不同浓度锑溶液(0、10、20、30和40 mg/L)和不同时间(24、48、96和144 h)培养下,斑马鱼体内不同酶活性的变化情况。研究结果表明,培养24 h时,不同浓度锑对斑马鱼体内除碱性磷酸酶以外的7种酶活性均有明显的抑制作用。随着锑胁迫时间增加,斑马鱼体内三磷酸腺苷酶、过氧化氢酶活性呈现先降低后增加的变化趋势;过氧化物酶、超氧化物歧化酶、乙酰胆碱酯酶、乳酸脱氢酶和酸性磷酸酶活性呈现"锯齿形"变化趋势;碱性磷酸酶酶活性呈现先增加后降低的变化趋势。综上分析表明锑对斑马鱼体内自由基调节、兴奋传导、能量代谢、物质运输、机体生长和免疫防御等生命过程都有明显的影响。     

氧化石墨烯对红细胞功能的影响

纳米材料的生物相容性是人们关注的热点。氧化石墨烯是一种被广泛应用于生物医学的纳米材料,但其毒性不容忽视。本文从溶血率、红细胞脆性、乙酰胆碱酯酶活性三方面研究了氧化石墨烯对血液系统的毒性。结果表明,红细胞的溶血率在氧化石墨烯浓度低于100 μg/mL时均低于8% (P<0.01);低浓度氧化石墨烯 (<5 μg/mL) 对红细胞的脆性没有显著影响,高浓度氧化石墨烯 (如10 μg/mL) 会提高红细胞的脆性 (P=0.01);氧化石墨烯能增加红细胞上乙酰胆碱酯酶的活性,浓度为20 μg/mL的直径>5 μm的氧化石墨烯 (LGO) 可将乙酰胆碱酯酶的活性提高42.67% (P<0.05)。之后利用分子动力学模拟研究氧化石墨烯与乙酰胆碱酯酶相互作用并提高其活性的机理,推测氧化石墨烯会附着在细胞膜上并提供一个电负性环境,帮助水解产物更快地从活性位点脱离,从而提高乙酰胆碱酯酶的活性。     

三种农药对红裸须摇蚊毒力和羧酸酯酶活性的影响

摇蚊是一种世界性分布的水生昆虫,常作为监测水环境污染指示生物。以红裸须摇蚊为对象,测定了氧化乐果、毒死蜱和三氟氯氰菊酯对红裸须摇蚊4龄幼虫毒力和体内羧酸酯酶活性的影响。结果表明,氧化乐果、毒死蜱和三氟氯氰菊酯12 h 致死中浓度LC₅₀分别为12.508、2.478和0.046 μg/L。低浓度(0.05 μg/L)氧化乐果处理3 h和12 h以及各浓度(除8 μg/L)氧化乐果处理48 h,摇蚊体内羧酸酯酶活性均高于对照,表现为诱导作用,其余各浓度各处理时间均表现为抑制减少。除0.125 μg/L和0.25 μg/L毒死蜱处理12 h对羧酸酯酶有诱导作用外,毒死蜱均抑制羧酸酯酶活性;而三氟氯氰菊酯也均抑制羧酸酯酶活性。因此,摇蚊羧酸酯酶可作为一种监测农药污染的生物化学标志物加以利用。     

五氯酚对斑马鱼胚胎的毒性效应研究

采用斑马鱼胚胎发育技术,对环境激素类物质五氯酚的毒性进行测定,结果表明,五氯酚(PCP)对胚胎的特定作用时间段是卵产出至发育6 h之内;PCP对胚胎发育有明显的抑制作用,会造成胚胎发育的畸形或死亡,不同时间染毒产生的可观察毒理学终点各异;随着PCP对发育48 h斑马鱼胚胎作用时间的减短,其致死效应敏感性降低,其中0 hpf组的LC0值最小,为70.8μg·L^-1,24hpf组LC0值最大,为831.8μg·L^-1;斑马鱼胚胎对孵化后0时染毒的PCP最为敏感,PCP对胚胎产生急性毒性效应的敏感指标:心胞囊肿、血液循环障碍、无心律＞孵化率降低＞停滞发育作用;斑马鱼胚胎最敏感的指标为48 h血液循环障碍和48 h半致死效应.     

Aquatic insects as a vector for Mycobacterium ulcerans

Mycobacterium ulcerans is an emerging environmental pathogen which causes chronic skin ulcers (i.e., Buruli ulcer) in otherwise healthy humans living in tropical countries, particularly those in Africa. In spite of epidemiological and PCR data linking M. ulcerans to water, the mode of transmission of this organism remains elusive. To determine the role of aquatic insects in the transmission of M. ulcerans, we have set up an experimental model with aquariums that mimic aquatic microenvironments. We report that M. ulcerans may be transmitted to laboratory mice by the bite of aquatic bugs (Naucoridae) that are infected with this organism. In addition, M. ulcerans appears to be localized exclusively within salivary glands of these insects, where it can both survive and multiply without causing any observable damage in the insect tissues. Subsequently, we isolated M. ulcerans from wild aquatic insects collected from a zone in the Daloa region of Ivory Coast where Buruli ulcer is endemic. Taken together, these results point to aquatic insects as a possible vector of M. ulcerans.     

Aquatic Insects as a Vector for Mycobacterium ulcerans

Mycobacterium ulcerans is an emerging environmental pathogen which causes chronic skin ulcers (i.e., Buruli ulcer) in otherwise healthy humans living in tropical countries, particularly those in Africa. In spite of epidemiological and PCR data linking M. ulcerans to water, the mode of transmission of this organism remains elusive. To determine the role of aquatic insects in the transmission of M. ulcerans, we have set up an experimental model with aquariums that mimic aquatic microenvironments. We report that M. ulcerans may be transmitted to laboratory mice by the bite of aquatic bugs (Naucoridae) that are infected with this organism. In addition, M. ulcerans appears to be localized exclusively within salivary glands of these insects, where it can both survive and multiply without causing any observable damage in the insect tissues. Subsequently, we isolated M. ulcerans from wild aquatic insects collected from a zone in the Daloa region of Ivory Coast where Buruli ulcer is endemic. Taken together, these results point to aquatic insects as a possible vector of M. ulcerans.     

Endosulfan increases seric interleukin-2 like (IL-2L) factor and immunoglobulin M (IgM) of Nile tilapia (Oreochromis niloticus) challenged with Aeromona hydrophila

Endosulfan is a persistent organochlorine insecticide which is extremely toxic to fish. It is known to induce immunological alterations in juvenile Nile tilapia (Oreochromis niloticus) such as increases in phagocytic activity and reactive oxygen species production of spleen macrophages. The purpose of the present study was to demonstrate the effects of acute exposure to a sublethal concentration of endosulfan (7 ppb, 96 h) on parameters of the adaptive humoral immune response of the aforementioned aquatic organism. The effect of endosulfan on the capacity of immune cells to produce interleukin-2 like (IL-2L) factor and immunoglobulin M (IgM) in response to a challenge with ½ LD50 of the infectious bacteria Aeromonas hydrophila was evaluated.Experimental results indicate that short, sublethal, endosulfan exposure triggers a succession of events beginning with non-specific activation of macrophages followed by an exacerbated synthesis of the IL-2L factor by activated B cells. This leads to significantly increased secretion of IgM and could in turn facilitate autoantibody production and the development of autoimmune pathologies.     

Degradation and detoxification of endosulfan isomers by a defined co-culture of two Bacillus strains

The degradation of alpha and beta isomers of endosulfan by a two-member bacterial co-culture was studied. Results were similar whether the two isomers were present individually or together, as in technical endosulfan. The degradation of both isomers was accompanied by the formation of endosulfan diol and endosulfan lactone. Accumulation of the metabolite, endosulfan sulfate was, however, not observed during the reaction with either of the isomers. The microbial degradation of endosulfan isomers was also accompanied by a decrease in its toxicity to the test organism Tubifex tubifex Müller.     

Effects of low concentration of endosulfan on proliferation, ERK1/2 pathway, apoptosis and senescence in Nile tilapia (Oreochromis niloticus) splenocytes

Endosulfan is a potent organochlorinated pesticide that is known to induce side effects in aquatic organisms, including Oreochromis niloticus (Nile tilapia). It has been previously shown that endosulfan induces oxidative stress and non-specific activation of splenic macrophages and exacerbated serum interleukin-2 synthesis in Nile tilapia. Endosulfan may promote proliferation of T cells through MAP kinase (MAPK) activated signal transductions. The ERK family of MAPKs includes ERK1 and ERK2. Phosphorylated ERK1/2 (pERK1/2) molecules are involved in many aspects of cellular survival, and are important for apoptosis or oxidative stress-induced senescence. In order to study the mechanisms by which endosulfan affects fish health, the present study was aimed at evaluating the in vitro effects of this insecticide on proliferation, the ERK1/2 pathway, apoptosis and cell senescence in splenocytes from Nile tilapia. Lymphoproliferation was evaluated by colorimetric method using the WST-1 assay. Flow cytometry was used to assess pERK1/2, apoptosis and senescence, using Annexin V-FITC and β-galactosidase respectively. Experimental data showed that exposure to 7 μg mL(-1) of endosulfan per se increased cellular proliferation, but decreased the lymphoproliferative response to mitogenic stimulus with PMA + ionomycin. Splenocytes exposed to endosulfan for 15-180 min showed significantly higher levels of pERK1/2 than the non-exposed control. Endosulfan mediated a decrease in etoposide-induced apoptosis and provoked cell senescence. In conclusion, exposure of immune cells to a low concentration of endosulfan deregulates their function and may facilitate the development of multiple diseases.     

Metabolic pathways utilized by Phanerochaete chrysosporium for degradation of the cyclodiene pesticide endosulfan.

Recent studies have shown that cultures of white rot fungi not favoring the production of lignin and manganese peroxidases are effective in degrading certain xenobiotics. In this study we have used endosulfan as a model xenobiotic to assess the enzymatic mechanisms of pesticide metabolism under ligninolytic (nutrient-deficient) and nonligninolytic (nutrient-rich) culture conditions. Rapid metabolism of this chlorinated pesticide occurred under each nutrient condition tested. However, the extent of degradation and the nature of the metabolic products differed for nutrient-deficient and nutrient-rich media. The pathways for endosulfan metabolism were characterized by analysis of the fungal metabolites produced. The major endosulfan metabolites were identified by gas chromatography-electron capture detection and gas chromatography-mass spectrometry as endosulfan sulfate, endosulfan diol, endosulfan hydroxyether, and a unknown metabolite tentatively identified as endosulfan dialdehyde. The nature of the metabolites formed indicates that this organism utilizes both oxidative and hydrolytic pathways for metabolism of this pesticide. Piperonyl butoxide, a known cytochrome P-450 inhibitor, significantly inhibited the oxidation of endosulfan to endosulfan sulfate and enhanced hydrolysis of endosulfan to endosulfan diol. We suggest that the metabolism of endosulfan is mediated by two divergent pathways, one hydrolytic and the other oxidative. Judging by the inactivity of extracellular fluid and partially purified lignin peroxidase in metabolizing endosulfan, we conclude that metabolism of this compound does not involve the action of extracellular peroxidases.     

Endosulfan induces oxidative stress and changes on detoxication enzymes in the aquatic macrophyte Myriophyllum quitense

Endosulfan (1) is a chlorinated insecticide still in use in both developed and emerging countries. Although its toxicity on animals has been studied in the last years, scarce information is available on its effects on plants. In this study, we exposed the aquatic macrophyte Myriophyllum quitense to environmentally relevant concentrations of endosulfan (microg/L) (1) for a short time, simulating exposures that might occur after either accidental spills or toxic run-off from agricultural areas. The main goal was to evaluate changes in both detoxication and antioxidant enzymatic systems of this plant upon exposure to endosulfan (1). Thus, we measured the activities of catalase (CAT), soluble and membrane associated glutathione-S-transferases (s- and m-GSTs) and glutathione reductase (GR), as well as the hydrogen peroxide (H2O2) content. Results showed that endosulfan (1) exerts oxidative stress on M. quitense, which was evidenced by the increase of CAT activity and the H2O2 content in exposed plants. At 5 microg/L endosulfan (1), we found a generalized induction of activities of tested enzymes, indicating that this xenobiotic activates the protection system of this plant, increasing its capacity to scavenge reactive oxygen species. On the other hand, we did not find significant changes at 0.02 microg/L endosulfan (1), which is the maximal concentration allowed for freshwater. We conclude that runoff events, which can produce significant amounts of endosulfan (1) in aquatic environments during short time, can result in oxidative stress on M. quitense, and probably on similar macrophytes.     

水生昆虫对汞的吸收、富集和水-陆转移

汞是一种人体非必需且有毒的重金属元素,全球性的汞污染因对人类健康具有损害而备受社会关注。自然界中的汞绝大部分会通过江河径流和雨雪尘土的沉降而进入水生生态系统,每年进入水生生态系统的汞至少有10 000吨。水生昆虫作为重要的消费者生物存在于水生生态食物网中,是其重要的组成部分,在水生生态系统的物质循环中扮演着重要角色。本文介绍了近年来水生昆虫与汞之间的相关研究,重点总结了水生昆虫对汞的吸收和富集程度,分析了水生昆虫在汞的水-陆转移中的作用。研究数据表明,水生昆虫对汞的吸收程度与环境因素有关,并通过不同的途径转移到陆地生态系统中,对陆地生态系统上层食物链的生物存在一定的威胁,同时也需注意在对水生昆虫进行开发利用的同时,考虑汞是否超标的因素。     

Life cycle and paratenesis of American gordiids (Nematomorpha: Gordiida)

To complete their life cycle, gordiids must make a transition from aquatic to terrestrial environments. However, epibenthic aquatic larvae and their terrestrial definitive hosts do not overlap in habitat. This has led many investigators to suggest that infections are acquired through the ingestion of insects, which become infected as aquatic larvae with gordiid cysts and subsequently carry gordiids to land. This proposed life cycle was experimentally tested using 3 common American species of gordiids: Gordius robustus, Paragordius varius, and Chordodes morgani. Cysts of all 3 species survived the metamorphosis of Tanytarsus sp., a midge. Subsequent infection trials of definitive hosts with cysts from imagos show that cysts surviving the metamorphosis of insects remained viable and free of host internal defense reaction. Data from naturally infected mayflies, Callibaetus sp., show that encystment and survival of gordiids within aquatic insects occur in nature. Paratenesis between paratenic hosts was also shown to be possible in these 3 species. This latter finding appears to indicate that cysts formed in spurious paratenic hosts may not be lost but may eventually transfer to normal paratenic hosts.     

STUDIES ON SELECTIVE TOXICITY OF SIX INSECTICIDES BETWEEN GREEN PEACH APHID AND LADYBIRDS

Abstract  The selective toxicity of six kinds of insecticides, including imidacloprid, imidacloprid + synergist (SV1), fenvalerate, endosulfan, methomyl and dimethoate, between the green peach aphid ( Myzus persicae Sulzer) and two species of ladybirds ( Coccinella septempunctata Linnaeus and Propylaea japonica Thunbery), was investigated in the laboratory. The reults showed that both imidacloprid WP and imidacloprid + synergist (SVl) EC possessed the highest toxicity to the aphids. Between C. septempunctata and M. persicae and between P. japonica and M. persicae , the selective toxicity ratios (STRs) of imidacloprid WP, imidacloprid+ synergist (SV1) EC and endosulfan EC were 37.6 and 13.0, 9.84 and 7.75, 54.0 and 7.28 respectively. All of them showed rather high selective toxicity. The STRs of fenvalerate EC, dimethoate EC and methomyl EC were all very low, ranging from 0.02 to 0.21, indicating their low degree of safety to the two species of ladybids. The results demomarated that imidacloprid WP and imidacloprid + SVl EC not only had rather high toxicity to the aphids, but also reduced strikingly the reproduction rate and fecundity of the survival aphids. Insecticides can induce the relative fitness of insects decrease. Among the six insecticides tested with M. persicae , the following were insecticides and the order of induction was: imidacloprid + SV1 imidacloprid endosulfan methomyl fenvalerate > dimethoate.