生鲜乳中二英毒性作用及其机理

二英是一类氯代含氧三环芳烃类持久性有机污染物,因为其特有的化学和物理特性,很容易在食物链中积累。二英包含多氯二苯并对二英(PCDDs)和多氯二苯并呋喃(PCDFs)两大类,其中2,3,7,8-四氯二苯并对二英(TCDD)是毒性最强的一种。本文主要就生鲜乳中PCDDs和PCDFs的含量、来源及其中TCDD的毒性作用及其机理进行概述,为相关研究提供一定参考。     

二噁英对动物源食品的污染与毒性

二噁英是由2个苯环通过2个氧原子连接而生成的芳香烃族化合物,分多氯代二苯并二噁英(PCDDs)和多氯代二苯并呋喃(PCDFs)2类.PCDDs是由2个氧桥连接的双苯环化合物,PCDFs是二苯呋喃环结构.     

二噁英的化学结构与毒性

20世纪的最后一个夏季 ,“二口恶英”事件 ,被媒体渲染得沸沸扬扬 ,引起了全世界广泛关注。“二口恶英”是什么东西 ?它的毒性有多强 ?毒性机理是如何评定的 ?科学家对“二口恶英”的化学结构和理化特性的分析 ,成为人们关心的焦点。1　分子结构及理化特性具有二口恶英活性及其更广泛的卤代芳烃化合物统称为二口恶英及其类似物。其化学结构见图1。图 1　二口恶英的化学结构　　目前媒体上引用的二口恶英术语仅仅理解为对一二口恶英 ,是十分片面的。实际上真正具有毒性的是在对一二口恶英的两侧 ,各结合一个苯环形成多氯代二苯并一对一二口恶…     

二垩英的毒害作用

1　二垩英类化合物性质及来源具有二垩英活性及其更广泛的卤代烃化合物统称二垩英及其类似物。而真正具有毒性的是在对 二垩英的两侧各结合1个苯环 ,苯环 8个与碳原子连接的氢被氯取代而形成的多氯代二苯二垩英 (PCDD )和多氯代二苯呋喃 (PCDF) ,因此PCDDS和PCDFS各有 75 ,13 5种同系物及异构体。而通常所说的二垩英是指 2 ,3 ,7,8四氯代二苯二垩英 (TCDD)和氯代二苯呋喃等 17种类似化合物。这一类化合物呈固体 ,熔点高 ,对热稳定 (85 0℃以上才会被破坏 ) ,难溶于水 ,易溶于脂肪及有机溶剂 (如二氯苯 ,氯仿 )中。此外 ,对酸 ,碱 …     

二噁英微生物降解的研究进展

二[口恶]英属于全球性污染物,其毒性大、稳定性强,难于代谢降解,微生物降解是清除污染区域二[口恶]英的主要技术,本文在对降解菌的筛选、目前筛选出的主要菌株、降解机理研究等方面作了简要论述,并提出了今后研究的方向和重点.     

饲料中二噁英类化合物的污染及检测

二噁英是一类多氯代含氧三环芳烃类化合物的统称,是高毒的持久性有机污染物,包括75种多氯代二苯并-对-二噁英(PCDDs)和135种多氯代二苯并呋喃(PCDD/Fs)。二噁英性质非常稳定,不易降解且极具富集性,通过空气、水、泥土和植物及脂质转移富集于食物链中,积聚于动物和人的脂肪组织中,对生态环境、畜禽和人类健康造成危害。文中综述了饲料中二噁英的主要污染来源及污染途径,总结了饲料中二噁英类物质的检测方法,包括化学分析法、免疫学分析法和生物学分析方法。     

来稿摘登

●警惕二口恶英污染今春先由比利时后波及荷、法、德，发生混有二口恶英（ｄｉｏｘｉｎ）动物油脂饲料污染肉、乳、蛋及其制品的严重事件，损失惨重，比国首相率政府集体辞职。二口恶英及其衍生物，包括有数百种化合物，其中２，３，７，８－四氯二苯－Ｐ－二口恶英（ＴＣ...     

2,3,7,8-四氯二苯并-对-二噁英对鱼类胚胎发育影响的研究进展

二噁英(dioxin)所以被称为"世纪之毒",因之是危害极大的环境激素,致畸、致癌和突变性强,可通过食物链富集进入鱼、人和其他动物体内,并在脂肪中积蓄,对机体健康构成严重威胁。其中尤以2,3,7,8-四氯二苯并-对-二噁英(2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD)的毒性最强,引起了全球的高度关注。文中着重综述TCDD对鱼类胚胎发育的影响、机理及目前预防TCDD对鱼类胚胎发育影响的研究进展,旨在更好地为研究TCDD对鱼类胚胎发育的影响、机理及预防措施提供参考。     

2,3,7,8-四氯二苯并-对-二噁英对鱼类生长的影响及投喂调控

二噁英(dioxin)可通过多种途径进入鱼、人和其他动物体,并在脂肪中积蓄,使机体畸形、突变和致癌等。其中2,3,7,8-四氯二苯并-对-二噁英(2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD)被称为"地球上毒性最强的物质"。文中主要综述TCDD对鱼类生长的影响及其机理,同时提出通过投喂无污染或抗污染毒害的饲料,积极地预防TCDD对鱼类生长的影响。旨在更好的研究TCDD对鱼类和其他水生生物的影响、机制与预防,控制TCDD对水环境的污染,保护鱼类和其他水生生物,生产健康、卫生和安全的渔业产品。     

动物饲料中的二恶英

二恶英 二恶英和二恶英类化合物是一个有400种以上不同分子的族类(75种多氯代二苯并二恶英-PCDD,135种多氯代二苯并呋喃-PCDF和209种多氯代联苯-PCB),其特点是具有共同的化学结构。其中,7种多氯代二苯并二恶英,13种多氯代二苯并味喃和11种多氯代联苯被认为会产生二恶英所特     

二恶英的毒性及其对畜牧业的影响

作为目前世界上最强的人类一级致癌物，二恶英对现代畜牧业的危害性日趋明显。本文就二恶英的性质、毒性、对畜牧业的危害、防控措施及目前的检测方法作一综述。     

Impacts and impact mechanisms of "dioxins" in humans and animals

"Dioxins" are used to specify polychlorinated dibenzo-p-dioxins (PCDD), dibenzo-furanes (F) and dioxin-like polychlorinated biphenyls (PCB's). Many of the congeners proved to be highly toxic; 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) is the most toxic congener, and probably the most toxic compound ever synthesized by man (the natural occurance of this substance is very low). The total concentration/-toxicity of a mixture of congeners (WHO-PCDD/F-TEQ, or including the PCB's WHO-PCDD/F-PCB-PCB-TEQ) is calculated by addition of the individual concentrations multiplied by respective toxicity equivalence factors TEF; the most toxic congener TCDD is defined as 1. The tolerable weekly intake TWI set by the European Commission is 14pg WHO-PCDD/F-TEQ/kg bw. The "body burden" of adults in industrial countries is about 2-6 ng WHO-PCDD/F-TEQ/kg bw., or about double this value if PCB's are also considered. There is a very broad range of toxic effects of "dioxins". Many of the congeners can induce toxic responses at very low "body burdens". The most sensitive effects are immunosuppression, developmental and reproductive toxicity, as well as neurological behavioral effects. These effects occur at "body burdens" whih are close to background exposure of the human. Cancerogenic effects are induced at higher exposure (Seveso, industrial exposure). TCDD was considered a "complete carcinogen" by the IARC (Group 1). There is a broad range of carcinogenic effects, and there is no "hallmark" effect. Most toxic effects induced by TCDD are mediated by binding to the Ah-receptor (Ah-R) which binds together with a second protein, ARNT, to the respone elements of a number of target genes, and thus modulates gene expression. "Dioxins" are strong promotors, but weak initiators. The multitude of interactions of the Ah-R and ARNT ("receptor cross-talk") results in numerous molecular and cellular effects. The TCDD-Ah-R complex can also bind to the response element of the estrogen receptor, and thus can block the effects of es-trogens. This explains the fact that TCDD can be an estrogen antagonist reducing or preventing mamma carcinoma. Other Ah-R ligands occur in vegetables (e.g. indoles, flavones) and will possibly be developed in the future as functional substances. PCB's have similar properties to TCDD if they can exist in a planar configuration (dioxin-like PCB's). The non-dioxin-like PCB's always occur together with "dioxins"; their toxixty cannot be adequately determined although they occur in high concenrations. The consumption of food contaminated with "dioxins" need not directly lead to a toxic effect. Due to the continous cumulation of "dioxins" repeated ingestion of contaminated food could result in an increase of the "body burden" and thus chronic toxicity. This shows that the exposure of the human to dioxins should be minimized wherever possible.     

Immunomodulatory effects of organochlorine mixtures upon in vitro exposure of peripheral blood leukocytes differ between free-ranging and captive southern sea otters (Enhydra lutris)

Organochlorines (OCs), notably polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are ubiquitous environmental contaminants. Contaminant-induced immunosuppression by OCs has been implicated as a co-factor in the deaths of thousands of marine mammals in infectious disease epizootics over the last two decades, and limited studies support the hypothesis that PCBs are immunomodulatory. This study represented a unique opportunity to assess the potential differences in susceptibility to OCs between captive and free-ranging sea otters originating from the same genetic population. In vitro immune assays were utilized to evaluate both innate (phagocytosis and respiratory burst) and acquired (mitogen-induced B and T lymphocyte proliferation) immune functions. Individual PCBs (138, 153, 169 and 180) as well as TCDD and all 26 possible combinations were tested. Mixtures were tested as they represent 'real life' exposure. Our results suggest that (1) different immune functions were sensitive to different OC mixtures in both magnitude and direction (enhancement/suppression) and (2) differences in sensitivities upon in vitro exposure to OCs occurred between free-ranging and captive otters. Differences in susceptibility could be explained by the acute stress of capture, the chronic stress of captivity or nutritional differences. Understanding differences in toxicity to different populations of sea otters will have important implications for risk assessment as well as conservation and management strategies.     

Short-term hormone release from adult female rat hypothalamic and pituitary explants is not altered by 2,3,7,8-tetrachlorodibenzo-p-dioxin

2, 3, 7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has adverse effects on reproduction, in part due to direct actions at the ovary. It is unclear whether effects are further mediated by glands that regulate ovarian function. We investigated whether effects of TCDD are mediated via the hypothalamic-pituitary axis. Hypothalamic and pituitary tissues were cultured in medium with and without TCDD. TCDD did not alter GnRH release from hypothalamic samples. It continued to be pulsatile with no differences in the average peak frequency, average peak amplitude, or baseline GnRH release. TCDD did not alter GnRH-induced release of gonadotropins from pituitary samples. There were no differences in average peak amplitude or baseline release. AhR, ARNT or ER alpha mRNA copy numbers in cultured pituitaries were not affected by TCDD. Our data suggest that TCDD effects on ovarian function are not mediated through the hypothalamic or pituitary release parameters tested in this study.     

二噁英微生物降解的研究进展

二口恶英属于全球性污染物,其毒性大、稳定性强,难于代谢降解,微生物降解是清除污染区域二口恶英的主要技术,本文在对降解菌的筛选、目前筛选出的主要菌株、降解机理研究等方面作了简要论述,并提出了今后研究的方向和重点。     

Oxidative stress inducers potentiate 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated pre-cardiac edema in larval zebrafish

We reported the involvement of oxidative stress and prostaglandins including thromboxane and prostacyclin in pre-cardiac edema (early edema) caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). While the involvement of oxidative stress in TCDD-induced toxicity has been frequently reported, the mechanism of its action is still unclear. In the present study, oxidative stress inducers including paraquat, hydrogen peroxide (H₂O₂) and rotenone augmented early edema (edema) induced by a low concentration of TCDD (0.1 ppb) at 55 hr post fertilization (hpf), while each of them alone did not cause edema. Edema caused by TCDD plus oxidative stress inducers was almost abolished by antioxidants, an antagonist for thromboxane receptor (ICI-192,605) and an agonist for prostacyclin receptor (beraprost), suggesting that the site of action of these inducers was in the regular signaling pathway after activation of aryl hydrocarbon receptor type 2 (AHR2) by TCDD. Oxidative stress inducers also enhanced edema caused by an agonist for the thromboxane receptor (U46619), and the enhancement was also inhibited by antioxidants. Sulforaphane and auranofin, activators of Nrf2 that is a master regulator of anti-oxidative response, did not affect U46619-evoked edema but almost abolished TCDD-induced edema and potentiation by paraquat in both TCDD- and U46619-induced edema. Taken together, the results suggest that oxidative stress augments pre-cardiac edema caused by TCDD via activation of thromboxane receptor-mediated signaling in developing zebrafish. As paraquat and other oxidative stress inducers used also are environmental pollutants, interaction between dioxin-like compounds and exogenous source of oxidative stress should also be considered.     

Does paternal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affect the sex ratio of offspring?

In 1976, men who were exposed to the highest concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) after an explosion at a chemical plant near Seveso, Italy, produced more girls than boys. However, few studies have examined the possibility that the exposure of laboratory animals to TCDD, especially that of males, could lead to a lower male/female sex ratio. The aim of this study was to investigate whether direct paternal exposure to TCDD affects the sex ratio of offspring using a relatively large-scale experimental design. Male ICR mice (n=120) were randomly assigned to three, one of which served as a vehicle control, the other two were administered TCDD orally with an initial loading dose of 2 or 2,000 ng TCDD/kg, followed by a weekly maintenance dose of 0.4 (T2/0.4 group) or 400 (T2000/400 group) ng/kg prior to mating. The major organs of each mouse were weighed and histopathologically and immunohistologically investigated, and the sex ratio of offspring [males/(males + females) x 100] was calculated in each dam. There were no significant effects on organ weights, or on the structure of the testis and epididymis between the control and TCDD-exposed males, but TCDD administration produced a significantly lower proportion of male offspring from T2000/400-exposed sires despite no alteration in litter size (Control: 53.1 +/- 1.7; T2/0.4: 48.8 +/- 2.5; T2000/400: 46.2 +/- 2.1). In addition, we further divided the T2000/400 group into 3 subgroups based on the proportion of CYP1A1-immunoreactive areas in the liver; there was a significant correlation between sex ratio and CYP1A1 immunoreactivity. Thus, the present study confirms that direct paternal exposure to TCDD might be associated with an alteration in the sex ratio of offspring. Possible mechanisms through which TCDD might decrease the fertility potential of Y-bearing gametes before conception are discussed.     

Interactions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with immune responses of rainbow trout

Chlorinated dioxins, as typified by the most potent isomer, TCDD, are immunosuppressive in mammalian species and can enhance the susceptibility to a number of diseases. In recent years chlorinated dioxins have been detected in fish in many freshwater and marine habitats. Thus far, the effects of these chemicals on the immune responses of fish have not been examined. We studied the influence of TCDD on the defense mechanisms of rainbow trout. Yearling trout were injected intraperitoneally with the vehicle, 0.1, 1.0 or 10 micrograms/kg of TCDD. Interactions with the humoral immune response to sheep red blood cells (SRBC) were assessed by the Jerne plaque assay using head kidney and spleen leukocytes. Serum antibody was measured by complement-mediated lysis of SRBC in a chromium release assay. Effects of TCDD on the cellular immune responses were evaluated by the response of thymic and splenic lymphocytes to Con A and PWM. In addition, the phagocytic activity of peritoneal macrophages was examined in vitro. Trout which received 0.1 or 1.0 micrograms/kg TCDD remained clinically normal, and defense mechanisms were unaltered in these fish. Trout which received 10 micrograms/kg of TCDD became hypophagic and exhibited fin necrosis, ascites and suppression of hematopoiesis. In this treatment group, Con A-induced blastogenesis of thymic and splenic lymphocytes was not significantly changed, however, suppression of the PWM-induced response of splenic lymphocytes occurred. No statistically significant alterations occurred in humoral immune responses, and phagocytic activity of peritoneal macrophages was not decreased. The dose-response curve for various biologic effects of TCDD in the rainbow trout appears different from that in sensitive mouse strains. The 30-day, single-dose, parenteral LD50 for TCDD in the C57BL mouse is 100 micrograms/kg, and TCDD suppresses both cell-mediated and humoral immune responses at 1-2 micrograms/kg in this mouse strain. In the rainbow trout, however, immunosuppression was evident only at doses of TCDD approaching the 80-day, single-dose, parenteral LD50 of 20 micrograms/kg.