硫丹杀虫剂对非靶动物的生物蓄积潜力和毒性

Syed M. Naqvi , Chetana Vaishnavi
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引用次数: 234

摘要

1. 硫丹杀虫剂是一种多氯化合物,用于控制多种昆虫;它几乎不溶于水,但很容易附着在粘土颗粒上,并在土壤和水中持续存在数年。它的作用方式涉及与温度升高正相关的重复性神经放电。这种化合物对大多数鱼类都有剧毒,并可能导致大量死亡。在鱼类中,它引起Na和K浓度的显著变化,降低血液中Ca2+和Mg的水平,抑制Na, K和Mg依赖性atp酶(在大脑中)。据报道,硫丹在海洋动物中具有生物蓄积性;然而,淡水动物(如小龙虾)在一定程度上积累了它,但在净化过程中它们迅速失去了这种化合物。硫丹对水生无脊椎动物的毒性通常小于对鱼类的毒性。然而,它会导致腺苷酸能量电荷、氧气消耗、血淋巴氨基酸、琥珀酸脱氢酶、心跳(贻贝)和渗透调节改变的减少。一般来说,哺乳动物比水生动物更不容易受到硫丹毒性的影响。对实验室哺乳动物进行的大多数研究可以总结为:(a)神经毒性:雄性大鼠比雌性大鼠对硫丹更敏感,硫丹会降低大脑和血浆乙酰胆碱酯酶的活性。硫丹I(一种代谢物)引起去甲肾上腺素、5-羟色胺和GABA的显著变化。(b)肾毒性:在大鼠中发现MFOs活性受到抑制;(c)肝毒性:在大鼠肝脏中发现化学诱导的氨基吡啶n -去甲基化酶和苯胺水解酶,并发生糖原水平降低;(d)血液学毒性:硫丹暴露导致红细胞谷胱甘肽还原酶、血红蛋白量、红细胞数量和平均红细胞体积显著降低。呼吸毒性:累及大鼠肺呼吸困难、急性肺气肿、紫绀和肺泡间区出血。生化方面:在大鼠中,硫丹引起葡萄糖-6-磷酸脱氢酶活性、血糖水平、微粒体和表面活性剂系统磷脂含量升高,并深刻诱导醇脱氢酶和胞质谷胱甘肽s -转移酶活性。显著降低小肠上皮Na+、K+、Mg2+ atp酶,血浆钙水平和碱性磷酸酶水平。免疫毒性:大鼠血清对破伤风毒素、IgG、IgM和γ球蛋白的抗体滴度显著降低。生殖毒性:大鼠精系上皮退行性改变,睾酮生成限制性酶(3β-羟基类固醇转移酶和17β-羟基类固醇转移酶)的诱导,生殖器官组织学改变,睾丸萎缩,卵巢囊肿的发生。第二性器官的重量也有所减轻。发育性、致畸性和遗传毒性:该杀虫剂引起大鼠胎儿对雷氏色素的吸收显著增加。骨骼异常包括体重过轻的胎儿,较小的第4和第5未僵化的胸骨。家兔无胎毒或致畸活性;然而,在鸡中,由于抗有丝分裂活性而发生蛋孵化和不育。硫丹对小鼠和仓鼠骨髓细胞造成显著的染色体畸变,并对精子细胞造成损伤。在果蝇中,性别连锁的隐性致死性被注意到了。在小鼠中,发生了显性致死突变;异常精子增多,数量减少。10.致癌毒性:没有报告通过任何途径接触B6C3F对小鼠或人类具有致癌作用。对人类的毒性:硫丹暴露在人类中表现出癫痫效应、多动、易怒、震颤、抽搐和瘫痪。一名摄入30%硫丹的20岁男性自杀未遂,导致缺氧,随后出现反复吸入性肺炎,心动过速性休克发作,前有心动过速和高血压。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bioaccumulative potential and toxicity of endosulfan insecticide to non-target animals

1. Endosulfan insecticide is a polychlorinated compound used for controlling a variety of insects; it is practically water-insoluble, but readily adheres to clay particles and persists in soil and water for several years. Its mode of action involves repetitive nerve-discharges positively correlated to increase in temperature. This compound is extremely toxic to most fish and can cause massive mortalities. In fish, it causes marked changes in Na and K concentrations, decrease in blood Ca2+ and Mg levels and inhibits Na, K and Mg-dependent ATPase (in brain).

2. Bioaccumulation of endosulfan is reported for marine animals; however, freshwater animals (e.g. crayfish) accumulate it to some extent, but they lose the compound rapidly during depuration. Endosulfan is generally less toxic to aquatic invertebrates than fish. However, it causes decreases in adenylate energy charge, oxygen consumption, hemolymph amino acids, succinate dehydrogenase, heart-beat (mussel) and altered osmoregulation.

3. Generally, mammals are less susceptible to endosulfan's toxicity than aquatic animals. The majority of studies conducted on laboratory mammals can be summarized, (a) Neurotoxicity: male rats are more sensitive than females to endosulfan, which decreases brain and plasma acetyleholinesterase activity. Endosulfan I (a metabolite) causes a significant change in norepinephrine, 5-HT and GABA. (b) Renal toxicity: inhibition of MFOs activity was noticed in rats; other effects included changes in proximal convoluted tubules and necrosis of the tubular epithelium, (c) Hepatotoxicity: chemically-induced aminopyrine N-demethylase and aniline hydrolase were found in rat liver, and reduction in the glycogen level occurred, (d) Hematologic toxicity: endosulfan exposure resulted in a significant decrease in the erythrocyte glutathione reductase, hemoglobin amount, RBC number and mean corpuscular volume.

4. Respiratory toxicity: involved dyspnea, acute emphysema, cyanosis and hemorrhages in the interalveolar partitions of rat's lungs.

5. Biochemical: in rats, endosulfan caused increased glucose-6-phosphate dehydrogenase activity, blood glucose level, phospholipid contents of the microsomal and surfactant system, and profoundly induced the activity of alcohol dehydrogenase and cytosolic glutathione S-transferases. It also decreased significantly Na+, K+ and Mg2+ ATPases, plasma calcium level and alkaline phosphatase in the intestinal epithelium.

6. Immunologic toxicity: rat serum antibody titer to tetanus toxin, IgG, IgM and gammaglobulins were significantly reduced.

7. Reproductive toxicity: degenerative changes in the seminiferous epithelium, induction of the rate-limiting enzyme in testosterone production (3β-hydroxysteroid transferase and 17β-hydroxysteroid transferase), histological changes in reproductive organs, testicular atrophy and the occurrence of ovarian cysts were noticed in rat. Reduction in the weight of secondary sex organ was also observed.

8. Developmental, teratogenic and genotoxicity: this insecticide caused a significant increase in the fetal résorption of rats. Skeletal abnormalities included underweight fetuses, small 4th and 5th unossified sternabrae. No fetotoxic or teratogenic activity was found in rabbits; however, in chickens, egg-hatchability and sterility occurred due to antimitotic activity. Endosulfan caused significant chromosomal aberrations in mouse and hamster bone-marrow cells and damage to spermatozoa cells. In Drosophila, sex-linked recessive lethals were noticed. In mice, dominant lethal mutations occurred; increase in abnormal sperm and decrease in count occurred.

9. Carcinogenic toxicity: not reported to be carcinogenic in B6C3F mice or humans by any route of exposure.

10. Toxicity to humans: endosulfan exposure has exhibited epileptic effects, hyperactivity, irritability, tremors, convulsions and paralysis in humans. A suicidal attempt by a 20-year old male who ingested 30% endosulfan caused hypoxia, followed by recurrent aspiration pneumonia, episodes of tachycardiogenic shock which was preceded by tachycardia and hypertension.

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