氢醌急性毒性和蓄积毒性的实验研究

目的：研究氢醌对小鼠和大鼠的急性毒性和蓄积毒性，为建立卫生标准提供资料。方法：选用昆明种小鼠６０只，Ｓ．Ｄ雌性大鼠３０只，以氢醌（ＨＱ）乳化液，分别按０～９００ｍｇ／ｋｇ和０～２１５０ｍｇ／ｋｇ各分５个剂量组，一次性灌胃染毒。选用昆明种小鼠５０只，Ｓ．Ｄ雌性大鼠２５只，以ＨＱ乙醇溶液，分别按０～３８４０ｍｇ／ｋｇ各分５个剂量组一次性皮肤涂布染毒；另选昆明种小鼠４０只，以剂量定期递增染毒法灌胃，起始染毒剂量为０．１ＬＤ５０，以后每４天递增剂量１．５倍，共２０天，后观察５天，再给予一个ＬＤ５０的ＨＱ水溶液。结果：ＨＱ的急性毒作用表现为抽搐、震颤、瘫痪、呼吸困难，最后死亡。小鼠经口ＬＤ５０为３９９．８ｍｇ／ｋｇ，大鼠经口ＬＤ５０为５８４ｍｇ／ｋｇ。小鼠经皮染毒最小致死量大于４８００ｍｇ／ｋｇ，大鼠为大于３８４０ｍｇ／ｋｇ。结论：ＨＱ急性毒性属中等毒类，于小鼠体内有轻度蓄积作用。     

丙烯腈对雄性ICR小鼠生殖细胞毒性

目的：探讨丙烯腈对雄性小鼠生细胞的毒性作用。方法：雄性ＩＣＲ小鼠以０、２．５、５、１０ｍｇ／ｋｇ体重剂量连续腹腔注射染毒５ｄ,２周后处死动物,观察睾丸中早期精细胞微核;ＩＣＲ雄性小鼠以０、６、１２、２４ｍｇ／ｋｇ体重连续灌胃染毒５ｄ后于每周末处死部分动物。连续５周,分析附睾精子畸形率。结果：早期精细胞微核实验结果表明,染毒剂量≥５．０ｍｇ／ｋｇ,早期精细胞微核明显增加,微核率与染毒剂量之间存在剂量     

氟化钠,氯化汞和亚砷酸钠对小鼠睾丸早期精细胞微核率的影响

采用Ｔａｔｅｓ微核试验法检测３种无机化学物对雄性小鼠生殖细胞染色体的损伤作用。不同剂量的氟化钠（１４ｍｇ／ｋｇ、２８ｍｇ／ｋｇ）、氯化汞（０．５ｍｇ／ｋｇ、１．０ｍｇ／ｋｇ）和亚砷酸钠（０．２５ｍｇ／ｋｇ、０．５ｍｇ／ｋｇ）分别经腹腔注射染毒，每天１次，连续３天，于首次染毒后第１５天杀鼠。测得微核率为７．２％，１０．０‰；６．４‰、５．６‰和３．４‰、３．０‰。其中氟化钠和氯化汞组的微核率与阴性对照组（２．２‰）比较．有显著差异．可以认为是雄性生殖细胞染色体断裂剂。根据染毒到制片的间隔时间判断，氟化钠和氯化主要作用于减数分裂前的Ｇ１和Ｓ期初级精母细胞。     

不同剂量尿烷诱发A/J系小鼠肺肿瘤

本研究用５周龄敏感系Ａ／Ｊ系小鼠一次尿烷不同剂量腹腔注射（１００，５０，２５，１２．５ｍｇ／ｋｇ），染毒１５ｗｋ后，观察肿瘤发生，发展及病理形态特征。结果发现，光镜下，Ａ／Ｊ系小鼠发瘤危险增加的最低剂量为２５ｍｇ／ｋｇ（ｐ〈０．０５），发瘤数和发瘤率均呈明显剂量反应关系，发瘤面积亦随剂量增大而增加。     

砷对小鼠子代生长发育的影响

我们研究了孕鼠接触砷对子代生长发育的影响，结果显示，染砷各组仔鼠机体砷和脑组织砷含量增高，大脑皮层神经细胞结构异常。０．７５ｍｇ／ｋｇ剂量组仔鼠表现为神经行为发育迟缓，外周血淋巴细胞α－醋酸萘酯酶（ＡＮＡＥ）阳性率降低．４．５０ｍｇ／ｋｇ剂量组仔鼠断乳后体重增长缓慢，血液胆碱酯酶活性降低，血清溶血素水平亦显著下降。表明砷可经母体影响胚胎和子代的生长发育。     

氢酯急性毒性和蓄积毒性的实验研究

研究氢醌对小鼠和大鼠的急性毒性和蓄积毒性，为建立卫生标准提供资料。方法：选用昆明种小鼠６０只，Ｓ．Ｄ雌性小刀３０只，以氢醌乳化液，分别按０－９００ｍｇ／ｋｇ和０－２１５０ｍｇ／ｋｇ各分５个剂量组，一次性灌胃染毒。选用昆明种小鼠５０只，Ｓ．Ｄ雌性大鼠２５只，以ＨＱ乙醇溶液，分别按０－３８４０，ｇ／ｋｇ各分５个剂量组一次性皮肤涂布染毒；另选昆明种小鼠４０只，以剂量定期递增染毒法灌胃，起始染毒剂量为０．     

苯并（a）芘对小鼠腹腔巨噬细胞功能影响的研究

以２０、１０、５ｍｇ／ｋｇ Ｂ（ａ）ｐ连续灌胃１０天染毒小鼠，观察Ｂ（ａ）ｐ对小鼠腹腔巨噬细胞（ＰＥＣ）吞噬功能及Ｆｃ受体功能的影响。结果表明，总剂量为２００ｍｇ／ｋｇ的Ｂ（ａ）ｐ染毒组，小鼠ＰＥＣ吞噬率为２５．９％，对照组为４３．９％，吞噬率下降近５０％；剂量为１００、５０ｍｇ／ｋｇ的Ｂ（ａ）ｐ染毒组，未见ＰＥＣ吞噬率有明显变化。在三个染毒剂量组，均未见小鼠ＰＥＣ Ｆｃ受体功能有明显的变化。     

TMD对小鼠亚慢性毒性及致突变作用研究

对氮丙啶类化合物ＴＭＤ的亚慢性及毒突变作用进行了研究。毒性试验按１０、２０、４０ｍｇ／ｋｇ三个剂量组给小鼠经口染毒，致突变试验选用Ａｍｅｓ试验、微核试验和精子畸形试验。结果显示，ＴＭＤ无明显蓄积。染毒３５天，４０，ｇ／ｋｇ组ＷＢＣ显著降低，Ｈｂ在２０和４０ｍｇ／ｋｇ组有显著降低；而染毒４５天剂量组ＷＢＣ、Ｈｂ、ＰＴ均有显著降低。血清ＧＰＴ、ＢＵＮ无明显变化。脏器系数中仅睾丸、卵巢与对照组间有极显著性差异（Ｐ〈０．０１），且呈剂量反应关系。病理检查发现雌性２０、４０ｍｇ／ｋｇ组卵巢各级卵细胞减少，雄性各剂量组均出现睾丸曲细精管明显损害。Ａｍｅｓ试验ＴＭＤ为强阳性物质。试验组微核率、精子畸形率比对照组极显著增高（Ｐ〈０．０１）。表明ＴＭＤ对造血系统影响明显，对生殖细胞具有明显损害和遗传毒性。     

铅染毒对大鼠神经行为功能及神经化学的影响

作者研究了铅染毒对大鼠神经行为功能、海马中单胺类递质及脑组织脂质过氧化水平的影响。结果显示，１ ３３３．３ｍｇ／ｋｇ剂量组（Ｐｂ－Ｂ为６．２３μｍｏｌ／Ｌ）大鼠学习记忆能力受到影响，２６６．７ｍｇ／ｋｇ（Ｐｂ－Ｂ为４．２０μｍｏｌ／Ｌ）和１３３３．３ｍｇ／ｋｇ剂量组大鼠的运动改变，情绪状态不稳定；海马中多巴胺递质及其代谢产物含量有随染毒剂量增高而降低的趋势，而脑组织中脂质过氧化水平有随染毒剂量升高     

硝基苯对小鼠睾丸细胞酶的作用

以剂量为１００ｍｇ／ｋｇ体重、５００ｍｇ／ｋｇ体重的硝基苯（ＮＢ）分别给雄性小白鼠经口染毒。染毒２天后，各染毒组的睾丸组织中Ｇ－６－ＰＤ、ＬＤＨ－ｘ、ＳＤＨ的活性均明显低于对照组。染毒４天后，染毒组Ｇ－６－ＰＤ活性恢复到对照水平；ＬＤＨ－ｘ的１００ｍｇ／ｋｇ体重组恢复到对照水平，而５００ｍｇ／ｋｇ组仍明显低于对照组；ＳＤＨ活性染毒组仍低于对照组。ＬＰＯ值在染毒２天、４天后与对照组相比均无显著差异。     

硝化甘油毒性研究

本文报道了硝化甘油的急性和亚慢性毒性。主要急性毒作用是对循环、中枢神经及血液系统的作用。大鼠及小鼠经口的LD50分别为428.4mg/kg和390.4mg/kg,小鼠腹腔注射LD50为252.5mg/kg。亚慢性毒性:200mg/kg剂量组12/14动物死亡,80及40mg/kg组出现明显中毒,20mg/kg组出现轻度中毒,中毒主要表现为高铁血红蛋白血症、睾丸组织萎缩及大剂量影响心脏舒缩功能。     

Toxicity of dichloropropanols

A rare outbreak of acute hepatic damage in workers exposed to dichloropropanols was reported in 1992. As there are no detailed reports of dichloropropanols (DCPs) toxicity and its mechanism, we reviewed the toxicity of dichloropropanols using our results. 1) A marked elevation of serum AST and ALT with massive necrosis of the liver was noted in the 1/2 x, the 1 x and 2 x LD50 (0.149 mg/kg) of 1, 3-dichloro-2-propanol(DC 2 P). Hepatic malondialdehyde level was significantly increased, and associated with a decrease in liver glutathione S-transferase activity and reduced glutathione content. It is suggested that the free radical is associated with DCPs. 2) A reduction of leukocytes, platelets and fibrinogen, and prolonged prothrombin time were observed in the 1 x LD50 of DC 2 P. 3) In the CA1 area of the hippocampus, inhibition of population spikes was reduced by the 1 x LD50 of DC 2 P. This research was completed with the assistance of several other papers concerning dichloropropanols toxicity.     

Investigations on the acute toxic, cytogenetic, and embryotoxic activity of phenyl isocyanate and diethoxyphosphoryl isocyanate

Phenyl isocyanate (I) and diethoxyphosphoryl isocyanate (II), used as intermediates in organic chemical syntheses, were tested for their acute toxic, cytogenetic, and embryotoxic activity on mice of different strains. The oral LD50 values for male CFLP mice were determined to be 196 mg/kg for I and 4080 mg/kg for II. Single oral doses of 1/40 and 1/20, respectively, of the LD50 of I (4.9 and 9.8 mg/kg) and II (102 and 204 mg/kg) did not cause any significant enhancement in the percentage of chromosome aberrations in bone marrow cells of CFLP mice. After oral administration of 9.8 mg/kg I and 204 mg/kg II to pregnant Halle-AB-Jena and Halle-DBA mice at various days of gestation (4, 7, 11, or 15), none of the compounds tested were embryotoxic.     

对二氯苯急性毒性的实验研究

目的 研究对二氯苯（P-DCB）的急性毒性,为制订职业性接触限值提供参考依据。方法 大鼠和小鼠各60只,均随机分成6组,每组10只,雌雄各半,大鼠以0、2400、左右162、4200、5500、7244mgP-DCB/kg,小鼠以0、1568、2510、4000、6400、10240mgP-DCB/kg一次灌胃,小鼠60只,随机分为6组,每组10只,雌雄各半,以0、3162、5011、8000、12589、19953mg/m^3P-DCB吸入2h。大鼠8只,小鼠10只,白兔6只,性别不限,以5000mgP-DCB/kg涂皮8h。结果 大鼠经口LD50为3609mg/kg,小鼠经口LD50为4262mg/kg,小鼠吸入LC50为10100mg/m^3。大鼠和小鼠经皮LD50均大于5000mg/kg,白兔经皮最低致死剂量（MLD）大于5000mg/kg。结论 P-DCB是一种低毒类化合物。     

工作场所空气中三氯硫磷卫生标准的研究

[目的 ]研究工作场所空气中三氯硫磷卫生标准。 [方法 ]测定三氯硫磷的急性和亚急性毒性 ,并进行现场接触工人的职业流行病学调查。 [结果 ]三氯硫磷的大鼠经口LD50 为 681mg/kg ,慢性吸入阈浓度 2 0 6mg/m3 ,刺激阈浓度 8 5mg/m3 (大鼠 )。工作场所空气中三氯硫磷浓度 0 5mg/m3 以下 ,未发现接触工人中毒症状。 [结论 ]建议工作场所空气中三氯硫磷最高容许浓度为 0 5mg/m3 。     

Oral toxicity of bismuth in rat: single and 28-day repeated administration studies

The consumption and production of bismuth are increasing, however there is very little information about the direct toxic effect of bismuth. The present study aimed to characterize the potential toxic effects of bismuth through oral administration and observation for fourteen days following single dose of 0 and 2,000 mg/kg (acute oral toxicity study), and repeated oral administration for twenty-eight days at dose levels of 0, 40, 200, and 1,000 mg/kg daily (28-d repeated oral dose toxicity study) to male and female Crj:CD (SD) IGS rats (SPF). We found no deaths and no abnormalities in clinical signs, body weights, and necropsy findings for any of the animals in the acute oral toxicity study and no changes attributable to bismuth in either males or females in the dose group up to 1,000 mg/kg of the 28-d repeated-dose toxicity study. Therefore, we determined that the lethal dose with a 50% mortality rate (LD50) is greater than 2,000 mg/kg and the no-observed-adverse-effect level (NOAEL) of bismuth is 1,000 mg/kg in both sexes. We conclude that the adverse toxic effects of bismuth as a simple metal substance are low compared to lead toxicity under the conditions tested in our studies.     

Acute toxicity and cholinesterase inhibition in chicks dosed orally with organophosphate insecticides

Acute toxic effects of three commonly used insecticidal preparations of the organophosphates chlorpyrifos, diazinon, and dichlorvos were examined in mixed breed broiler chicks, and cholinesterase activity in plasma and brain were measured. The acute (24 h) oral median lethal doses (LD50) of chlorpyrifos, diazinon, and dichlorvos were 10.79 mg kg(-1), 6.32 mg kg(-1), and 6.30 mg kg(-1), respectively, as determined by the up-and-down method in chicks. Signs of cholinergic toxicosis in the chicks appeared within two hours after dosing, and they included salivation, lacrimation, gasping, frequent defecation, drooping of wings, tremors, convulsions, and recumbency before death. Halving the oral LD50 of chlorpyrifos (5 mg kg(-1)), diazinon (3 mg kg(-1)), and dichlorvos (3 mg kg(-1)) caused immobility and wing drooping, but not the clinical signs of cholinergic toxicity. However, at full LD50 doses of these insecticides, chicks showed clinical signs of cholinergic toxicity similar to those seen in the LD50 experiments. Two out of six chicks died within two hours after treatment with LD50 doses of chlorpyrifos and dichlorvos, whereas LD50 dosing with diazinon caused death in three out of six chicks. Compared to control values, the insecticides reduced plasma and whole brain cholinesterase activities by 29% to 84% and 18% to 77%, respectively, depending on the dose. The decrease in plasma cholinesterase correlated well (r=0.82) with that of the brain. These data suggest that organophosphate insecticides administered orally at LD50 doses induce clinical signs of cholinergic poisoning and concurrently reduce brain and plasma cholinesterase activities in chicks.     

农药三唑磷和杀虫单对小鼠的联合毒作用研究

目的　用急性毒性试验方法研究即将投入批量生产的混配农药“18%三唑磷·杀虫单微乳剂”联合毒作用类型。　方法　用改进寇氏法分别测定农药三唑磷、杀虫单单剂及其二者质量混合比为 3 :1、1:1、1:3的三种混合农药对 KM小鼠的急性经口 L D50 ,用联合毒作用系数 K值法判断混合物的联合毒作用类型。　结果　农药三唑磷和杀虫单 L D50 分别为 12 .3 2 mg/kg和 10 0 .5 mg/kg,二者的等毒性比约为 8:1;三唑磷与杀虫单质量混合比为 3 :1,1:1,1:3的三种混合农药的 L D50 分别为 2 7.2 3 mg/kg,40 .5 4mg/kg和 85 .92 mg/kg,其联合毒作用系数 K值分别为 0 .5 8,0 .5 4,0 .42。　结论　三唑磷与杀虫单混合比在 3 :1～ 1:3之间混合物的联合毒作用属相加作用     

Benefit of nanocarrier of magnetic magnesium in rat malathion-induced toxicity and cardiac failure using non-invasive monitoring of electrocardiogram and blood pressure

Medical management in acute organophosphate (OP) poisoning is not always successful because of tissue hypoxia which results in a reduction of heart contractility and cell damage. This study reports improvement of malathion (MAL)-induced cardiac failure by a nanocarrier of magnetic isotope of Mg (PMC16). A rat model of acute MAL poisoning was set up. PMC16 nanoparticle at doses of 0.05, 0.1, 0.2 LD50 = 896 mg/kg) were administered intravenously (iv) 30 minutes after a single intraperitoneal (ip) injection of MAL (0.25 LD50= 207 mg/kg). Atropine (AT; 40 mg/kg, ip) plus pralidoxime (PAM; 40 mg/kg, ip) and magnesium sulfate (MgSO?; 600 mg/kg, iv) were used as standard therapy or controls. Anesthetized animals were monitored for heart rate, electrocardiogram, blood pressure, and blood oxidative stress biomarkers like cellular lipid peroxidation, total thiol molecules, antioxidant power, gamma glutamil transpeptidase, and acetylcholinesterase (AChE) as a marker of OP toxicity. Results indicated that after MAL administration, heart rate and BP decreased and R-R duration increased. PMC16 markedly restored BP at all doses as compared with MgSO?. PMC16 at the dose of 0.05 LD50 significantly increased BP in comparison to AT + PAM. PMC16 restored heart rate at dose of 0.2 LD50 and reduced lipid peroxidation at dose of 0.05 LD50 as compared to MgSO?. PMC16 also improved total antioxidant power at all doses when compared to AT + PAM and reduced GGT activity at dose of 0.2 LD50 but did not affect total thiol molecules. MgSO? could improve MAL-induced reduction of total antioxidant power. After 24 h, PMC16 significantly improved MAL-suppressed AChE activity at doses of 0.05 and 0.1 LD50. PMC16 at all doses significantly recovered MAL-induced arrhythmia when compared to standard therapies. It is concluded that PMC16 is able to control OP-induced cardiac failure and toxicity.     

Strong acute toxicity, severe hepatic damage, renal injury and abnormal serum electrolytes after intravenous administration of cadmium fluoride in rats

Cadmium fluoride (CdF) is commonly used as an insulator for ulta high speed mass telecommunications equipment, and there is a considerable risk that industrial workers will inhale CdF particles. Despite the possibility that acute exposure can cause harmful systemic effects, there are no studies to date that address the health consequences of acute CdF exposure. This study therefore aimed to determine the acute lethal dose of CdF and its effects on various target organs, including the liver and kidney. We also determined the effect of CdF on serum electrolytes and acid-base balance. The effective lethal dose was determined and dose-response study was conducted after intravenous administration of CdF in rats. The 24 h LD(50) of CdF was determined to be 3.29 mg/kg. The dose-response study used doses of 1.34, 2.67, 4.01 mg/kg CdF. Saline or sodium fluoride solution were used for controles. Severe hepatocellular injury was induced at doses greater than 2.67 mg/kg, as demonstrated by AST and ALT activities greater than 1,500 IU/l in rats injected with a dose of 4.01 mg/kg. Acute renal failure was induced at doses greater than 2.67 mg/kg. Decreased serum Ca, increased serum K and metabolic acidosis were induced at a dose of 4.01 mg/kg. Decreased serum Ca was caused by exposure to ionized F. CdF has the strongest lethal and hepatic toxicity among all Cd containing compounds.