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马拉硫磷的一种杂质会改变大鼠肺细支气管上皮的形态。

An impurity of malathion alters the morphology of rat lung bronchiolar epithelium.

作者信息

Imamura T, Gandy J, Fukuto T R, Talbot P

出版信息

Toxicology. 1983 Jan;26(1):73-9. doi: 10.1016/0300-483x(83)90058-6.

DOI:10.1016/0300-483x(83)90058-6
PMID:6829031
Abstract

Oral administration of O,O,S-trimethyl phosphorothioate (OOS), an impurity in technical malathion, caused morphological changes in the bronchiolar epithelium of rat lungs. OOS-treated rat lungs had fewer but larger Clara (non-ciliated) cells than lungs from control rats given either corn oil or purified malathion. Moreover, lactate dehydrogenase (LDH) activity in bronchopulmonary lavage fluid was significantly higher in OOS than in control rats. We interpret these data to mean that OOS, and/or its metabolite(s) causes a lesion in the lung. Because of the widespread agricultural use of technical malathion, future work should address the significance of our findings and the possible toxic effect of OOS on lung tissue.

摘要

技术级马拉硫磷中的杂质O,O,S-三甲基硫代磷酸酯(OOS)经口服后,导致大鼠肺细支气管上皮出现形态学变化。与给予玉米油或纯化马拉硫磷的对照大鼠的肺相比,经OOS处理的大鼠肺中克拉拉(无纤毛)细胞数量更少但体积更大。此外,OOS处理组大鼠支气管肺泡灌洗液中的乳酸脱氢酶(LDH)活性显著高于对照组大鼠。我们将这些数据解读为OOS及其代谢物会导致肺部损伤。鉴于技术级马拉硫磷在农业中的广泛使用,未来的研究应探讨我们研究结果的意义以及OOS对肺组织可能产生的毒性作用。

相似文献

1
An impurity of malathion alters the morphology of rat lung bronchiolar epithelium.马拉硫磷的一种杂质会改变大鼠肺细支气管上皮的形态。
Toxicology. 1983 Jan;26(1):73-9. doi: 10.1016/0300-483x(83)90058-6.
2
Phenobarbital pretreatment protects against morphologic changes in rat bronchiolar epithelium caused by an impurity of malathion.苯巴比妥预处理可预防由马拉硫磷杂质引起的大鼠细支气管上皮形态学改变。
Am J Pathol. 1983 Jun;111(3):350-3.
3
Morphological alterations of rat lung bronchiolar epithelium produced by various trialkyl phosphorothioates.各种硫代磷酸三烷基酯对大鼠肺细支气管上皮的形态学改变。
Toxicology. 1984 Jul;32(1):37-46. doi: 10.1016/0300-483x(84)90032-5.
4
Cellular responses to O,O,S-trimethyl phosphorothioate-induced pulmonary injury in rats.
Toxicol Appl Pharmacol. 1985 Aug;80(1):51-7. doi: 10.1016/0041-008x(85)90100-0.
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Effect of drug metabolism inducer and inhibitor on O,O,S-trimethyl phosphorothioate-induced delayed toxicity in rats.
Chem Biol Interact. 1983 Jul 1;45(1):53-64. doi: 10.1016/0009-2797(83)90042-x.
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Sequential and dose-dependent alterations in rat bronchiolar epithelium during O,O,S-trimethyl phosphorothioate induced delayed toxicity.硫代磷酸O,O,S-三甲基酯诱导的大鼠迟发性毒性过程中细支气管上皮的顺序性和剂量依赖性改变
J Pathol. 1984 Jun;143(2):127-37. doi: 10.1002/path.1711430207.
7
A phosphorothionate isomer protects against the pneumotoxicity caused by O,O,S-trimethyl phosphorothioate.一种硫代磷酸酯异构体可预防由O,O,S-三甲基硫代磷酸酯引起的肺毒性。
Toxicol Appl Pharmacol. 1987 Mar 15;87(3):498-508. doi: 10.1016/0041-008x(87)90256-0.
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Role of metabolic activation, covalent binding, and glutathione depletion in pulmonary toxicity produced by an impurity of malathion.代谢活化、共价结合和谷胱甘肽耗竭在马拉硫磷一种杂质所致肺部毒性中的作用。
Toxicol Appl Pharmacol. 1984 Mar 15;72(3):476-83. doi: 10.1016/0041-008x(84)90124-8.
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Lung injury and delayed toxicity produced by O,S,S-trimethyl phosphorodithioate, an impurity of malathion.马拉硫磷的一种杂质O,S,S-三甲基二硫代磷酸酯所导致的肺损伤和迟发性毒性。
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Development of tolerance to a pneumotoxic impurity of malathion.对马拉硫磷的一种肺毒性杂质产生耐受性。
J Toxicol Environ Health. 1985;15(2):279-91. doi: 10.1080/15287398509530654.

引用本文的文献

1
Ultrastructural changes in rat Clara cells induced by a single dose of O,S,S-trimethyl phosphorodithioate.单次剂量的O,S,S-三甲基二硫代磷酸酯诱导大鼠克拉拉细胞的超微结构变化
Arch Toxicol. 1984 Nov;56(1):59-65. doi: 10.1007/BF00316355.
2
Mechanism of protection against pneumotoxicity caused by O,S,S-trimethyl phosphorodithioate.O,S,S-三甲基二硫代磷酸酯所致肺毒性的防护机制
Arch Environ Contam Toxicol. 1986 Jan;15(1):87-96. doi: 10.1007/BF01055253.
3
Neonatal death and lung injury in rats caused by intrauterine exposure to O,O,S-trimethylphosphorothioate.
宫内暴露于O,O,S-三甲基硫代磷酸酯导致的新生大鼠死亡和肺损伤。
Arch Toxicol. 1988 Apr;61(5):378-86. doi: 10.1007/BF00334619.
4
Immature alveolar/blood barrier and low disaturated phosphatidylcholine in fetal lung after intrauterine exposure to O,O,S-trimethylphosphorothioate.宫内暴露于硫代磷酸三甲基酯后胎儿肺中未成熟的肺泡/血液屏障及低不饱和磷脂酰胆碱。
Arch Toxicol. 1989;63(4):331-5. doi: 10.1007/BF00278648.