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乙酰胺苯脲对柔嫩艾美耳球虫内源性发育阶段的超微结构影响

Ultrastructural effects of acetamizuril on endogenous phases of Eimeria tenella.

作者信息

Liu Lili, Chen Huiya, Fei Chenzhong, Wang Xiaoyang, Zheng Wenli, Wang Mi, Zhang Keyu, Zhang Lifang, Li Tao, Xue Feiqun

机构信息

Key Laboratory of Veterinary Drug Safety Evaluation and Residues Research, Chinese Academy of Agricultural Sciences, Shanghai Veterinary Research Institute, CAAS, No.518 Ziyue Rd, Minhang Dist., Shanghai, 200241, People's Republic of China.

出版信息

Parasitol Res. 2016 Mar;115(3):1245-52. doi: 10.1007/s00436-015-4861-9. Epub 2015 Dec 28.

Abstract

To explore the primary stage or site of action of acetamizuril (AZL), a novel triazine anticoccidial compound, the ultrastructural development of Eimeria tenella at different endogenous stages was studied in experimentally infected chickens treated with a single oral dose of 15 mg/kg AZL. As a result of drug action, the differentiations of second-generation schizonts and microgamonts were largely inhibited and merozoites became irregular in shape. Meanwhile, the outer membrane blistering and perinuclear space enlargement were obvious in the second-generation schizonts and microgamonts, which were never observed in the classic triazine anticoccidiosis drug diclazuril-treated E. tenella. The chromatin aggregation, anachromasis, and marginalization were visible in merozoites and microgamonts. Furthermore, the abnormal evagination of microgametes finally resulted in the degeneration of microgamonts and the failure of subsequent fertilization. The most marked micromorphological alteration occurring in the macrogamonts was the WFB2. Even if the fertilization occurred, the formation of oocyst wall became malformed and the zygote proceeded to the obvious degeneration. In addition, mitochondria swelling and cytoplasm vacuolization were discerned in respective intracellular stages, while endoplasmic reticulum and Golgi body swelling was less seen. These alterations may be the causes leading to the final death of E. tenella and also provide some information for further exploring the mechanism of action of AZL at the molecular level.

摘要

为探究新型三嗪类抗球虫化合物乙酰氨基嘧嗪(AZL)的主要作用阶段或作用位点,在经单剂量口服15 mg/kg AZL处理的实验性感染鸡中,研究了柔嫩艾美耳球虫在不同内生阶段的超微结构发育情况。药物作用的结果显示,第二代裂殖体和小配子体的分化受到很大抑制,裂殖子形状变得不规则。同时,第二代裂殖体和小配子体出现明显的外膜起泡和核周间隙增大,这在经典三嗪类抗球虫药地克珠利处理的柔嫩艾美耳球虫中从未观察到。裂殖子和小配子体中可见染色质聚集、色质减退和边缘化现象。此外,小配子的异常外翻最终导致小配子体退化以及后续受精失败。在大配子体中出现的最显著微观形态改变是WFB2。即使发生受精,卵囊壁的形成也会畸形,合子会明显退化。此外,在各个细胞内阶段可观察到线粒体肿胀和细胞质空泡化,而内质网和高尔基体肿胀较少见。这些改变可能是导致柔嫩艾美耳球虫最终死亡的原因,也为进一步从分子水平探索AZL的作用机制提供了一些信息。

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