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首页> 外文期刊>Parasitology >4-Nitrobenzaldehyde thiosemicarbazone: a new compound derived from S-(-)-limonene that induces mitochondrial alterations in epimastigotes and trypomastigotes of Trypanosoma cruzi
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4-Nitrobenzaldehyde thiosemicarbazone: a new compound derived from S-(-)-limonene that induces mitochondrial alterations in epimastigotes and trypomastigotes of Trypanosoma cruzi

机译：4-硝基苯甲醛硫半脲：一种由S-（-）-柠檬烯衍生的新化合物，可引起克氏锥虫的副鞭毛和锥毛鞭毛虫的线粒体改变。

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摘要

Trypanosoma cruzi is the causative agent of Chagas' disease, a parasitic disease that remains a serious health concern with unsatisfactory treatment. Drugs that are currently used to treat Chagas' disease are partially effective in the acute phase but ineffective in the chronic phase of the disease. The aim of the present study was to evaluate the antitrypanosomal activity and morphological, ultrastructural and biochemical alterations induced by a new molecule, 4-nitrobenzaldehyde thiosemicarbazone (BZTS), derived from S-(-)-limonene against epimastigote, trypomastigote and intracellular amastigote forms of T. cruzi. BZTS inhibited the growth of epimastigotes (IC50=92m), intracellular amastigotes (IC50=323m) and inhibited the viability of trypomastigotes (EC50=143m). BZTS had a CC50 of 3745m in LLCMK2 cells. BZTS induced rounding and distortion of the cell body and severely damaged parasite mitochondria, reflected by extensive swelling and disorganization in the inner mitochondrial membrane and the presence of concentric membrane structures inside the organelle. Cytoplasmic vacuolization, endoplasmic reticulum that surrounded organelles, the loss of mitochondrial membrane potential, and increased mitochondrial O-2 production were also observed. Our results suggest that BZTS alters the ultrastructure and physiology of mitochondria, which could be closely related to parasite death.
机译：克氏锥虫是恰加斯氏病的病原体，恰加斯氏病是一种寄生虫病，治疗效果欠佳仍是严重的健康问题。当前用于治疗恰加斯氏病的药物在疾病的急性期部分有效，但在疾病的慢性期无效。本研究的目的是评估由S-（-）-li烯衍生的新分子4-硝基苯甲醛硫代半碳环素（BZTS）诱导的抗锥虫活性以及形态，超微结构和生化改变，以对抗表鞭毛，色粉体和胞内mas体形式。 T. cruzi。 BZTS抑制了表鞭毛纲动物的生长（IC50 = 92m），细胞内的变形虫（IC50 = 323m），并抑制了类锥虫的生存（EC50 = 143m）。 BZTS在LLCMK2细胞中的CC50为3745m。 BZTS诱导细胞体变圆和变形，并严重破坏了寄生虫线粒体，这反映在线粒体内膜的广泛肿胀和紊乱以及细胞器内部同心膜结构的存在。还观察到细胞质空泡化，包围细胞器的内质网，线粒体膜电位的丧失和线粒体O-2产量的增加。我们的结果表明BZTS改变了线粒体的超微结构和生理，这可能与寄生虫死亡密切相关。

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