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首页> 外文期刊>Journal of Parasitology >NITROPHENIDE (MEGASUL™) BLOCKS EIMERIA TENELLA DEVELOPMENT BY INHIBITING THE MANNITOL CYCLE ENZYME MANNITOL-1-PHOSPHATE DEHYDROGENASE
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NITROPHENIDE (MEGASUL™) BLOCKS EIMERIA TENELLA DEVELOPMENT BY INHIBITING THE MANNITOL CYCLE ENZYME MANNITOL-1-PHOSPHATE DEHYDROGENASE

机译：硝基苯酚（MEGASUL™）通过抑制甘露醇循环酶甘露醇-1-磷酸脱氢酶来阻止黄疸病的发展。

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摘要

Unsporulated oocysts of the protozoan parasite Eimeria tenella contain high levels of mannitol, which is thought to be the principal energy source for the process of sporulation. Biosynthesis and utilization of this sugar alcohol occurs via a metabolic pathway known as the mannitol cycle. Here, results are presented that suggest that 3-nitrophenyl disulfide (nitrophenide, Megasul™), an anticoccidial drug commercially used in the 1950s, inhibits mannitol-1-phosphate dehydrogenase (M1PDH), which catalyzes the committed enzymatic step in the mannitol cycle. Treatment of E. tenella-infected chickens with nitrophenide resulted in a 90% reduction in oocyst shedding. The remaining oocysts displayed significant morphological abnormalities and were largely incapable of further development. Nitrophenide treatment did not affect parasite asexual reproduction, suggesting specificity for the sexual stage of the life cycle. Isolated oocysts from chickens treated with nitrophenide exhibited a dose-dependent reduction in mannitol, suggesting in vivo inhibition of parasite mannitol biosynthesis. Nitrophenide-mediated inhibition of M1PDH was observed in vitro using purified native enzyme. Moreover, M1PDH activity immunoprecipitated from E. tenella-infected cecal tissues was significantly lower in nitrophenide-treated compared with untreated chickens. Western blot analysis and immunohistochemistry showed that parasites from nitrophenide-treated and untreated chickens contained similar enzyme levels. These data suggest that nitrophenide blocks parasite development at the sexual stages by targeting M1PDH. Thus, targeting of the mannitol cycle with drugs could provide an avenue for controlling the spread of E. tenella in commercial production facilities by preventing oocyst shedding.
机译：原生动物寄生艾美球虫的未孢子卵囊含有高水平的甘露醇，这被认为是孢子形成过程的主要能源。这种糖醇的生物合成和利用是通过称为甘露醇循环的代谢途径进行的。在这里，提出的结果表明3-硝基苯基二硫化物（硝基苯，Megasul™）是一种在1950年代商业化使用的抗球虫药，它抑制了甘露醇-1-磷酸脱氢酶（M1PDH），该酶催化了甘露醇循环中固定的酶促步骤。用硝基苯甲醚处理感染艾美球虫的鸡，可使卵囊脱落减少90％。其余的卵囊表现出明显的形态异常，并且在很大程度上不能进一步发育。硝基苯哌啶酮治疗不影响寄生虫的无性繁殖，表明对生命周期性阶段的特异性。从用硝基苯酚处理的鸡中分离出的卵囊表现出甘露醇的剂量依赖性降低，表明体内对寄生虫甘露醇生物合成的抑制作用。使用纯化的天然酶体外观察到硝基苯介导的对M1PDH的抑制。此外，与未经处理的鸡相比，经硝基苯处理的鸡从大肠杆菌感染的盲肠组织中免疫沉淀的M1PDH活性显着降低。 Western印迹分析和免疫组织化学表明，硝基苯处理和未处理的鸡肉中的寄生虫含有相似的酶水平。这些数据表明，硝基苯酚通过靶向M1PDH来阻止性阶段的寄生虫发育。因此，用药物靶向甘露醇循环可以通过防止卵囊脱落为商业生产设施中的大肠杆菌的扩散提供途径。

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