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首页> 外文期刊>Cell and Tissue Research >Alzheimer's disease-related amyloid-beta(1-42) peptide induces the loss of human sperm function
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Alzheimer's disease-related amyloid-beta(1-42) peptide induces the loss of human sperm function

机译：阿尔茨海默氏症的疾病相关的淀粉样蛋白β（1-42）肽诱导人体精子的损失

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Characteristically identified as the main component of senile plaques present in patients suffering from Alzheimer's disease, A beta has been detected in human testis and reproductive fluids, but its effect on spermatozoa has not been addressed. The present study evaluated whether the most toxic and aggregant amyloid precursor protein (APP)-proteolytic product, amyloid-beta(1-42) (A beta(1-42)), was capable of affecting sperm functionality. Normozoospermic samples were either exposed to different A beta(1-42) doses or to the untreated and scrambled controls for a maximum of 48 h at 37 A degrees C and 5%CO2, and motility, viability and mitochondrial status were evaluated. Additionally, tyrosine phosphorylation was analyzed by immunocytochemistry and acrosomal integrity through PSA-FITC. A shorter treatment period was used to monitor prompt Ca2+ responses. A beta(1-42) peptide decreased motility before inducing mitochondrial impairment (p < 0.05; n = 6). Both outcomes became more pronounced with time, reaching their maximal decrease at 48 h, where even 1 mu M produced undesirable effects (p < 0.05; n = 6). A beta(1-42) peptide also decreased cell survival (p < 0.05; n = 6). Furthermore, although no effects on tyrosine phosphorylation were observed (p > 0.05; n = 6), reduced acrosomal integrity was detected (p < 0.05; n = 7), which was not correlated with viability loss (p > 0.05). In parallel, all A beta(1-42) concentrations elicited a [Ca2+](i) rise but a significant difference was only observed at 20 mu M (p < 0.05; n = 7) and a tendency was obtained with 10 mu M (p = 0.053; n = 7). In conclusion, A beta(1-42) peptide oligomers impair sperm function in vitro, although further studies are required to determine the clinical relevance of these findings.
机译：特征性地鉴定为患有阿尔茨海默病患者患者的老年斑块的主要成分，在人类睾丸和生殖液中检测到β，但其对精子的影响尚未得到解决。本研究评估了最有毒和聚集的淀粉样蛋白前体蛋白（APP） - 蛋白质溶液产物，淀粉样蛋白β（1-42）（β（1-42））是否能够影响精子官能度。常规血压样品在不同的β（1-42）中被暴露于不同的β（1-42），或者在37℃和5％CO 2下最多48小时的未处理和加糖的对照，并评估运动性，活力和线粒体状态。另外，通过PSA-FITC通过免疫细胞化学和仿体素完整性分析酪氨酸磷酸化。较短的治疗期用于监测提示CA2 +响应。在诱导线粒体损伤之前，β（1-42）肽减少了运动性（P <0.05; n = 6）。两种结果随时间变得更加明显，达到48小时的最大减少，在1亩m产生不期望的影响（P <0.05; n = 6）。 β（1-42）肽也降低了细胞存活率（P <0.05; n = 6）。此外，尽管观察到对酪氨酸磷酸化的影响（p> 0.05; n = 6），但检测到减少的仿毒剂完整性（P <0.05; n = 7），其与活性损失不相关（p> 0.05）。平行，所有β（1-42）浓度引发了[Ca2 +]（I）升高，但仅在20μm（p <0.05; n = 7）下观察到显着差异，并且用10μm获得趋势（p = 0.053; n = 7）。总之，β（1-42）肽低聚物在体外损害精子功能，尽管需要进一步研究以确定这些发现的临床相关性。

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