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铁补充对缺铁大鼠睾丸功能和生精作用的影响。

Effects of Iron Supplementation on Testicular Function and Spermatogenesis of Iron-Deficient Rats.

机构信息

Division of Urology, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.

Division of Experimental Surgery Center, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.

出版信息

Nutrients. 2022 May 14;14(10):2063. doi: 10.3390/nu14102063.

Abstract

Iron deficiency is the most common micronutrient deficiency in the world. Previous studies have shown that iron deficiency increases oxidative stress and decreases antioxidant enzymes, and studies of male infertility indicated that oxidative stress may affect male reproductive functions. The aim of this study was to investigate the effects of iron supplementation on spermatogenesis and testicular functions in iron-deficient rats. Three-week-old male Sprague Dawley (SD) rats were randomly divided into two groups: an iron-adequate control (AI group, 35 ppm FeSO4) and an iron-deficient group (ID group, <5 ppm FeSO4). After three weeks, the iron-deficient group was divided into an original iron-deficient group and five iron-supplemented groups, the latter fed diets containing different doses of FeSO4 (6, 12, 18, 24, and 35 ppm). After five weeks, blood and testis tissue were analyzed. We presented as median (interquartile range, IQR) for continuous measurements and compared their differences using the Kruskal−Wallis test followed by the Mann−Whitney U test among groups. The results showed that as compared with the AI group, the ID group had significantly lower serum testosterone and poorer spermatogenesis (The medians (QR) were 187.4 (185.6−190.8) of AI group vs. 87.5 (85.7−90.4) of ID group in serum testosterone, p < 0.05; 9.3 (8.8−10.6) of AI group vs. 4.9 (3.4−5.4) of ID group in mean testicular biopsy score (MTBS], p < 0.05); iron supplementation reversed the impairment of testis tissue. In the testosterone biosynthesis pathway, iron supplementation improved the lowered protein expressions of hydroxysteroid dehydrogenases caused by iron deficiency. Additionally, decreased activities of glutathione peroxidase and catalase, and increased cleaved-caspase 8 and caspase 3 expression, were found in the iron-deficient rats. The iron-supplemented rats that received > 12 ppm FeSO4 exhibited improvements in antioxidant levels. In conclusion, iron supplementation can abrogate testis dysfunction due to iron deficiency through regulation of the testicular antioxidant capacity.

摘要

缺铁是世界上最常见的微量营养素缺乏症。先前的研究表明,缺铁会增加氧化应激并降低抗氧化酶水平,而男性不育症的研究表明,氧化应激可能会影响男性生殖功能。本研究旨在探讨铁补充对缺铁大鼠精子发生和睾丸功能的影响。将 3 周龄雄性 Sprague Dawley(SD)大鼠随机分为两组:铁充足对照组(AI 组,35 ppm FeSO4)和缺铁组(ID 组,<5 ppm FeSO4)。3 周后,缺铁组分为原缺铁组和 5 个铁补充组,后者喂食含有不同剂量 FeSO4(6、12、18、24 和 35 ppm)的饮食。5 周后,分析血液和睾丸组织。我们呈现连续测量的中位数(四分位距,IQR),并使用 Kruskal-Wallis 检验比较组间差异,然后使用 Mann-Whitney U 检验进行比较。结果表明,与 AI 组相比,ID 组的血清睾酮明显降低,精子发生较差(中位数(IQR)分别为 AI 组的 187.4(185.6-190.8)与 ID 组的 87.5(85.7-90.4),p <0.05;AI 组的 9.3(8.8-10.6)与 ID 组的 4.9(3.4-5.4),p <0.05);铁补充逆转了睾丸组织的损伤。在睾酮生物合成途径中,铁补充改善了缺铁引起的羟甾类脱氢酶蛋白表达降低。此外,还发现缺铁大鼠的谷胱甘肽过氧化物酶和过氧化氢酶活性降低,caspase 8 和 caspase 3 表达增加。接受>12 ppm FeSO4 补充的铁补充大鼠抗氧化水平提高。总之,铁补充可以通过调节睾丸抗氧化能力来消除缺铁引起的睾丸功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7f6d/9144601/da5b6911a648/nutrients-14-02063-g001.jpg

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