Marín de Jesús Sergio, Vigueras-Villaseñor Rosa María, Cortés-Barberena Edith, Hernández-Rodríguez Joel, Pérez-Aguirre Sonia Guadalupe, Montes Sergio, Carrizales-Yáñez Leticia, Arrieta-Cruz Isabel, Arteaga-Silva Marcela
Doctorado en Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, Av. Ferrocarril San Rafael Atlixco 186, Col. Leyes de Reforma 1ª. Sección, Alcaldía Iztapalapa, Ciudad de México C.P. 09340, Mexico.
Laboratorio de Biología de la Reproducción, Instituto Nacional de Pediatría, Av. Insurgentes Sur 3700-Letra C, Insurgentes Cuicuilco, Coyoacán, Ciudad de México C.P. 04530, Mexico.
Int J Mol Sci. 2025 May 10;26(10):4589. doi: 10.3390/ijms26104589.
Sperm maturation involves changes in plasma membrane glycosylation for fertilization. Cadmium (Cd) exerts a negative effect by disrupting testicular and epididymal function, altering antioxidant activity. Zinc (Zn) is an essential element known for its antioxidant properties, role in testosterone synthesis, and support of spermatogenesis. However, its effect on sperm membrane glycosylation, as well as endocrine and antioxidant activity, after exposure to Cd has remained unexplored. This study evaluated the impact of Zn on epididymal sperm glycosylation, endocrine activity, and antioxidant activity in Cd-exposed rats. Four groups of male Wistar rats were analyzed: control, Cd-exposed, Zn-supplemented, and Zn + Cd groups. On postnatal day 90, tissues and blood were collected for Zn and Cd quantification, testosterone levels, antioxidant activity, histological analysis, and sperm quality. The results showed that Cd concentration increased significantly, reduced testosterone levels, modified antioxidant activity, and caused structural damage in the epididymis. The Cd-exposed group showed disrupted glycosylation and distribution patterns and reduced sperm quality. The Zn + Cd group showed lower Cd accumulation, preserved testosterone levels, restored antioxidant activity, and preserved glycosylation patterns and sperm quality. This study highlights the protective role of Zn in mitigating Cd-induced reproductive toxicity, probably through the competitive inhibition of Cd uptake and antioxidant support, thereby preserving fertility.
精子成熟涉及质膜糖基化的变化以实现受精。镉（Cd）通过破坏睾丸和附睾功能、改变抗氧化活性而产生负面影响。锌（Zn）是一种必需元素，以其抗氧化特性、在睾酮合成中的作用以及对精子发生的支持而闻名。然而，其在暴露于镉后对精子膜糖基化以及内分泌和抗氧化活性的影响仍未得到探索。本研究评估了锌对镉暴露大鼠附睾精子糖基化、内分泌活性和抗氧化活性的影响。分析了四组雄性Wistar大鼠：对照组、镉暴露组、补锌组和锌 + 镉组。在出生后第90天，收集组织和血液用于锌和镉定量、睾酮水平、抗氧化活性、组织学分析和精子质量评估。结果表明，镉浓度显著增加，睾酮水平降低，抗氧化活性改变，并导致附睾结构损伤。镉暴露组显示糖基化和分布模式紊乱，精子质量下降。锌 + 镉组显示镉积累减少，睾酮水平保持，抗氧化活性恢复，糖基化模式和精子质量得以保留。本研究强调了锌在减轻镉诱导的生殖毒性方面的保护作用，可能是通过竞争性抑制镉摄取和提供抗氧化支持，从而维持生育能力。
