Santiago-Andres Yorgui, Hernández Álvarez Elizabeth, Ochoa Gutierrez Daniel, Morton Bermea Ofelia, Fiordelisio Tatiana
Laboratorio de Neuroendocrinología Comparada, Facultad de Ciencias, Universidad Nacional Autónoma de México, Ciudad Universitaria, Ciudad de México, México.
Posgrado en Ciencias Biológicas, Unidad de Posgrado, Edificio D, Primer Piso, Circuito de Posgrados, Ciudad Universitaria, Ciudad de México, México.
J Endocrinol. 2025 Oct 7;267(1). doi: 10.1530/JOE-25-0161. Print 2025 Oct 1.
Cadmium is a heavy metal found widely in the environment, originating from industrial emissions, mining activities, phosphate fertilizers, and cigarette smoke. It is an endocrine-disrupting chemical that mimics essential metals such as calcium and zinc, interfering with hormone signaling. Due to its long biological half-life, cadmium bioaccumulates in organisms, raising concerns about its long-term effects on endocrine and reproductive health. Cadmium's reproductive toxicity is well documented, with studies highlighting its impact on gonadotropin regulation and testicular function. However, its specific effects on calcium (Ca2+) signaling in gonadotrophs remain poorly understood. This study aims to determine whether cadmium disrupts Ca2+-dependent signaling mechanisms essential for gonadotropin secretion. To address this, we used an adult male mouse model to assess pituitary cadmium accumulation, gonadotroph responsiveness to GnRH, and alterations in Ca2+ mobilization patterns. Our results show that cadmium exposure leads to pituitary bioaccumulation, prolonged endocrine disruption, and gonadotroph hyperplasia. Initially, gonadotroph responsiveness to GnRH declines, but over time, altered Ca2+ oscillation patterns and increased gonadotropin secretion emerge. A transition from normal oscillatory Ca2+ signaling to biphasic responses was observed, along with sustained phospholipase C-β (PLCβ) activation, suggesting persistent intracellular signaling disruptions. In addition, cadmium exposure resulted in testicular atrophy, increased apoptosis, and reduced sperm count. Testosterone levels declined, while the gonadotroph population increased, highlighting an imbalance in endocrine regulation. These findings suggest that cadmium induces reproductive toxicity through a combination of direct testicular damage and disruption of gonadotroph calcium signaling and hormone secretion, leading to testicular dysfunction that is relevant to public health.
镉是一种在环境中广泛存在的重金属,源于工业排放、采矿活动、磷肥和香烟烟雾。它是一种内分泌干扰化学物质,可模拟钙和锌等必需金属,干扰激素信号传导。由于其较长的生物半衰期,镉会在生物体内生物累积,引发人们对其对内分泌和生殖健康长期影响的担忧。镉的生殖毒性已有充分记录,研究突出了其对促性腺激素调节和睾丸功能的影响。然而,其对促性腺细胞中钙(Ca2+)信号传导的具体影响仍知之甚少。本研究旨在确定镉是否会破坏促性腺激素分泌所必需的Ca2+依赖性信号传导机制。为解决这一问题,我们使用成年雄性小鼠模型来评估垂体镉的累积、促性腺细胞对促性腺激素释放激素(GnRH)的反应以及Ca2+动员模式的变化。我们的结果表明,镉暴露会导致垂体生物累积、长期内分泌干扰和促性腺细胞增生。最初,促性腺细胞对GnRH的反应下降,但随着时间的推移,会出现Ca2+振荡模式改变和促性腺激素分泌增加。观察到从正常的振荡性Ca2+信号传导转变为双相反应,同时磷脂酶C-β(PLCβ)持续激活,表明细胞内信号传导持续受到破坏。此外,镉暴露导致睾丸萎缩、细胞凋亡增加和精子数量减少。睾酮水平下降,而促性腺细胞数量增加,突出了内分泌调节的失衡。这些发现表明,镉通过直接的睾丸损伤以及破坏促性腺细胞钙信号传导和激素分泌,诱导生殖毒性,导致与公共卫生相关的睾丸功能障碍。