Yazğan Yener, Keleş Ömer Faruk, Bayir Mehmet Hafit, Çiçek Hacı Ahmet, Ahlatcı Adem, Yıldızhan Kenan
Department of Biophysics, Faculty of Medicine, Kastamonu University, Kastamonu 37100, Türkiye.
Department of Pathology, Faculty of Veterinary Medicine, Van Yuzuncu Yil University, Van 65080, Türkiye.
Toxics. 2025 Jul 22;13(8):611. doi: 10.3390/toxics13080611.
Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity.
镉（CAD）是一种普遍存在的环境污染物，会带来严重的心脏毒性风险。心脏、肾脏、肝脏和大脑只是一些会因这种剧毒重金属CAD而遭受严重损害的重要器官。CAD的心脏毒性机制与氧化损伤和炎症有关。硒（SEL）是一种具有抗炎、抗凋亡和抗氧化特性的微量元素，可以作为膳食补充剂。SEL是一种对人类和动物营养至关重要的矿物质，能显著抑制重金属CAD的生物毒性。本研究旨在通过活性氧（ROS）诱导的聚（ADP-核糖）聚合酶-1（PARP-1）/腺苷二磷酸核糖（ADPR）/瞬时受体电位阳离子通道蛋白2（TRPM2）途径，评估硒对CAD所致心血管损伤的预防作用。SEL在减轻炎症和氧化反应方面显示出令人鼓舞的结果。除了通过灌胃给予25 mg/kg CAD外，大鼠还腹腔注射0.5 mg/kg SEL和3 mg/kg 2-氨基乙基亚苯基硼酸酯（2-APB），持续五天。组织病理学检查结果显示，CAD组大鼠心脏的形态学变化特征为明显的坏死、心肌细胞变性和血管充血。与CAD组大鼠相比, SEL组、2-APB组和SEL+2-APB组大鼠心脏的形态学改变较少。此外，给予CAD的大鼠心脏中丙二醛（MDA）、总氧化剂（TOS）、活性氧（ROS）、半胱天冬酶（Casp-3-9）和肿瘤坏死因子-α（TNF-α）增加，而谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）和总抗氧化剂（TAS）减少。SEL改善了抗氧化剂水平，避免了组织损伤，并降低了心脏MDA、TOS和ROS。在给予CAD的大鼠中，SEL降低了心脏PARP-1、TRPM2、TNF-α和半胱天冬酶水平。总之，SEL通过降低氧化应激和心脏损伤以及调节ROS/PARP-1/TRPM2途径，预防了CAD的心脏毒性。
