Candida albicans is the most common pathogenic fungus in humans, causing cutaneous and life-threatening systemic infections. In this study, we confirmed using propidium iodide influx that gold nanoparticles (AuNPs), which are promising materials for use as antimicrobial agents, did not affect the membrane permeability of C. albicans. Thus, the fungal cell death mechanisms induced by AuNPs were assessed at intracellular levels including DNA damage, mitochondrial dysfunction, and reactive oxygen species (ROS) overproduction. AuNPs interacted with C. albicans DNA leading to increased nuclear condensation and DNA fragmentation. Changes in the mitochondria induced by AuNPs involving mass, Ca²⁺ concentrations, and membrane potential indicated dysfunction, though the level of intracellular and mitochondrial ROS were maintained. Although ROS signaling was not disrupted, DNA damage and mitochondrial dysfunction triggered the release of mitochondrial cytochrome c into the cytosol, metacaspase activation, and phosphatidylserine externalization. Additionally, the AuNPs-induced apoptotic pathway was not influenced by N-acetylcysteine, an ROS scavenger. This indicates that ROS signaling is not linked with the apoptosis. In conclusion, AuNPs induce ROS-independent apoptosis in C. albicans by causing DNA damage and mitochondria dysfunction.

白色念珠菌是人类中最常见的致病真菌，可引起皮肤和危及生命的全身感染。在这项研究中，我们证实了使用碘化丙啶的涌入，金纳米颗粒（AuNPs）是有前途的用作抗菌剂的材料，它不会影响C的膜通透性。白色的。因此，在细胞内水平评估了AuNPs诱导的真菌细胞死亡机制，包括DNA损伤，线粒体功能障碍和活性氧（ROS）过量产生。AuNP与C相互作用。白色念珠菌DNA导致核浓缩和DNA片段增多。涉及质量，Ca ^2+的AuNPs诱导的线粒体变化尽管维持了细胞内和线粒体ROS的水平，但浓度和膜电位均表明功能障碍。尽管ROS信号没有被破坏，但DNA损伤和线粒体功能障碍触发了线粒体细胞色素c释放到细胞质中，metaspaspase激活和磷脂酰丝氨酸外在化。另外，AuNPs诱导的凋亡途径不受ROS清除剂N-乙酰半胱氨酸的影响。这表明ROS信号传导与细胞凋亡无关。总之，AuNPs诱导了C细胞中ROS的独立凋亡。白色念珠菌会引起DNA损伤和线粒体功能障碍。