Fumonisin B₁ (FB₁) is a typical mycotoxin that widely contaminates food crops and their products and is known to be neurotoxic. In diverse dietary patterns, organisms are at risk of co-exposure to FB₁ and the heavy metal cadmium (Cd), but how Cd affects the toxic damaging effects of FB₁ is unknown. Therefore, this study explored the potential mechanism of co-exposure of Cd and FB₁ using a Caenorhabditis elegans (C. elegans) model. Our findings indicate that co-exposure with FB₁ (200 μg/mL) and Cd (25, 100, and 200 μg/mL) for 24 h significantly aggravated oxidative stress damage and mitochondrial dysfunction in dose-dependent. This included abnormal expression of mitochondrial membrane proteins and disruptions in the division and fusion processes of mitochondria. Moreover, the co-exposure to Cd and FB₁ induced ferroptosis, characterized by abnormally high levels of unstable ferrous iron and alterations in the expression levels of ferroptosis-related genes such as aat-9, acs-17, gpx-1, ftn-1, and frh-1. Collectively, these results underscore the aggravating effect of combined exposure to FB₁ and Cd on mitochondrial dysfunction and ferroptosis pathways in C. elegans. This study offers a novel perspective for exploring the mixture toxicity between FB₁ and Cd.

中文翻译：

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镉和伏马菌素 B1 共暴露对秀丽隐杆线虫线粒体功能障碍和铁死亡途径的影响


伏马菌素 B₁ （FB₁） 是一种典型的霉菌毒素，广泛污染粮食作物及其产品，已知具有神经毒性。在不同的饮食模式中，生物体有共同暴露于 FB₁ 和重金属镉 （Cd） 的风险，但 Cd 如何影响 FB₁ 的毒性破坏作用尚不清楚。因此，本研究使用秀丽隐杆线虫 （C. elegans） 模型探讨了 Cd 和 FB₁ 共同暴露的潜在机制。我们的研究结果表明，与 FB₁ （200μg/mL） 和 Cd （25、100 和 200μg/mL） 共暴露 24 小时显着加重了剂量依赖性的氧化应激损伤和线粒体功能障碍。这包括线粒体膜蛋白的异常表达以及线粒体分裂和融合过程的破坏。此外，Cd 和 FB₁ 的共同暴露诱导了铁死亡，其特征是异常高水平的不稳定亚铁和铁死亡相关基因（如 aat-9、acs-17、gpx-1、ftn-1 和 frh-1）表达水平的改变。总的来说，这些结果强调了 FB₁ 和 Cd 联合暴露对秀丽隐杆线虫线粒体功能障碍和铁死亡途径的加重作用。本研究为探索 FB₁ 和 Cd 之间的混合物毒性提供了新的视角。