Rodak Kamil, Bęben Dorota, Birska Monika, Siwiela Oliwia, Kokot Izabela, Moreira Helena, Radajewska Anna, Szyjka Anna, Kratz Ewa Maria
Department of Laboratory Diagnostics, Division of Laboratory Diagnostics, Faculty of Pharmacy, Wroclaw Medical University, Borowska Street 211A, 50-556 Wroclaw, Poland.
Student Research Club, "Biomarkers in Medical Diagnostics", Department of Laboratory Diagnostics, Division of Laboratory Diagnostics, Faculty of Pharmacy, Wroclaw Medical University, Borowska Street 211A, 50-556 Wroclaw, Poland.
Antioxidants (Basel). 2024 Mar 13;13(3):342. doi: 10.3390/antiox13030342.
Exposure to aluminum (Al) and its compounds is an environmental factor that induces neurotoxicity, partially through oxidative stress, potentially leading to the development of neurodegenerative diseases. Components of the diet, such as caffeinated coffee, may play a significant role in preventing these diseases. In the present study, an experimental model of PC12 cells (rat pheochromocytoma tumor cells) was developed to investigate the influence of caffeine and caffeinated coffee on neurotoxicity induced by Al compounds and/or oxidative stress. For the induction of neurotoxicity, aluminum maltolate (Almal) and HO were used. The present study demonstrates that 100 μM Almal reduced cell survival, while caffeinated coffee with caffeine concentrations of 5 μg/mL and 80 μg/mL reversed this effect, resulting in a higher than fivefold increase in PC12 cell survival. However, despite the observed antioxidant properties typical for caffeine and caffeinated coffee, it is unlikely that they are the key factors contributing to cell protection against neurotoxicity induced by both oxidative stress and Al exposure. Moreover, the present study reveals that for coffee to exert its effects, it is possible that Al must first activate certain mechanisms within the cell. Therefore, various signaling pathways are discussed, and modifications of these pathways might significantly decrease the risk of Al-induced neurotoxicity.
接触铝及其化合物是一种环境因素，可诱发神经毒性，部分是通过氧化应激，这可能会导致神经退行性疾病的发展。饮食中的成分，如含咖啡因的咖啡，可能在预防这些疾病方面发挥重要作用。在本研究中，建立了PC12细胞（大鼠嗜铬细胞瘤肿瘤细胞）实验模型，以研究咖啡因和含咖啡因的咖啡对铝化合物和/或氧化应激诱导的神经毒性的影响。为了诱导神经毒性，使用了苹果酸铝（Almal）和HO。本研究表明，100μM的Almal降低了细胞存活率，而咖啡因浓度为5μg/mL和80μg/mL的含咖啡因的咖啡逆转了这种作用，导致PC12细胞存活率提高了五倍以上。然而，尽管观察到咖啡因和含咖啡因的咖啡具有典型的抗氧化特性，但它们不太可能是保护细胞免受氧化应激和铝暴露诱导的神经毒性的关键因素。此外，本研究表明，咖啡要发挥其作用，铝可能必须首先激活细胞内的某些机制。因此，讨论了各种信号通路，对这些通路的修饰可能会显著降低铝诱导的神经毒性风险。
