Impaired mitochondrial function and oxidative stress in rat cortical neurons: Implications for gadolinium-induced neurotoxicity

摘要: Gadolinium (Gd), a rare-earth lanthanides metal, is widely utilized for various industrial and medical purposes, particularly in brain magnetic resonance imaging. However, its potential effects on the impairment of central nervous system remain uncertain, especially with regard to mitochondria, primary target metal-induced neural injury. This study investigates gadolinium mitochondrial energy metabolism, ROS accumulation, cell death toward cortical neurons. Results show that metabolic activity mitochondria significantly decreased as early 3 h after exposure cells chloride. Subsequently, significant elevation intracellular ROS, decrease ATP synthesis, depolarization membrane potential, release cytochrome c activation caspase-3 were observed. Following these changes, increased LDH into culture medium DNA fragmentation detected. Inhibition both could reduce Gd-induced neuron death. All results suggest cause apoptosis primarily by inhibiting function inducing oxidative stress. The present work provides new insight toxicological mechanism