Original article Cytochrome C oxidase activity and nitric oxide synthase in the rat brain following aluminium intracerebral application

Stevanović, Ivana; Jovanović, Marina; Čolić, Miodrag; Ninković, Milica; Jelenković, A; Mihajlovic, R.

doi:10.5114/fn.2013.35957

Cited by 3 publications

(1 citation statement)

References 22 publications

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“…Rao et al [ 209 ] have shown that the ROS formation and mitochondrial respiratory activity, as well as glutathione depletion, were increased in the glial cells after being treated with Al for 24 h. Other groups have also depicted that Al exposure increased ROS formation and impaired the cytochrome c oxidase, which impaired mitochondrial functions in various neuronal cell types, including PC12 [ 210 , 211 , 212 ], SH-SY5Y neuroblastoma cells [ 213 , 214 ], and rat and cerebellar granule neuronal cells [ 42 , 215 ]. Mitochondrial dysfunction was also observed in in vivo studies [ 216 , 217 ]. Acute exposure to 50 μM Al maltonate via intracisternal injection caused the release of cytochrome c (cyt-c), accompanied by decreased Bcl-2, upregulated Bax, p53, and caspase-3, and DNA fragmentation in the mitochondria of rabbit brain [ 218 ].…”

Section: Molecular Mechanisms Of Metal-induced Mitochondrial Dysfunctionmentioning

confidence: 94%

Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Cheng

Yang

Tao

et al. 2021

Toxics

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Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system.

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