Inhibition of respiratory processes by overabundance of zinc in neuronal cells.
Studies suggest that excessive amounts of free zinc ions can cause neuron death by interfering with the energy production process. The sites of the cell oxidation activity of zinc are the glycolytic enzymes, the Krebs cycle components and the respiratory chain. Further consequences of reduced access to energy are: increased production of reactive forms of oxygen, decrease of the mitochondrial membrane potential and decreased level of ATP. Also, the toxicity of zinc accelerates the supply of extra amounts of this element to the mitochondria, which results in their increased permeability.
Floriańczyk
Bolesław
B
Department of Environmental Hygiene, Institute of Agricultural Medicine, 20-090 Lublin, Poland. bolkofs@poczta.onet.pl
Trojanowski
Tomasz
T
D000818:Animals; D019069:Cell Respiration / Q000187:drug effects; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D009474:Neurons / Q000737:chemistry* / Q000378:metabolism*; D015032:Zinc / Q000633:toxicity*
D015032:Zinc