Impairment of mitochondrial energy metabolism in different regions of rat brain following chronic exposure to aluminium.
The present study was designed with an aim to evaluate the effects of chronic aluminium exposure (10 mg/kg b.wt, intragastrically for 12 weeks) on mitochondrial energy metabolism in different regions of rat brain in vivo. Mitochondrial preparations from aluminium treated rats revealed significant decrease in the activity of various electron transport complexes viz. cytochrome oxidase, NADH cytochrome c reductase and succinic dehydrogenase as well, in the hippocampus region. The decrease in the activity of these respiratory complexes was also seen in the other two regions viz. corpus striatum and cerebral cortex, but to a lesser extent. This decrease in the activities of electron transport complexes in turn affected the ATP synthesis and ATP levels adversely in the mitochondria isolated from aluminium treated rat brain regions. We also studied the spectral properties of the mitochondrial cytochromes viz. cyt a, cyt b, cyt c1, and cyt c in both control and treated rat brains. The various cytochrome levels were found to be decreased following 12 weeks of aluminium exposure. Further, these impairments in mitochondrial functions may also be responsible for the production of reactive oxygen species and impaired antioxidant defense system as observed in our study. The electron micrographs of neuronal cells depicted morphological changes in mitochondria as well as nucleus only from hippocampus and corpus striatum regions following 12 weeks exposure to aluminium. The present study thus highlights the significance of altered mitochondrial energy metabolism and increased ROS production as a result of chronic aluminium exposure in different regions of the rat brain.
Kumar
Vijay
V
Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160 012, India.
Bal
Amanjit
A
Gill
Kiran Dip
KD
D000255:Adenosine Triphosphate / Q000378:metabolism; D000535:Aluminum / Q000494:pharmacology*; D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D003580:Cytochromes / Q000378:metabolism; D004579:Electron Transport / Q000187:drug effects; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects*; D005978:Glutathione / Q000378:metabolism; D008297:Male; D008854:Microscopy, Electron; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism*; D009245:NADH Dehydrogenase / Q000378:metabolism; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010710:Phosphates / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013778:Tetrazolium Salts; D013844:Thiazoles
D003580:Cytochromes; D010710:Phosphates; D017382:Reactive Oxygen Species; D013778:Tetrazolium Salts; D013844:Thiazoles; D000255:Adenosine Triphosphate; D000535:Aluminum; D013385:Succinate Dehydrogenase; D009245:NADH Dehydrogenase; D003576:Electron Transport Complex IV; C022616:thiazolyl blue; D005978:Glutathione