title: Effect of aluminium-induced Alzheimer like condition on oxidative energy metabolism in rat liver, brain and heart mitochondria.
abstract: Prolonged exposure of rats to aluminium (Al) can result in an Alzheimer-like condition. To get better insights into the biochemical defects underlying AD, senility and ageing we exposed rats for long durations (90-100 days) to soluble salt of aluminium (AlCl3) and checked its influence on mitochondrial respiratory activity in the liver, brain and heart. In the liver and brain mitochondria the ADP/O ratio was impaired with NAD+ linked substrates. State three respiration decreased with glutamate in the liver. For succinate, the ADP/O ratio decreased in the liver mitochondria while state three and four respiration decreased in the brain mitochondria. In both the tissues respiration rates decreased with ascorbate + TMPD as the substrate. In the heart mitochondria ADP/O ratios with NAD+ linked substrates decreased, while respiration rates increased with all the substrates except for ascorbate + TMPD. Temperature kinetics data showed different effects on ATPase in the mitochondria from the three tissues. Data on lipid/phospholipid profiles suggested that the observed changes in energy metabolism were not mediated via lipid changes. Long-term exposure to Al resulted in approximately 100% increase in Al content of liver and brain mitochondria but in the heart there was phenomenal 11-fold increase, indicating thereby that the effects of Al exposure were indirect rather than direct due to Al accumulation.
authors.affiliation: Department of Biochemistry, Faculty of Science, MS University of Baroda, India.
authors.forename: C V
authors.initials: CV
authors.lastname: Swegert
authors.forename: K R
authors.initials: KR
authors.lastname: Dave
authors.forename: S S
authors.initials: SS
authors.lastname: Katyare
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000375:Aging / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000077410:Aluminum Chloride; D017607:Aluminum Compounds / Q000633:toxicity*; D000544:Alzheimer Disease / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001831:Body Temperature; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D002712:Chlorides / Q000633:toxicity*; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism*; D010085:Oxidative Phosphorylation / Q000187:drug effects*; D051381:Rats
chemical_list: D017607:Aluminum Compounds; D002712:Chlorides; D000077410:Aluminum Chloride; D018698:Glutamic Acid; D000244:Adenosine Diphosphate; D000251:Adenosine Triphosphatases