1. Effect of aluminium-induced Alzheimer like condition on oxidative energy metabolism in rat liver, brain and heart mitochondria.
- Author
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Swegert CV, Dave KR, and Katyare SS
- Subjects
- Adenosine Diphosphate metabolism, Adenosine Triphosphatases metabolism, Aging drug effects, Aging metabolism, Aging pathology, Aluminum Chloride, Alzheimer Disease chemically induced, Alzheimer Disease pathology, Animals, Body Temperature, Brain drug effects, Disease Models, Animal, Glutamic Acid metabolism, Male, Membrane Fluidity drug effects, Mitochondria, Heart drug effects, Mitochondria, Liver drug effects, Rats, Aluminum Compounds toxicity, Alzheimer Disease metabolism, Brain metabolism, Chlorides toxicity, Energy Metabolism drug effects, Mitochondria, Heart metabolism, Mitochondria, Liver metabolism, Oxidative Phosphorylation drug effects
- 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.
- Published
- 1999
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