Effect of aluminium-induced Alzheimer like condition on oxidative energy metabolism in rat liver, brain and heart mitochondria.

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.