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 ≃ 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.
| Original language | English |
|---|---|
| Pages (from-to) | 27-42 |
| Number of pages | 16 |
| Journal | Mechanisms of Ageing and Development |
| Volume | 112 |
| Issue number | 1 |
| DOIs | |
| State | Published - Dec 7 1999 |
| Externally published | Yes |
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Keywords
- Aluminium
- Alzheimer's disease
- ATPase
- Membrane fluidity
- Mitochondria
- Oxidative phosphorylation
ASJC Scopus subject areas
- Aging
- Biochemistry
- Developmental Biology
- Developmental Neuroscience
Cite this
Effect of aluminium-induced Alzheimer like condition on oxidative energy metabolism in rat liver, brain and heart mitochondria. / Swegert, Cyril V.; Dave, Kunjan R; Katyare, Surendra S.
In: Mechanisms of Ageing and Development, Vol. 112, No. 1, 07.12.1999, p. 27-42.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of aluminium-induced Alzheimer like condition on oxidative energy metabolism in rat liver, brain and heart mitochondria
AU - Swegert, Cyril V.
AU - Dave, Kunjan R
AU - Katyare, Surendra S.
PY - 1999/12/7
Y1 - 1999/12/7
N2 - 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 ≃ 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.
AB - 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 ≃ 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.
KW - Aluminium
KW - Alzheimer's disease
KW - ATPase
KW - Membrane fluidity
KW - Mitochondria
KW - Oxidative phosphorylation
UR - http://www.scopus.com/inward/record.url?scp=0032701899&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032701899&partnerID=8YFLogxK
U2 - 10.1016/S0047-6374(99)00051-2
DO - 10.1016/S0047-6374(99)00051-2
M3 - Article
C2 - 10656181
AN - SCOPUS:0032701899
VL - 112
SP - 27
EP - 42
JO - Mechanisms of Ageing and Development
JF - Mechanisms of Ageing and Development
SN - 0047-6374
IS - 1
ER -