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Calcium transport in rat liver mitochondria

Juzu, HA 1982 , 'Calcium transport in rat liver mitochondria', PhD thesis, University of Tasmania.

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In the present study, it was found that various components of the rat cytosol affect Ca²⁺ transport into and out of mitochondria when examined in vitro.
The ³H-palmitate-binding protein when saturated with palmitate caused Ca²⁺ release. The Ca-binding protein and albumin helped prolong Ca²⁺ retention in the mitochondria.
Palmitoyl CoA and palmitate caused release of Ca²⁺ from preloaded mitochondria. On the other hand palmitoylcarnitine caused Ca²⁺ retention.
The mitochondria were able to accumulate 4 - 9 % of the externally added Mg²⁺. The presence of varying concentration of external Mg²⁺ did not inhibit or increase Ca²⁺ uptake by the mitochondria, however, the extra Mg²⁺ accumulated prolonged Ca²⁺ retention in the mitochondria. During Ca²⁺ release from the mitochondria, there was a corresponding release of mitochondrial Mg²⁺. During Ca²⁺ retention, the level of mitochondrial Mg²⁺ remained steady.
ATP or respiratory substrate was required for Ca²⁺ uptake. The presence of both respiratory substrate and ATP favoured Ca²⁺ retention.
During Ca²⁺ release induced by palmitoyl CoA, PEP or glucose plus hexokinase, the total ATP concentration (i.e. that in the medium plus mitochondria) decreased, while the total AMP increased. During prolonged Ca²⁺ retention in the mitochondria, a high concentration of total ATP and a low concentration of total AMP was observed.
The findings of Lehninger et al (1978) (that a more oxidised steady state of the mitochondrial pyridine nucleotide
favours Ca²⁺ release and a relatively reduced state favours Ca²⁺ retention) was confirmed and further extended in this study. The adenine nucleotides were not significantly different from the control during Ca²⁺ release in the presence of the oxidants of mitochondrial NADH such as acetoacetate or oxaloacetate. Bovine serum albumin or ethane-1-hydroxy-diphosphonic acid (EHDP), substances known to help Ca²⁺ retention in the mitochondria, caused the Ca²⁺ released from the mitochondria by oxaloacetate to be taken up again.
Externally added NAD⁺ and possibly NADH prolonged Ca²⁺ retention in the mitochondria. On the other hand, NADPH caused an earlier Ca²⁺ release. NADP⁺ did not affect Ca²⁺ uptake or release,
The effect of cAMP on Ca²⁺ release was reinvestigated in the present study based on the findings of Lehninger et al (1978) and Christiansen (1977). Cyclic AMP caused Ca²⁺ release provided that palmitoyl CoA or palmitoylcarnitine were substrates and that the mitochondria prepared from fed rats were used within 1 hr after isolation. It was also noted in this study that the mitochondria isolated from starved rats had a lower NADH/NAD⁺ ratio and released their Ca²⁺ earlier than the mitochondria from fed rats. It was suggested that cAMP stimulates Ca²⁺ release from the mitochondria presumably by altering the redox state of the mitochondrial pyridine nucleotides.

Item Type: Thesis - PhD
Authors/Creators:Juzu, HA
Keywords: Liver cells, Calcium in the body, Biological transport, Mitochondria
Copyright Holders: The Author
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Copyright 1980 the Author - The University is continuing to endeavour to trace the copyright owner(s) and in the meantime this item has been reproduced here in good faith. We would be pleased to hear from the copyright owner(s).

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Thesis (Ph.D.)--University of Tasmania, 1982. Bibliography: l. 234-249

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