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Uptake of copper by mouse hepatocytes
H J McArdle1, S M Gross, D M Danks
1Murdoch Institute for Research Into Birth Defects, Royal Children's Hospital, Parkville, Victoria, Australia.
Journal of Cellular Physiology
|August 1, 1988
Summary
Mouse hepatocytes efficiently uptake copper through a process influenced by amino acids but independent of cellular energy. This suggests distinct pathways for copper and histidine transport, aiding in modeling hepatic copper absorption.
Area of Science:
- Hepatology
- Cell Biology
- Biochemistry
Background:
- Hepatocytes are crucial for metal ion homeostasis.
- Understanding copper uptake mechanisms is vital for metabolic research.
Purpose of the Study:
- To investigate copper uptake kinetics in mouse hepatocytes.
- To elucidate the factors influencing copper transport and its relationship with amino acids.
Main Methods:
- Primary mouse hepatocytes were used, both freshly isolated and cultured.
- Copper uptake was measured under various conditions, including presence of amino acids and ATP depletion.
- Inhibitors like N-ethyl maleimide and Pronase were employed to probe transport mechanisms.
Main Results:
- Hepatocyte copper uptake exhibited biphasic kinetics in suspension and linear uptake in culture.
- Uptake showed saturation but did not follow simple Michaelis-Menten kinetics.
- Histidine and other amino acids stimulated copper uptake, while copper did not affect histidine uptake.
- Copper uptake was independent of intracellular adenosine triphosphate (ATP) levels.
- N-ethyl maleimide and Pronase significantly reduced copper uptake.
Conclusions:
- Copper and histidine appear to be transported via distinct pathways in hepatocytes.
- The uptake mechanism is not directly energy-dependent (ATP-dependent).
- A novel model for hepatocyte copper uptake is proposed, integrating new findings with existing data.