Abstract
Background and Objective: In Wilson’s disease, copper metabolism is impaired due to defective copper transporting protein ATP7B, resulting in copper accumulation in liver and brain and causing damage to liver and brain tissues. Published data suggest that one of the possible treatments for Wilson’s disease is curcumin—a compound found in the root of Curcuma longa. In this study, we tested whether curcumin affects copper transport and excretion in HepG2 hepatocytes carrying wildtype ATP7B. Materials and Methods: We examined the impact of 5 µM and 25 µM curcumin on the transport of copper in HepG2 cells incubated with 20 µM and 100 µM CuCl2, as well as copper excretion from cells. First, immunofluorescent staining and co-localization analysis were carried out in HepG2 cells using confocal laser scanning microscope and Nikon NIS Elements software. Second, a concentration of copper extracted into cell culture medium was determined using atomic absorption spectrometry. Results: The analysis of the co-localization between Golgi complex and ATP7B revealed that both 5 µM and 25 µM doses of curcumin improve the ability of liver cells to transport copper to plasma membrane at 20 µM CuCl2, but not at 100 µM CuCl2 concentration. However, atomic absorption spectrometry showed that curcumin rather promotes copper absorption into liver cell line HepG2 than excretion of it. Conclusions: Curcumin accelerates the transport of copper within liver cells, but does not promote copper excretion from HepG2 cells.
Highlights
Copper is an important microelement necessary for the functioning of several cellular processes [1,2,3,4].excessive accumulation of copper in tissues leads to oxidative stress, cell death [5,6,7] and damage of cellular proteins, lipids and nucleic acids [8,9]
Fifteen percent of the absorbed copper is delivered to tissues, while 85% is excreted from the body through gall (98%) or urine (2%), indicating that liver is the main organ for copper homeostasis [11]
We tested the basic effect of increasing copper concentrations on translocation of ATP7B (Figure 1)
Summary
Excessive accumulation of copper in tissues leads to oxidative stress, cell death [5,6,7] and damage of cellular proteins, lipids and nucleic acids [8,9]. In Wilson’s disease, copper metabolism is impaired due to defective copper transporting protein ATP7B, resulting in copper accumulation in liver and brain and causing damage to liver and brain tissues. We tested whether curcumin affects copper transport and excretion in HepG2 hepatocytes carrying wildtype ATP7B. Results: The analysis of the co-localization between Golgi complex and ATP7B revealed that both 5 μM and 25 μM doses of curcumin improve the ability of liver cells to transport copper to plasma membrane at 20 μM CuCl2 , but not at 100 μM CuCl2 concentration
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