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Nystatin affects zinc uptake in human fibroblasts
Biological Trace Element Research
|August 1, 1996
Summary
Cellular zinc uptake may involve potocytosis, a process inhibited by nystatin. This drug and the acrodermatitis enteropathica mutation both reduce zinc transport velocity across cell membranes.
Area of Science:
- Cell Biology
- Biochemistry
- Membrane Transport
Background:
- The precise mechanisms of cellular zinc transport remain unidentified.
- Zinc uptake is temperature-dependent, suggesting involvement of membrane dynamics like endocytosis or potocytosis.
Purpose of the Study:
- To investigate the role of potocytosis in cellular zinc uptake.
- To determine the effects of nystatin, a potocytosis inhibitor, on zinc uptake in normal and acrodermatitis enteropathica (AE) fibroblasts.
Main Methods:
- Fibroblasts were incubated with nystatin or DMSO, then exposed to 65zinc.
- Zinc uptake kinetics were analyzed using Michaelis-Menten models.
- Nystatin's effect on zinc internalization and binding was assessed.
Main Results:
- Nystatin significantly inhibited zinc uptake in both normal and AE fibroblasts.
- Nystatin reduced both K(m) and Vmax in normal cells, and Vmax in AE cells.
- The AE mutation alone reduced Vmax, indicating impaired zinc transport.
Conclusions:
- Potocytosis may play a role in cellular zinc uptake, as inhibited by nystatin.
- Nystatin reduces zinc transport velocity across the cell membrane.
- The AE mutation impairs cellular zinc transport by reducing Vmax.