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Related Concept Videos

What are Membranes?01:54

What are Membranes?

A key characteristic of life is the ability to separate the external environment from the internal space. To do this, cells have evolved semi-permeable membranes that regulate the passage of biological molecules. Additionally, the cell membrane defines a cell’s shape and interactions with the external environment. Eukaryotic cell membranes also serve to compartmentalize the internal space into organelles, including the endomembrane structures of the nucleus, endoplasmic reticulum and Golgi...
What are Membranes?01:24

What are Membranes?

A cell's plasma membrane demarcates the cell's borders and determines the nature of its interaction with the environment. Cells exclude certain substances, take in others, and excrete some others in controlled quantities. The plasma membrane must be flexible to allow certain cells, such as red and white blood cells, to change their shape while passing through narrow capillaries. These are the more obvious plasma membrane functions. In addition, the plasma membrane's surface carries markers that...
Membrane Fluidity01:26

Membrane Fluidity

Membrane fluidity is explained by the fluid mosaic model of the cell membrane, which describes the plasma membrane structure as a mosaic of components—including phospholipids, cholesterol, proteins, and carbohydrates—that gives the membrane a fluid character.
Mosaic nature of the membrane
The mosaic characteristic of the membrane helps the plasma membrane remain fluid. The integral proteins and lipids exist as separate but loosely-attached molecules in the membrane. The membrane is a relatively...
Enlargement of the Plasma Membrane01:22

Enlargement of the Plasma Membrane

Cell division and enlargement are processes that require precise control. The control ensures that cell division cannot proceed unless the cell has grown to a specific size. A spherical, dividing cell requires an approximately 1.6X increase in its surface area to double its volume. The secretory pathway also has a significant role in cell membrane enlargement. Secretory vesicles that bud off from the Golgi apparatus and later fuse with the plasma membrane during exocytosis are a major source of...
What are Membranes?01:24

What are Membranes?

A cell's plasma membrane demarcates the cell's borders and determines the nature of its interaction with the environment. Cells exclude certain substances, take in others, and excrete some others in controlled quantities. The plasma membrane must be flexible to allow certain cells, such as red and white blood cells, to change their shape while passing through narrow capillaries. These are the more obvious plasma membrane functions. In addition, the plasma membrane's surface carries markers that...
Plasma Membrane in Bacteria and Archaea01:27

Plasma Membrane in Bacteria and Archaea

The plasma membrane is an essential cellular structure responsible for maintaining cellular integrity and regulating the selective transport of molecules. While bacteria and archaea share the fundamental function of plasma membranes, their structural and molecular differences reflect adaptations to distinct ecological and physiological challenges.Bacterial Plasma MembranesBacterial plasma membranes are predominantly composed of phospholipids with fatty acid chains ester-linked to a glycerol...

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Related Experiment Video

Updated: Jul 24, 2026

Determination of Plasma Membrane Partitioning for Peripherally-associated Proteins
11:11

Determination of Plasma Membrane Partitioning for Peripherally-associated Proteins

Published on: June 15, 2018

Role of zinc in plasma membrane function.

B L O'Dell1

  • 1Department of Biochemistry, University of Missouri, Columbia, MO 65211, USA.

The Journal of Nutrition
|May 10, 2000
PubMed
Summary

Zinc deficiency impairs cell membrane function, particularly calcium uptake, leading to issues like bleeding and neuropathy. Restoring zinc levels quickly reverses these effects, suggesting a defect in calcium channels is the primary biochemical issue.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Nutritional Science

Background:

  • Plasma zinc concentration is a standard measure of zinc status but is insufficient alone.
  • Zinc deficiency can manifest in various physiological impairments, including bleeding disorders and neurological issues.
  • Identifying the primary biochemical defect in zinc deficiency is crucial for understanding its pathogenesis.

Purpose of the Study:

  • To identify the first limiting biochemical defect in animals fed zinc-deficient diets.
  • To investigate the role of plasma membrane proteins and calcium uptake in zinc deficiency.
  • To elucidate the mechanisms underlying impaired platelet aggregation and neuropathy in zinc-deficient states.

Main Methods:

  • Induction of zinc deficiency in animal models (rats and guinea pigs).

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Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay

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Last Updated: Jul 24, 2026

Determination of Plasma Membrane Partitioning for Peripherally-associated Proteins
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Determination of Plasma Membrane Partitioning for Peripherally-associated Proteins

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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells
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Atomic Absorbance Spectroscopy to Measure Intracellular Zinc Pools in Mammalian Cells

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Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay

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  • Assessment of platelet aggregation, red blood cell osmotic fragility, and synaptic vesicle function.
  • Analysis of plasma membrane protein changes and calcium ion (Ca2+) uptake.
  • Evaluation of the effects of dietary zinc repletion and in vitro glutathione treatment.
  • Main Results:

    • Zinc deficiency impairs platelet aggregation and red blood cell integrity, linked to decreased Ca2+ uptake and plasma membrane sulfhydryl concentration.
    • Neuropathy and impaired synaptic vesicle Ca2+ uptake were observed in zinc-deficient guinea pigs.
    • These impairments were rapidly reversible with dietary zinc repletion or in vitro glutathione treatment.
    • A defect in calcium channels, potentially due to an abnormal sulfhydryl redox state, is postulated as the primary issue.

    Conclusions:

    • A defect in calcium channels is likely the first limiting biochemical defect in zinc deficiency.
    • Impaired calcium uptake and subsequent second-messenger dysfunction result from an abnormal sulfhydryl redox state in membrane channel proteins.
    • Understanding this mechanism provides insight into the cellular basis of zinc deficiency symptoms and potential therapeutic targets.