Electric field pulses induce reversible shape transformation of human erythrocytes.

Molecular membrane biology · 1997 · Mixed · Low evidence

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MixedLow evidencePaper 4119

Study snapshot

PublicationMolecular membrane biology · 1997

Study typein_vitro

Reported directionMixed

Evidence ratingLow

Abstract

Electric field pulses > 2-3 kV cm-1, long known to induce membrane poration and fusion of erythrocytes as well as to enhance the transbilayer mobility of phospholipids and to perturb aminophospholipid asymmetry, are shown to induce, at 0 degree C, transformation of the discocytic cells into echinocytes and spheroechinocytes. The extent of transformation increases with strength, duration and number of pulses. Its time course is biphasic, a major rapid phase (t/2 approximately 5 s) being followed by a minor one, lasting for 2-3 h. Shape transformation goes along with the exofacial exposure of phosphatidylserine (PS), detected by FITC-annexin V binding and quantified by a calibration curve established via externally inserted dilauroylphosphatidylserine. Incubation of these echinocytes at 37 degrees C leads to a rapid recovery of the discocytic shape followed by slower formation of stomatocytes. Shape recovery is temperature dependent (Ea approximately 100 kJ/mol), and can be impaired by depletion of ATP or Mg++ and by addition of vanadate or fluoride. Shape recovery and stomatocyte formation go along with a rapid loss of annexin binding in about 45% of the cells while the rest maintains its binding capacity. In the presence of vanadate, annexin binding increases in all cells. The results are discussed in the light of the bilayer couple concept of erythrocyte shape and the enhanced transverse mobility of phospholipids. Echinocyte formation is most likely caused by the reorientation of endofacial aminophospholipids to the outer leaflet of the bilayer. Shape recovery and stomatocyte formation probably result from a continuous reinternalization of PS via the ATP dependent aminophospholipid translocase, but may also be supported by downhill movement of PC to the inner leaflet and by other yet unidentified processes.

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AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro

Effect directionmixed

PopulationHuman erythrocytes (in vitro)

Sample sizeNot supplied

ExposureNot supplied

Evidence strengthLowConfidence: 74% · Peer reviewed: yes

Main findings

Electric field pulses >2–3 kV/cm at 0°C induced transformation of human erythrocytes from discocytes into echinocytes and spheroechinocytes, with greater transformation at higher pulse strength, duration, and number. Shape transformation was accompanied by exofacial PS exposure (annexin V binding). Incubation at 37°C led to rapid recovery of discocytic shape followed by slower stomatocyte formation; recovery was temperature-dependent and could be impaired by ATP or Mg++ depletion and by vanadate or fluoride, with annexin binding decreasing in ~45% of cells during recovery while others maintained binding capacity.

Outcomes measured

Erythrocyte shape transformation (discocytes to echinocytes/spheroechinocytes; recovery to discocytes; stomatocyte formation)
Exofacial phosphatidylserine (PS) exposure measured by FITC-annexin V binding
Dependence of transformation on pulse strength, duration, and number
Temperature dependence and effects of ATP/Mg++ depletion and inhibitors (vanadate, fluoride) on recovery/annexin binding

Limitations

No sample size reported in abstract
Exposure parameters beyond field strength threshold (e.g., exact pulse duration/number) not fully specified in abstract
In vitro erythrocyte model; generalizability to in vivo health outcomes not addressed

View raw extracted JSON

{
  "study_type": "in_vitro",
  "exposure": {
    "band": null,
    "source": "electric field pulses",
    "frequency_mhz": null,
    "sar_wkg": null,
    "duration": null
  },
  "population": "Human erythrocytes (in vitro)",
  "sample_size": null,
  "outcomes": [
    "Erythrocyte shape transformation (discocytes to echinocytes/spheroechinocytes; recovery to discocytes; stomatocyte formation)",
    "Exofacial phosphatidylserine (PS) exposure measured by FITC-annexin V binding",
    "Dependence of transformation on pulse strength, duration, and number",
    "Temperature dependence and effects of ATP/Mg++ depletion and inhibitors (vanadate, fluoride) on recovery/annexin binding"
  ],
  "main_findings": "Electric field pulses >2–3 kV/cm at 0°C induced transformation of human erythrocytes from discocytes into echinocytes and spheroechinocytes, with greater transformation at higher pulse strength, duration, and number. Shape transformation was accompanied by exofacial PS exposure (annexin V binding). Incubation at 37°C led to rapid recovery of discocytic shape followed by slower stomatocyte formation; recovery was temperature-dependent and could be impaired by ATP or Mg++ depletion and by vanadate or fluoride, with annexin binding decreasing in ~45% of cells during recovery while others maintained binding capacity.",
  "effect_direction": "mixed",
  "limitations": [
    "No sample size reported in abstract",
    "Exposure parameters beyond field strength threshold (e.g., exact pulse duration/number) not fully specified in abstract",
    "In vitro erythrocyte model; generalizability to in vivo health outcomes not addressed"
  ],
  "evidence_strength": "low",
  "confidence": 0.74,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electric field pulses",
    "erythrocytes",
    "electroporation",
    "echinocytes",
    "spheroechinocytes",
    "stomatocytes",
    "phosphatidylserine",
    "annexin V",
    "aminophospholipid asymmetry",
    "ATP-dependent translocase"
  ],
  "suggested_hubs": []
}

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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.3109/09687689709048182
PubMed: 9491371

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