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Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore
Published on: January 21, 2020
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Eryptosis in lead-exposed workers.
Itzel-Citlalli Aguilar-Dorado1, Gerardo Hernández2, Martha-Angelica Quintanar-Escorza3
1Biochemistry Department, Centro de Investigación y Estudios Avanzados IPN, México, DF, Mexico.
Toxicology and Applied Pharmacology
|December 3, 2014
Summary
Lead exposure in workers significantly increases eryptosis, a red blood cell removal process, potentially through oxidative stress and calcium influx. This finding highlights a critical mechanism in lead intoxication.
Area of Science:
- Toxicology
- Hematology
- Cell Biology
Background:
- Eryptosis is the physiological removal of aged or damaged erythrocytes.
- Lead exposure is known to induce eryptosis in erythrocytes.
- Understanding the mechanisms of lead-induced eryptosis is crucial for managing lead intoxication.
Purpose of the Study:
- To investigate the levels of eryptosis in lead-exposed workers.
- To explore the potential role of oxidative stress in lead-induced eryptosis.
- To identify molecular pathways involved in lead intoxication-related eryptosis.
Main Methods:
- Blood samples were collected from lead-exposed and non-exposed male workers.
- Assays were performed to measure δ-aminolevulinic acid dehydratase (δALAD) activity, thiobarbituric acid-reactive substance (TBARS) concentration, and reduced/oxidized glutathione (GSH/GSSG) ratio.
- Intracellular free calcium concentration ([Ca(2+)]i), μ-calpain activity, adenosine triphosphate (ATP) concentration, and phosphatidylserine (PS) externalization were analyzed.
Main Results:
- Lead-exposed workers showed significantly reduced δALAD activity and increased TBARS concentration, indicating oxidative stress.
- A lower GSH/GSSG ratio and higher [Ca(2+)]i and μ-calpain activity were observed in lead-exposed erythrocytes.
- Significant phosphatidylserine externalization was detected in lead-exposed workers, a marker of eryptosis.
Conclusions:
- Lead intoxication in workers induces eryptosis.
- The mechanism involves oxidative stress, reduced glutathione, increased intracellular calcium, and μ-calpain activation.
- Further research is needed to understand the physiopathology and chronic complications of lead-induced eryptosis.

