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Related Concept Videos

Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Cellular Injury II: Classification01:21

Cellular Injury II: Classification

Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical injury...
In vitro Mutagenesis01:16

In vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
Cellular Injury IlI: Cellular Death01:11

Cellular Injury IlI: Cellular Death

Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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Related Experiment Video

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Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

[Cellular damage in vitro].

M Wendisch1, J Drechsel, R Freudenberg

  • 1Klinik und Poliklinik für Nuklearmedizin, Universitätsklinikum Dresden, Fetscherstr. 74, 01307 Dresden, Germany. maria.wendisch@uniklinikum-dresden.de

Nuklearmedizin. Nuclear Medicine
|July 30, 2009
PubMed
Summary
This summary is machine-generated.

Iodine-131 (131I) causes greater DNA damage and cell death in thyroid cells than Rhenium-188 (188Re) due to its higher linear energy transfer (LET), even at lower intracellular uptake.

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Area of Science:

  • Radiochemistry
  • Cellular Biology
  • Radiation Oncology

Context:

  • Cellular damage from ionizing radiation is influenced by dose, radiation quality (Linear Energy Transfer - LET), and radionuclide uptake.
  • Understanding these factors is crucial for effective targeted radionuclide therapy.

Purpose:

  • To investigate the differential effects of two beta-emitting radionuclides, Rhenium-188 (188Re) and Iodine-131 (131I), on the PCCl3 thyroid cell line.
  • To analyze the impact of intracellular radionuclide accumulation on cellular damage and survival.

Summary:

  • Thyroid cell line PCCl3 was exposed to 188Re-perrhenate and 131I-sodium iodide with and without perchlorate to modulate uptake.
  • DNA damage (Olive Tail Moment) and clonogenic cell survival were measured.
  • In the absence of perchlorate, lower 131I uptake resulted in higher radiotoxicity, increased DNA damage, and reduced cell survival compared to 188Re.

Impact:

  • 131I induced greater DNA damage and cell death than 188Re, attributed to its lower mean beta energy and higher LET.
  • This suggests 131I's higher radiotoxicity may stem from its physical characteristics and potential cross-fire effects, informing therapeutic strategies.