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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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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,...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Measuring Mitochondrial Function of Na&#239;ve and Effector CD8 T Cells
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Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells

Published on: March 28, 2025

Cell passage-associated transient high oxygenation causes a transient decrease in cellular glutathione and affects T

Melissa M Grant1, Helen R Griffiths

  • 1Life and Health Sciences, Aston University, Birmingham B4 7ET, UK.

Environmental Toxicology and Pharmacology
|July 26, 2011
PubMed
Summary

Routine cell culture maintenance temporarily reduces glutathione, a key antioxidant, impacting cell responses. This transient effect, lasting hours, can skew results in toxicity and proliferation studies.

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In Vivo Assessment of Alveolar Macrophage Efferocytosis Following Ozone Exposure
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Published on: October 22, 2019

Area of Science:

  • Cell Biology
  • Biochemistry
  • Immunology

Background:

  • Cell line maintenance is crucial for experimental consistency.
  • Cellular antioxidant levels, like glutathione, can influence cell function.
  • The impact of routine cell passage on cellular redox state and subsequent responses is not well understood.

Purpose of the Study:

  • To investigate the effect of routine cell culture maintenance on cellular glutathione levels.
  • To determine if changes in glutathione impact the response of Jurkat T cells to apoptotic and mitogenic stimuli.
  • To highlight a critical time window post-passage that may affect experimental outcomes.

Main Methods:

  • Assessed glutathione levels in HSB-CCRF-2, Jurkat T, and PC12 cell lines post-media replenishment.
  • Measured methotrexate-induced apoptosis and phytohaemagglutinin (PHA)-stimulated interleukin-2 (IL-2) production in Jurkat T cells at various time points after passage.
  • Quantified apoptotic nucleoids and IL-2 concentration to assess cell response.

Main Results:

  • Cell passage decreased glutathione by up to 42% in HSB-CCRF-2 cells within 120 minutes, returning to baseline within 5 hours.
  • Methotrexate-induced apoptosis was reduced when cells were exposed 30 minutes post-passage compared to untreated cells.
  • Interleukin-2 production was increased by 34% when cells were stimulated 2 hours post-passage compared to unstimulated cells.

Conclusions:

  • Routine cell passage transiently alters cellular glutathione levels and redox state in non-adherent cell lines.
  • This transient window can lead to under- or over-estimation of cell responses to cytotoxic and mitogenic agents.
  • Experimental timing relative to cell passage is critical for accurate assessment of cell function and drug efficacy.