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Related Concept Videos

Disorders of Leukocytes01:27

Disorders of Leukocytes

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Leukocyte disorders can lead to either leukopenia, characterized by an abnormally low leukocyte count, or leukocytosis, marked by a very high leukocyte number.
Leukopenia may result from bone marrow disorders, autoimmune diseases, and infectious diseases. For example, conditions such as multiple myeloma and aplastic anemia can impair the bone marrow's ability to produce adequate leukocytes. Similarly, autoimmune diseases like lupus and viral infections such as HIV can prompt the immune...
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Chromosome Preparation From Cultured Cells
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Do chromosome changes in blood cells implicate formaldehyde as a leukemogen?

Richard J Albertini1, Debra A Kaden2

  • 1a Department of Pathology , University of Vermont , Burlington , VT , USA.

Critical Reviews in Toxicology
|September 30, 2016
PubMed
Summary
This summary is machine-generated.

Formaldehyde (FA) is a mutagenic chemical. While endogenous FA is vital, exogenous FA exposure can cause DNA damage, but evidence does not support FA

Keywords:
DNA adductRisk assessmentbone marrowchromosome aberrationcomet assayhuman healthleukemialymphomamicronucleus testmutation

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Area of Science:

  • Toxicology
  • Genetics
  • Occupational Health

Background:

  • Formaldehyde (FA) is an endogenous and exogenous chemical with mutagenic properties.
  • Exogenous FA, from sources like methanol, can increase in vivo concentrations, potentially leading to DNA damage.
  • FA induces DNA monoadducts, DNA-DNA, and DNA-protein cross-links, primarily at contact sites, while methanol may cause systemic adducts.

Purpose of the Study:

  • To evaluate the genotoxicity of formaldehyde exposure.
  • To assess the evidence for formaldehyde-induced DNA damage and chromosome aberrations in humans.
  • To investigate the potential of formaldehyde as a human leukemogen.

Main Methods:

  • Review of existing human occupational studies and animal data on formaldehyde exposure.
  • Analysis of studies examining DNA adducts, DNA-protein cross-links, and chromosome aberrations in blood cells (PBLs) and bone marrow (BM) or hematopoietic precursor cells (HPCs).
  • Consideration of oxidative stress and reactive aldehyde formation as potential mechanisms of distal DNA damage.

Main Results:

  • Formaldehyde exposure primarily causes DNA damage at initial contact sites.
  • Studies on chromosome aberrations in FA-exposed humans and animals have yielded mixed or negative results.
  • Evidence from circulating blood cells and hematopoietic precursor cells does not convincingly support formaldehyde's classification as a human leukemogen.

Conclusions:

  • Current evidence does not strongly support formaldehyde's classification as a human leukemogen based on observed genetic changes in circulating blood cells.
  • While FA can induce DNA damage and oxidative stress, its systemic genotoxic effects and leukemogenic potential in humans require further investigation.
  • Distinguishing in vivo from in vitro occurrences and managing confounding exposures remain challenges in assessing FA's health risks.