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Related Concept Videos

Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
DNA Microarrays02:34

DNA Microarrays

Microarrays are high-throughput and relatively inexpensive assays that can be automated to analyze large quantities of data at a time. They are used in genome-wide studies to compare gene or protein expression under two varied conditions, such as healthy and diseased states. Microarrays consist of glass or silica slides on which probe molecules are covalently attached through surface functionalization. Most commonly, the slides are prepared through the chemisorption of silanes to silica...
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.
Cancer Prevention02:59

Cancer Prevention

Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
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The Lambda Select cII Mutation Detection System
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Published on: April 26, 2018

Classification of polycyclic aromatic hydrocarbons based on mutagenicity in lung tissue through DNA microarray.

Minoru Hirano1, Shiho Tanaka, Osamu Asami

  • 1Toyota Central R&D Labs., Inc., Nagakute, Aichi 480-1192, Japan.

Environmental Toxicology
|September 3, 2011
PubMed
Summary

Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants linked to lung cancer. DNA microarrays reveal that mutagenic PAHs, unlike nonmutagenic ones, activate p53-downstream genes in lung cells, aiding mutagenicity classification.

Keywords:
DNA damageDNA microarrayPAHcancercytochrome P450lungmetabolic activationmutagenicityp53polycyclic aromatic hydrocarbon

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Published on: March 20, 2018

Area of Science:

  • Environmental toxicology
  • Molecular biology
  • Genomics

Background:

  • Polycyclic aromatic hydrocarbons (PAHs) are pervasive environmental pollutants from organic matter combustion.
  • PAH exposure increases risks for lung cancer, asthma, and other inflammatory/allergic conditions.
  • Toxicogenomics utilizes DNA microarrays to study pollutant effects on cellular processes.

Purpose of the Study:

  • To assess the mutagenicity of PAHs in lung tissue.
  • To investigate the role of metabolic activation in PAH-induced DNA damage.
  • To differentiate mutagenic from nonmutagenic PAHs using genome-wide expression profiling.

Main Methods:

  • Human alveolar epithelial type II cells (A549) were exposed to pyrene (nonmutagenic PAH) and benzo-[a]-pyrene, 1-nitropyrene, or 1,8-dinitropyrene (mutagenic PAHs).
  • Genome-wide microarray expression profiling was employed to compare cellular responses.
  • Inhibitors of cytochrome P450 (α-naphthoflavone) and p53 (pifithrin-α) were used to probe molecular pathways.

Main Results:

  • Both mutagenic and nonmutagenic PAHs upregulated xenobiotic response genes like CYP1B1.
  • Only mutagenic PAHs significantly upregulated DNA damage-induced genes, specifically p53-downstream genes such as p21 (CDKN1A).
  • Inhibitor treatments blocked benzo-[a]-pyrene-induced p21 expression, confirming the involvement of metabolic activation and p53 signaling.

Conclusions:

  • Lung epithelial cells metabolically activate PAHs, leading to DNA damage.
  • The activation of p53-downstream genes is a key indicator of PAH mutagenicity.
  • DNA microarray expression profiles can effectively classify the mutagenicity of PAHs in lung tissue.