Exam 10: Damage to Nuclear Structuresdna: Mutagenesis and Carcinogenesis

What kind of mutations does N-ethyl N-nitrosourea cause?

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Question 1

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Point mutations with AT to TA transversions or AT to GC transitions.

How is the cis-dichloro, diaminoplatinum compound (cis-platinum) a cross-linking agent?

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It reacts with water during metabolism and a chloride is released. A second water can also be added similarly. The compound can then react with the nitrogens, especially the nitrogen of guanine.

What is the difference between genotoxic carcinogens and cell proliferation agents?

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A genotoxic agent such as a metal or its activated metabolite modifies DNA in some form that can be found by adduct formation, mutations, etc. A cell proliferation agent such a TCDD changes expression of DNA by binding to a receptor such as the Ah (or estrogenic agents bind to the ER receptors) and cause cell proliferation. This does not initiate cancer but provides mitogenic influences that promote cancer and can increase the mutation rate based on the increased rate of growth of cells (dysplasias).

Why would interference with topoisomerase II cause clastogenesis?

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Question 4

How was thimerosal's (used in vaccine production) damage to the nuclear membrane assessed?

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Question 5

How is the Comet assay interpreted?

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Question 6

Why are PAHs involved in frameshift mutations?

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Question 7

Showing 1 - 7 of 7

What kind of mutations does N-ethyl N-nitrosourea cause?

How is the cis-dichloro, diaminoplatinum compound (cis-platinum) a cross-linking agent?

What is the difference between genotoxic carcinogens and cell proliferation agents?

Why would interference with topoisomerase II cause clastogenesis?

How was thimerosal's (used in vaccine production) damage to the nuclear membrane assessed?

How is the Comet assay interpreted?

Why are PAHs involved in frameshift mutations?

Biological Research in Toxicology

Development of the Field of Toxicology

Toxicology Terms and How They Relate to Organisms

Hazard, Exposure, and Risk Modeling

Absorption and Transport of Toxicants Through Membranes: Toxic Damage to Membranes

Receptor-Mediated Toxicities on the Outside of Cells

Detoxication and Activation by Cells: Metabolism of the Original Toxicant

Damage to Cytosolic and Endoplasmic Reticulum Activities

Damage to Mitochondrial and Chloroplast Activities

Selective Genetic Sensitivity of Cells to Toxicants

Nutritional Toxicity and Sensitivity

Routes of Administration and Which Organs Are Most Likely Impacted Based on Route and Toxicokinetic Models

Forensic Toxicity Testing

The Skin and Eye: Most Likely Exposure Routes and Toxicities Due to Contact Exposure and Dose Toxicities

Gastrointestinal System Toxicity and Oral Exposure Gi Tract, Pancreas, Liver

The Lung and Gill Exposures Representing Toxic Concentrationsmodel for Environmental Toxicology

The Cardiovascular System As Conduit for a Dose Becoming a Dosage: Exposure and Toxicities

Bone Marrow and Immune Organ Toxicity Via Lymphatic and Blood Transport

The Nervous System and Exposure to Lipophilic Toxicants or Transported Neurotoxic Agents

Toxicity to Neuroendocrine Organs and Endocrine Disruption

Toxicity to Reproductive Organs and Developmental Toxicity

Excretion of Hydrophilic Toxicants and Metabolites and Kidney Toxicity

Dispersion Modeling in Air, Water, and Soil: Likely Route of Exposure and Most Sensitive Organism Based on Dispersion and Concentration

Agricultural Chemicals Pesticides and Fertilizers: Exposure and Impacts

Industrial Chemicals That Biodegrade: Organic Chemical Exposures and Impacts

Ndustrial Chemicals That Change Lipophilicity but Do Not Biodegrade: Metal Impacts

Industrial Chemicals That Cause Atmospheric Changes and Direct Versus Indirect Toxicity: Gases, Vapors, Aerosols, and Radiation

Toxicity of Pharmaceuticals and Personal Care Products Ppcps Into Water

Venoms and Injection Toxicity Versus Poisonous Animals or Cells and Ingestion or Contact Toxicity

Poisonous Plants or Plant Cells and Ingestion or Contact Toxicity

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