Exam 7: Detoxication and Activation by Cells: Metabolism of the Original Toxicant

Which inducers of CYPs lead to tolerance to medications while which ones cause more activation of procarcinogens?

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Question 1

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Phenobarbital causes more tolerance to medications while PAHs and dibenzodioxins cause more activation of compounds to carcinogens. Peroxisome proliferators may cause more cancer via this proliferative activity while also altering CYP isozyme composition.

What is the key reactant in the cytochrome P450 catalytic cycle and how is it formed?

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It is the doubly reduced oxygen which may be represented by the short-lived perferryl oxygen intermediate or the phorphyrin radical species. This is produced by a two electron reduction of the heme iron CYPs by cytochrome P450 reductase and transfer to the bound oxygen. The binding of the substrate to the heme iron precedes these reaction steps and leads to an oxidized substrate and the other oxygen forming water.

Which enzymes metabolize arachidonic acid and inhibition of these enzymes led to the development (therapeutic medications) and adverse effects (toxicity) of NSAIDS?

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Question 3

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The Cyclooxygenases (COX) form the prostaglandins and thromboxane and are known their Non-Steroidal Anti-Inflammatory Drug actions as well as unwelcome ulcers and hemorrhage.

Why does the metabolism of ethanol lead to a more toxic product to begin its conversion to a less toxic compound?

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Question 4

Indicate the possible phase 2 metabolites that may indicate the formation of a less toxic intermediate versus one that indicates a reactive intermediate.

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Question 5

Why is the benzoyl-CoA reductase a key enzyme in the difference between the metabolism of anaerobic bacteria and facultative anaerobes?

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Question 6

Which enzyme class metabolizes/oxidizes various amines depending on its isozyme?

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Question 7

What reactions reduce toxicity by CYPs and which ones lead to less toxic products?

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Question 8

Which enzymes metabolize catecholamines and indolamines and their inhibition was used early on to help with depression, but also could lead to hypertension in cheese eaters?

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Question 9

Showing 1 - 9 of 9

Which inducers of CYPs lead to tolerance to medications while which ones cause more activation of procarcinogens?

What is the key reactant in the cytochrome P450 catalytic cycle and how is it formed?

Which enzymes metabolize arachidonic acid and inhibition of these enzymes led to the development (therapeutic medications) and adverse effects (toxicity) of NSAIDS?

Why does the metabolism of ethanol lead to a more toxic product to begin its conversion to a less toxic compound?

Indicate the possible phase 2 metabolites that may indicate the formation of a less toxic intermediate versus one that indicates a reactive intermediate.

Why is the benzoyl-CoA reductase a key enzyme in the difference between the metabolism of anaerobic bacteria and facultative anaerobes?

Which enzyme class metabolizes/oxidizes various amines depending on its isozyme?

What reactions reduce toxicity by CYPs and which ones lead to less toxic products?

Which enzymes metabolize catecholamines and indolamines and their inhibition was used early on to help with depression, but also could lead to hypertension in cheese eaters?

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

Damage to Cytosolic and Endoplasmic Reticulum Activities

Damage to Mitochondrial and Chloroplast Activities

Damage to Nuclear Structuresdna: Mutagenesis and Carcinogenesis

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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