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Related Concept Videos

Sulfur Assimilation01:20

Sulfur Assimilation

Sulfur is an essential element in biological systems, contributing to synthesizing key biomolecules, including amino acids such as cysteine and methionine, and cofactors such as coenzyme A and biotin. Microorganisms primarily assimilate sulfur as sulfate (SO₄²⁻) from the environment, which must undergo a series of biochemical transformations before it can be incorporated into cellular components. As sulfate is highly oxidized, it must undergo assimilatory sulfate reduction to become...
Drug Metabolism: Phase II Reactions01:14

Drug Metabolism: Phase II Reactions

Phase II reactions are essential for the detoxification and elimination of drugs from the body. These reactions involve the conjugation of parent drugs or their phase I metabolites with endogenous molecules, resulting in more hydrophilic drug conjugates. The primary conjugation reactions in this phase are sulfation and glucuronidation. Both sulfation and glucuronidation typically produce biologically inactive metabolites. However, in some cases involving prodrugs, active metabolites may be...
Phase I Reactions: Oxidation of Aliphatic and Aromatic Carbon-Containing Systems01:19

Phase I Reactions: Oxidation of Aliphatic and Aromatic Carbon-Containing Systems

Phase I biotransformation reactions are integral to drug metabolism, predominantly involving oxidative, reductive, and hydrolytic transformations. Chief among these are oxidative reactions, which enhance the hydrophilicity of xenobiotics and introduce polar functional groups to facilitate their elimination from the body.
Oxidation reactions are fundamental in aromatic carbon-containing systems. An example is the hydroxylation of phenobarbital, a process that transforms it into...
Phase II Reactions: Miscellaneous Conjugation Reactions01:19

Phase II Reactions: Miscellaneous Conjugation Reactions

Phase II biotransformations are detoxification mechanisms that conjugate xenobiotics with endogenous substances, neutralizing their toxicity.
A key example involves the conjugation of cyanide ions, which impair cellular respiration and alter hemoglobin into non-oxygen-carrying cyanmethemoglobin. To neutralize this threat, a sulfur atom from thiosulphate is transferred to the cyanide ion, catalyzed by the enzyme rhodanese, resulting in an inactive compound called thiocyanate. The production of...
Bioactivation and Tissue Toxicity01:25

Bioactivation and Tissue Toxicity

Bioactivation is a metabolic process that transforms less reactive substances into highly reactive metabolites, initiating tissue toxicity. This transformation can lead to various toxic effects, including carcinogenesis and teratogenesis. Reactive metabolites are classified into two main types: electrophiles and free radicals.Electrophiles are electron-deficient species and are produced primarily by the enzyme cytochrome P-450 during the metabolism of compounds containing carbon, nitrogen, or...
Phase II Reactions: Sulfation and Conjugation with α-Amino Acids01:19

Phase II Reactions: Sulfation and Conjugation with α-Amino Acids

Sulfation and α-amino acid conjugation are two critical biotransformation reactions in drug metabolism. Sulfation, a phase II biotransformation reaction, involves adding a polar sulfate group to a drug, enhancing its water solubility and promoting excretion. This process can either co-occur with or occur independently of glucuronidation. Nonmicrosomal sulfotransferase enzymes catalyze the process. The reaction involves 3'-phosphoadenosine-5'-phosphosulfate or PAPS coenzyme activation, sulfur...

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Related Experiment Video

Updated: Jul 16, 2026

Preparation of DMMTAV and DMDTAV Using DMAV for Environmental Applications: Synthesis, Purification, and Confirmation
06:23

Preparation of DMMTAV and DMDTAV Using DMAV for Environmental Applications: Synthesis, Purification, and Confirmation

Published on: March 9, 2018

Molecular processes in cellular arsenic metabolism.

David J Thomas1

  • 1Experimental Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, 109 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA. thomas.david@epa.gov

Toxicology and Applied Pharmacology
|April 3, 2007
PubMed
Summary

Understanding how inorganic arsenic (iAs) and its metabolites accumulate, metabolize, and bind in cells is key to its toxicity. A conceptual model, evolving into a quantitative one, aids in studying iAs cellular behavior and its toxic effects.

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Last Updated: Jul 16, 2026

Preparation of DMMTAV and DMDTAV Using DMAV for Environmental Applications: Synthesis, Purification, and Confirmation
06:23

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Published on: March 9, 2018

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Area of Science:

  • Environmental toxicology
  • Molecular biology
  • Computational toxicology

Background:

  • Inorganic arsenic (iAs) is a known toxin and carcinogen.
  • Understanding the molecular mechanisms of iAs accumulation, metabolism, and binding is crucial for elucidating its toxic and carcinogenic actions.

Purpose of the Study:

  • To develop a conceptual model of molecular processes involved in arsenical influx, metabolism, binding, and efflux in cells.
  • To refine this model into a quantitative framework for predicting the kinetic and dynamic behavior of iAs and its metabolites.

Main Methods:

  • Construction of a non-quantitative conceptual model of cellular arsenical processing.
  • Incorporation of experimental data to develop a quantitative mathematical model.
  • Leveraging tools for manipulating arsenical transport and methylation enzyme activity.

Main Results:

  • The conceptual model provides a framework for experimental design and prediction.
  • The quantitative model will enable kinetic and dynamic estimations of iAs and its metabolites in cells.
  • The model can be integrated into pharmacokinetic and dose-response models.

Conclusions:

  • A refined conceptual and quantitative model of cellular iAs metabolism is essential for understanding its toxicity.
  • This model can inform the development of biologically based dose-response models for arsenicals.
  • Further development requires tools to manipulate cellular arsenical transport and metabolism.