Related Experiment Video

Updated: Jun 17, 2026

Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases
14:57

Spectrophotometric Screening for Potential Inhibitors of Cytosolic Glutathione S-Transferases

Published on: October 10, 2020

Isothiocyanate exposure, glutathione S-transferase polymorphisms, and colorectal cancer risk

Gong Yang1, Yu-Tang Gao, Xiao-Ou Shu

  • 1Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA. gong.yang@vanderbilt.edu

The American Journal of Clinical Nutrition
|January 1, 2010
PubMed
Abstract

Insights

High urinary isothiocyanate levels may reduce colorectal cancer risk, particularly for individuals with specific Glutathione S-transferase (GST) gene variations (GSTM1 and GSTT1 null genotypes). This suggests a potential protective effect modified by genetic factors.

Area of Science:

  • Nutritional Epidemiology
  • Cancer Prevention
  • Pharmacogenomics

Background:

  • Isothiocyanates from cruciferous vegetables show anticarcinogenic potential in lab studies.
  • Glutathione S-transferases (GSTs) metabolize isothiocyanates, and genetic variations may influence their activity.

Purpose of the Study:

  • To prospectively assess the link between urinary isothiocyanate levels and colorectal cancer risk.
  • To investigate if GST genotypes modify this association.

Main Methods:

  • A nested case-control study within the Shanghai Women's Health Study.
  • Involved 322 colorectal cancer cases and 1251 controls.
  • Measured urinary isothiocyanate concentrations and analyzed GSTM1/GSTT1 genotypes.

Main Results:

  • Urinary isothiocyanates showed an inverse association with colorectal cancer risk.
  • This inverse association was significant for GSTM1-null and GSTT1-null genotypes.
  • The strongest protective effect (OR 0.51) was observed in individuals with both null genotypes for GSTM1 and GSTT1.

Conclusions:

  • Isothiocyanate exposure appears to lower colorectal cancer risk.
  • The protective effect of isothiocyanates is significantly modified by GSTM1 and GSTT1 genetic variations.

More Related Videos

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform06:21

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform

Published on: May 10, 2024

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

Related Concept Videos

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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...
Phase II Reactions: Glutathione Conjugation and Mercapturic Acid Formation01:22

Phase II Reactions: Glutathione Conjugation and Mercapturic Acid Formation

Glutathione, a tripeptide made up of glutamate, cysteine, and glycine, is a critical player in the detoxification of drugs and xenobiotics via a process known as glutathione conjugation or mercapturic acid formation. This phase II biotransformation reaction involves the covalent binding of glutathione to a drug or its metabolite, enhancing the compound's water solubility and enabling its excretion.
Several distinctive characteristics distinguish glutathione conjugation from other phase II...
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...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...