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Arylamine activating sulfotransferase in liver

K Nagata1, K Yoshinari, S Ozawa

  • 1Division of Drug Metabolism and Molecular Toxicology, Faculty of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.

Mutation Research
|May 12, 1997
PubMed

Insights

Researchers investigated the role of sulfotransferases (SULT1) in activating carcinogenic N-hydroxy-arylamines. They identified a human gene similar to rat ST1C1 but found no detectable expression in human liver samples, suggesting it may not mediate this activation pathway.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Toxicology

Background:

  • Carcinogenic N-hydroxy-arylamines and -arylamides are activated by mammalian enzymes, leading to DNA damage.
  • Cytosolic sulfotransferases (SULT1) in rat and human livers are implicated in this metabolic activation process.

Purpose of the Study:

  • To identify and characterize a human orthologue of rat ST1C1, an enzyme involved in arylamine metabolic activation.
  • To assess the expression and potential role of the human ST1C1 orthologue in human liver.

Main Methods:

  • Screening of an EMBL genomic library using rat ST1C1 cDNA to identify homologous human sequences.
  • Sequencing of hybridized clones to determine nucleotide and amino acid homology.
  • Western blot analysis using anti-rat ST1C1 antibody and RT-PCR with human ST1C1 probes to detect protein and mRNA in human liver samples.

Main Results:

  • A human gene with high sequence homology to rat ST1C1 was identified in the 3'-terminal region.
  • No detectable protein band for the human ST1C1 orthologue was observed in Western blots of human liver samples.
  • No detectable mRNA for the human ST1C1 orthologue was found in human liver samples using RT-PCR.

Conclusions:

  • The identified human ST1C1 orthologue shows significant sequence similarity to its rat counterpart.
  • Despite sequence homology, the human ST1C1 orthologue does not appear to be expressed in human liver, suggesting it may not play a significant role in the metabolic activation of N-hydroxy-arylamines in this tissue.

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