Immunohistochemical localization and activity of glutathione transferase zeta (GSTZ1-1) in rat tissues

Hoffman B.M. Lantum, Raymond B. Baggs, Daria M. Krenitsky, Philip G. Board, M. W. Anders*

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    29 Citations (Scopus)

    Abstract

    Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of a range of α-haloacids, including dichloroacetic acid (DCA), and the penultimate step in the tyrosine degradation pathway. DCA is a rodent carcinogen and a common drinking water contaminant. DCA also causes multiorgan toxicity in rodents and dogs. The objective of this study was to determine the expression and activities of GSTZ1-1 in rat tissues with maleylacetone and chlorofluoroacetic acid as substrates. GSTZ1-1 protein was detected in most tissues by immunoblot analysis after immunoprecipitation of GSTZ1-1 and by immunohistochemical analysis; intense staining was observed in the liver, testis, and prostate; moderate staining was observed in the brain, heart, pancreatic islets, adrenal medulla, and the epithelial lining of the gastrointestinal tract, airways, and bladder; and sparse staining was observed in the renal juxtaglomerular regions, skeletal muscle, and peripheral nerve tissue. These patterns of expression corresponded to GSTZ1-1 activities in the different tissues with maleylacetone and chlorofluoroacetic acid as substrates. Specific activities ranged from 258 ± 17 (liver) to 1.1 ± 0.4 (muscle) nmol/min/mg of protein with maleylacetone as substrate and from 4.6 ± 0.89 (liver) to 0.09 ± 0.01 (kidney) nmol/min/mg of protein with chlorofluoroacetic acid as substrate. Rats given DCA had reduced amounts of immunoreactive GSTZ1-1 protein and activities of GSTZ1-1 in most tissues, especially in the liver. These findings indicate that the DCA-induced inactivation of GSTZ1-1 in different tissues may result in multiorgan disorders that may be associated with perturbed tyrosine metabolism.

    Original languageEnglish
    Pages (from-to)616-625
    Number of pages10
    JournalDrug Metabolism and Disposition
    Volume30
    Issue number6
    DOIs
    Publication statusPublished - 2002

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