Characterization and Localization of Glutathione‐S‐Transferases in Rat Brain and Binding of Hormones, Neurotransmitters, and Drugs

Abramovitz, Mark; Homma, Hisato; Ishigaki, Seishi; Tansey, Francine A.; Cammer, Wendy; Listowsky, Irving

doi:10.1111/j.1471-4159.1988.tb13228.x

Cited by 100 publications

(53 citation statements)

References 42 publications

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“…GSTZ1-1 was expressed only in some neurons of the central nervous system. This pattern of expression is unique to GSTZ1-1; GSTA and GSTM are expressed mostly in the choroid plexus, ventricular lining, and vascular epithelia; GSTP and GSTO are expressed only in astrocytes or glial cells; and microsomal GST1 is expressed in most regions in the brain (Abramovitz et al, 1988;Carder et al, 1990;Terrier et al, 1990;Campbell et al, 1991;Johnson et al, 1993;Juronen et al, 1996;Otieno et al, 1997;Sherratt et al, 1997;Yin et al, 2001) (Table 1). No staining was observed in a peripheral nerve embedded in skeletal muscle, indicating that GSTZ1-1 may not be expressed in peripheral nerves (Fig.…”

Section: Fig 2 Immunoblot Analysis Of Immunoprecipitated Gstz1-1 Prmentioning

confidence: 99%

“…Tubules/germ Ϫ Ϫ ϩ ϩ ϩ ϩ Hayes and Mantle, 1986;Terrier et al, 1990;Campbell et al, 1991;Hussey and Hayes, 1993;Sundberg et al, 1993;Gandy et al, 1996;Sherratt et al, 1997;Yin et al, 2001 Sertoli Abramovitz et al, 1988;Carder et al, 1990;Terrier et al, 1990;Campbell et al, 1991;Johnson et al, 1993;Juronen et al, 1996;Otieno et al, 1997;Sherratt et al, 1997;Yin et al, 2001 Cortical neurons Terrier et al, 1990;Campbell et al, 1991;Sundberg et al, 1993;Yin et al, 2001 Mucous cells Hayes and Mantle, 1986;Terrier et al, 1990;Campbell et al, 1991;Sundberg et al, 1993;Juronen et al, 1996;Sherratt et Terrier et al, 1990;Campbell et al, 1991;Rozell et al, 1993;Sundberg et al, 1993;Juronen et al, 1996;Otieno et al, 1997;Sherratt et al, 1997;Yin et al, 2001 Proximal tubule Campbell et al, 1991;Sundberg et al, 1993 Campbell et al, 1991;Sundberg et al, 1993;Sherratt et al, 1997;Yin et al, 2001 Hayes and Mantle, 1986;…”

Section: Tissuesmentioning

confidence: 99%

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Immunohistochemical Localization and Activity of Glutathione Transferase Zeta (GSTZ1–1) in Rat Tissues

Lantum

Baggs²,

Krenitsky³

et al. 2002

Drug Metab Dispos

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ABSTRACT:Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of a range of ␣-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.Glutathione transferases (GST 1 ) are a multigene family of phase II drug-metabolizing enzymes that catalyze the conjugation of glutathione with a range of endogenous and exogenous substrates (Armstrong, 1997;Salinas and Wong, 1999). Soluble and membrane-bound GSTs are expressed in many tissues, and soluble GSTs constitute 1 to 5% of total cytosolic protein (Morgenstern et al., 1984;Sundberg et al., 1993;Rowe et al., 1997). Activities with model substrates and the subcellular localization of GSTA, GSTM, GSTP, GSTT, and GSTO class GSTs and of microsomal GST1 have been previously characterized (Meyer et al., 1991;Hiratsuka et al., 1994;Mannervik and Widersten, 1995;Armstrong, 1997;Otieno et al., 1997;Yin et al., 2001).The expression of GSTs is regulated pre-and post-translationally in a tissue-specific manner resulting in protein products that differ quantitatively in different tissues (Tu et al., 1983;Rozell et al., 1993;Rowe et al., 1997). Testes express the highest amount of total GST protein per milligram cytosolic protein followed by the liver, brain, pancreas, adrenals, heart, and lung (DePierre and Morgenstern, 1983;Listowsky et al., 1998). Major GST-expressing tissues are the principal sites for drug and chemical metabolism indicative of the role of GSTs in the biotransformation of xenobiotics (Pabst et al., 1973;Armstrong, 1997). Studies...

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Section: Fig 2 Immunoblot Analysis Of Immunoprecipitated Gstz1-1 Prmentioning

confidence: 99%

Section: Tissuesmentioning

confidence: 99%

Immunohistochemical Localization and Activity of Glutathione Transferase Zeta (GSTZ1–1) in Rat Tissues

Lantum

Baggs²,

Krenitsky³

et al. 2002

Drug Metab Dispos

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“…Ependyma also have transport systems and distinct enzymes able to remove endogenous and exogenous toxins from the nervous system (Abramovitz et al, 1988;Cammer et al, 1989;Carder et al, 1990). In addition, ependyma express ZO1, occludin, cadherin, α-catenin and β-catenin which are some of junctional complex proteins known to provide the anatomical basis of the CNS barriers (Lippoldt et al, 2000a;Petrov et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Differential changes in junctional complex proteins suggest the ependymal lining as the main source of leukocyte infiltration into ventricles in murine neurocysticercosis

Alvarez

Teale

2007

Journal of Neuroimmunology

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The blood brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCB) limit the influx of immune mediators and bloodstream compounds into the central nervous system (CNS). Upon injury or infection, the integrity of these barriers is compromised and leukocyte infiltration occurs. The BCB is located in the choroid plexuses (CPs) found within ventricles of the brain, and it is considered one of the main routes of cellular infiltration into the CNS into healthy individuals. Our group recently showed that in a murine model of neurocysticercosis (NCC), there is a moderate increase in infiltration of leukocytes into ventricles, but the BCB is hardly compromised. To elucidate the role played by CPs and surrounding ependyma in leukocyte infiltration at ventricular sites, we analyzed changes in the expression of junctional complex proteins in animals intracranially infected with Mesocestoides corti. The results indicate that infection does not change the expression pattern of junctional complex proteins in CPs, but structural alterations and disappearance of these proteins were evident in ependyma adjacent to the internal leptomeninges. The kinetics and magnitude of these changes directly correlated with the extent of leukocyte infiltration through ependyma and with the expression and activity of MMPs. The results of this study indicate that the anatomical elements of the BCB are minimally disrupted during the course of murine NCC. Thus, most of the leukocytes infiltrating ventricles appear to extravasate through pial vessels located in the internal leptomeninges juxtaposed to the ependyma layer and then traverse the ependyma cells. In addition, MMP activity seems to be involved in this process. These results provide evidence for a previously undescribed entry route for leukocytes into the CNS.

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“…The localization of GST in astroglial and ependymal cells has been evidenced immunocytochemically in the Gunn rat cerebellum (this study and also refer to 28, 29) and for the normal rat brain (1,35,36). These cells are suggested to play an important role in transporting materials to and maintaining the ionic environment of neurons (41).…”

Section: Discussionmentioning

confidence: 61%

DEVELOPMENTAL CHANGES IN THE ACTIVITY OF GLUTATHIONE S-TRANSFERASE AND ITS IMMUNOCYTOCHEMICAL LOCALIZATION IN THE HYPOPLASTIC CEREBELLUM OF JAUNDICED GUNN RATS

Sato¹,

Asaoka

Semba³

et al. 1988

Biomed. Res.

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Developmental changes in the activity of glutathione S-transferase (GST) and its immunocytochemical localization were studied in the cerebella of homozygous (j/j) and heterozygous (j/+) Gunn rats. The activity of jaundiced j/j rats began to increase after 8 days of life and reached twice as high as that of non-jaundiced j/+ rats at 15-20 days, chronologically coincident with the development of bilirubin

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Characterization and Localization of Glutathione‐S‐Transferases in Rat Brain and Binding of Hormones, Neurotransmitters, and Drugs

Cited by 100 publications

References 42 publications

Immunohistochemical Localization and Activity of Glutathione Transferase Zeta (GSTZ1–1) in Rat Tissues

Immunohistochemical Localization and Activity of Glutathione Transferase Zeta (GSTZ1–1) in Rat Tissues

Differential changes in junctional complex proteins suggest the ependymal lining as the main source of leukocyte infiltration into ventricles in murine neurocysticercosis

<b>DEVELOPMENTAL CHANGES IN THE ACTIVITY OF GLUTATHIONE <i>S</i>-TRANSFERASE AND ITS IMMUNOCYTOCHEMICAL LOCALIZATION IN THE HYPOPLASTIC CEREBELLUM OF JAUNDICED GUNN RATS</b>

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