Trypanosoma cruzi

Choline acetyltransferase activity in tissues of susceptible and resistant mice infected with the Brazil strain

Herbert B. Tanowitz, Peter Davies, Stephen M. Factor, Takashi Minase, Ahvie Herskowitz, Murray Wittner

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

In order to ascertain if there were biochemical differences in the autonomic nervous system of both C57BL/6-(resistant) and C3H/HeJ-(susceptible) mice infected with the "Brazil" strain of Trypanosoma cruzi we studied the depletion of the enzyme, choline acetyltransferase (EC 2.3.1.6) in the hearts and brains of these infected mice. In the hearts of C3H/HeJ mice, a 30-35% depletion of choline acetyltransferase was evident by day 7 of infection, a time characterized by lack of obvious parasitemia and frank morphological changes in the myocardium or atrial ganglia. When these mice were moribund (day 25) the depletion of choline acetyltransferase was approximately 40%. Myocardial inflammation, necrosis, and increased pseudocyst numbers were evident as the infection proceeded and as the parasitemia rose. In addition, right atrial ganglia were involved with inflammatory cells but were devoid of amastigotes. In resistant (B6) mice choline acetyltransferase levels were not depleted during the course of infection. Brain choline acetyltransferase levels were significantly depleted in moribund C3H mice but there were no frank morphological changes. Extracts of T. cruzi were devoid of any substances capable of inhibiting choline acetyltransferase. Choline acetyltransferase depletion in the hearts of infected susceptible animals precedes morphological alteration. Depletion of this enzyme may be utilized as an early parameter of infection.

Original languageEnglish (US)
Pages (from-to)269-278
Number of pages10
JournalExperimental Parasitology
Volume51
Issue number2
DOIs
StatePublished - 1981

Fingerprint

Choline O-Acetyltransferase
Trypanosoma cruzi
Brazil
Parasitemia
Inbred C3H Mouse
Infection
Ganglia
Autonomic Nervous System
Brain
Enzymes
Myocardium
Necrosis
Inflammation

Keywords

  • Carditis
  • CAT
  • Chagas' disease
  • Choline acetyltransferase (EC 2.3.1.6)=CAT
  • Cholinergic nerves
  • Hemoflagellate
  • Mouse
  • Nervous system, autonomic
  • Protozoa, parasitic
  • Trypanosoma cruzi

ASJC Scopus subject areas

  • Immunology
  • Parasitology
  • Infectious Diseases

Cite this

Trypanosoma cruzi : Choline acetyltransferase activity in tissues of susceptible and resistant mice infected with the Brazil strain. / Tanowitz, Herbert B.; Davies, Peter; Factor, Stephen M.; Minase, Takashi; Herskowitz, Ahvie; Wittner, Murray.

In: Experimental Parasitology, Vol. 51, No. 2, 1981, p. 269-278.

Research output: Contribution to journalArticle

Tanowitz, Herbert B. ; Davies, Peter ; Factor, Stephen M. ; Minase, Takashi ; Herskowitz, Ahvie ; Wittner, Murray. / Trypanosoma cruzi : Choline acetyltransferase activity in tissues of susceptible and resistant mice infected with the Brazil strain. In: Experimental Parasitology. 1981 ; Vol. 51, No. 2. pp. 269-278.
@article{4af394cc1d46446cb261224230367170,
title = "Trypanosoma cruzi: Choline acetyltransferase activity in tissues of susceptible and resistant mice infected with the Brazil strain",
abstract = "In order to ascertain if there were biochemical differences in the autonomic nervous system of both C57BL/6-(resistant) and C3H/HeJ-(susceptible) mice infected with the {"}Brazil{"} strain of Trypanosoma cruzi we studied the depletion of the enzyme, choline acetyltransferase (EC 2.3.1.6) in the hearts and brains of these infected mice. In the hearts of C3H/HeJ mice, a 30-35{\%} depletion of choline acetyltransferase was evident by day 7 of infection, a time characterized by lack of obvious parasitemia and frank morphological changes in the myocardium or atrial ganglia. When these mice were moribund (day 25) the depletion of choline acetyltransferase was approximately 40{\%}. Myocardial inflammation, necrosis, and increased pseudocyst numbers were evident as the infection proceeded and as the parasitemia rose. In addition, right atrial ganglia were involved with inflammatory cells but were devoid of amastigotes. In resistant (B6) mice choline acetyltransferase levels were not depleted during the course of infection. Brain choline acetyltransferase levels were significantly depleted in moribund C3H mice but there were no frank morphological changes. Extracts of T. cruzi were devoid of any substances capable of inhibiting choline acetyltransferase. Choline acetyltransferase depletion in the hearts of infected susceptible animals precedes morphological alteration. Depletion of this enzyme may be utilized as an early parameter of infection.",
keywords = "Carditis, CAT, Chagas' disease, Choline acetyltransferase (EC 2.3.1.6)=CAT, Cholinergic nerves, Hemoflagellate, Mouse, Nervous system, autonomic, Protozoa, parasitic, Trypanosoma cruzi",
author = "Tanowitz, {Herbert B.} and Peter Davies and Factor, {Stephen M.} and Takashi Minase and Ahvie Herskowitz and Murray Wittner",
year = "1981",
doi = "10.1016/0014-4894(81)90115-6",
language = "English (US)",
volume = "51",
pages = "269--278",
journal = "Experimental Parasitology",
issn = "0014-4894",
publisher = "Academic Press Inc.",
number = "2",

}

TY - JOUR

T1 - Trypanosoma cruzi

T2 - Choline acetyltransferase activity in tissues of susceptible and resistant mice infected with the Brazil strain

AU - Tanowitz, Herbert B.

AU - Davies, Peter

AU - Factor, Stephen M.

AU - Minase, Takashi

AU - Herskowitz, Ahvie

AU - Wittner, Murray

PY - 1981

Y1 - 1981

N2 - In order to ascertain if there were biochemical differences in the autonomic nervous system of both C57BL/6-(resistant) and C3H/HeJ-(susceptible) mice infected with the "Brazil" strain of Trypanosoma cruzi we studied the depletion of the enzyme, choline acetyltransferase (EC 2.3.1.6) in the hearts and brains of these infected mice. In the hearts of C3H/HeJ mice, a 30-35% depletion of choline acetyltransferase was evident by day 7 of infection, a time characterized by lack of obvious parasitemia and frank morphological changes in the myocardium or atrial ganglia. When these mice were moribund (day 25) the depletion of choline acetyltransferase was approximately 40%. Myocardial inflammation, necrosis, and increased pseudocyst numbers were evident as the infection proceeded and as the parasitemia rose. In addition, right atrial ganglia were involved with inflammatory cells but were devoid of amastigotes. In resistant (B6) mice choline acetyltransferase levels were not depleted during the course of infection. Brain choline acetyltransferase levels were significantly depleted in moribund C3H mice but there were no frank morphological changes. Extracts of T. cruzi were devoid of any substances capable of inhibiting choline acetyltransferase. Choline acetyltransferase depletion in the hearts of infected susceptible animals precedes morphological alteration. Depletion of this enzyme may be utilized as an early parameter of infection.

AB - In order to ascertain if there were biochemical differences in the autonomic nervous system of both C57BL/6-(resistant) and C3H/HeJ-(susceptible) mice infected with the "Brazil" strain of Trypanosoma cruzi we studied the depletion of the enzyme, choline acetyltransferase (EC 2.3.1.6) in the hearts and brains of these infected mice. In the hearts of C3H/HeJ mice, a 30-35% depletion of choline acetyltransferase was evident by day 7 of infection, a time characterized by lack of obvious parasitemia and frank morphological changes in the myocardium or atrial ganglia. When these mice were moribund (day 25) the depletion of choline acetyltransferase was approximately 40%. Myocardial inflammation, necrosis, and increased pseudocyst numbers were evident as the infection proceeded and as the parasitemia rose. In addition, right atrial ganglia were involved with inflammatory cells but were devoid of amastigotes. In resistant (B6) mice choline acetyltransferase levels were not depleted during the course of infection. Brain choline acetyltransferase levels were significantly depleted in moribund C3H mice but there were no frank morphological changes. Extracts of T. cruzi were devoid of any substances capable of inhibiting choline acetyltransferase. Choline acetyltransferase depletion in the hearts of infected susceptible animals precedes morphological alteration. Depletion of this enzyme may be utilized as an early parameter of infection.

KW - Carditis

KW - CAT

KW - Chagas' disease

KW - Choline acetyltransferase (EC 2.3.1.6)=CAT

KW - Cholinergic nerves

KW - Hemoflagellate

KW - Mouse

KW - Nervous system, autonomic

KW - Protozoa, parasitic

KW - Trypanosoma cruzi

UR - http://www.scopus.com/inward/record.url?scp=0019492763&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019492763&partnerID=8YFLogxK

U2 - 10.1016/0014-4894(81)90115-6

DO - 10.1016/0014-4894(81)90115-6

M3 - Article

VL - 51

SP - 269

EP - 278

JO - Experimental Parasitology

JF - Experimental Parasitology

SN - 0014-4894

IS - 2

ER -