Effect of short-term exposure to hexachlorophene on rat brain marker enzymes

MEI PING Kung, Petera Nickerson, Frances M. Sansone, James R. Olson, Paul J. Kostyniak, Maureen A. Adolf, Pamela J Lein, Jerome A. Roth

Research output: Contribution to journalArticle

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Abstract

Effect of Short-Term Exposure to Hexachlorophene on Rat Brain Cell Specific Marker Enzymes.KUNG, M-P., NICKERSON, P. A., SANSONE, F. M., OLSON, J. R., KOSTYNIAK, P. J., ADOLF, M. A., LIEN, P. J., AND ROTH, J. A. (1988). Fundam. Appl Toxicol 11, 519-527. Seven cell specific marker enzymes in brain and optic nerve and morphological evaluation by light microscopy were used to characterize the neurotoxicity associated with exposure of rats to hexachlorophene (HCP, 40 mg/kg/day, po, for 9 days). In vitro exposure to HCP at concentrations up to 100mm had no direct inhibitory effect on the marker enzymes, validating their use in evaluating brain function in vivo. Rats exhibited a reduction in body weight gain, weakness, and ataxia of the hind limbs by the ninth day of HCP exposure. At 24 hr following the last day of exposure to HCP, the activities of the three neuron specific enzymes, glutamic acid decarboxylase, tyrosine hydroxylase, and choline acetyltransferase, in rat brain were unchanged from 3 those of the vehicle-treated control group. Of the two astroglial enzyme markers measured, a small but significant increase was observed in the activity of nonneuronal enolase in the cerebellum and glutamine synthetase in the hippocampus of HCP-treated rats. The optic nerve appeared to be the most sensitive tissue in that the activity of both the astroglial marker, nonneuronal enolase, and the myelin marker, 2',3'-cyclic nuceleotide phosphohydrolase, was significantly decreased following HCP exposure. This decrease in enzyme activity is consistent with the histo-4 logical observations demonstrating extensive vacuolization and edema in the optic nerve after exposure to HCP.

Original languageEnglish (US)
Pages (from-to)519-527
Number of pages9
JournalToxicological Sciences
Volume11
Issue number1
DOIs
StatePublished - 1988
Externally publishedYes

Fingerprint

Hexachlorophene
Rats
Brain
Enzymes
Optic Nerve
Optics
Phosphopyruvate Hydratase
Glutamate-Ammonia Ligase
Glutamate Decarboxylase
Choline O-Acetyltransferase
Tyrosine 3-Monooxygenase
Enzyme activity
Phosphoric Monoester Hydrolases
Neurons
Optical microscopy
Ataxia
Myelin Sheath
Cerebellum
Weight Gain
Microscopy

ASJC Scopus subject areas

  • Molecular Biology
  • Embryology
  • Cell Biology
  • Genetics
  • Developmental Biology
  • Toxicology

Cite this

Kung, MEI. PING., Nickerson, P., Sansone, F. M., Olson, J. R., Kostyniak, P. J., Adolf, M. A., ... Roth, J. A. (1988). Effect of short-term exposure to hexachlorophene on rat brain marker enzymes. Toxicological Sciences, 11(1), 519-527. https://doi.org/10.1093/toxsci/11.1.519

Effect of short-term exposure to hexachlorophene on rat brain marker enzymes. / Kung, MEI PING; Nickerson, Petera; Sansone, Frances M.; Olson, James R.; Kostyniak, Paul J.; Adolf, Maureen A.; Lein, Pamela J; Roth, Jerome A.

In: Toxicological Sciences, Vol. 11, No. 1, 1988, p. 519-527.

Research output: Contribution to journalArticle

Kung, MEIPING, Nickerson, P, Sansone, FM, Olson, JR, Kostyniak, PJ, Adolf, MA, Lein, PJ & Roth, JA 1988, 'Effect of short-term exposure to hexachlorophene on rat brain marker enzymes', Toxicological Sciences, vol. 11, no. 1, pp. 519-527. https://doi.org/10.1093/toxsci/11.1.519
Kung MEIPING, Nickerson P, Sansone FM, Olson JR, Kostyniak PJ, Adolf MA et al. Effect of short-term exposure to hexachlorophene on rat brain marker enzymes. Toxicological Sciences. 1988;11(1):519-527. https://doi.org/10.1093/toxsci/11.1.519
Kung, MEI PING ; Nickerson, Petera ; Sansone, Frances M. ; Olson, James R. ; Kostyniak, Paul J. ; Adolf, Maureen A. ; Lein, Pamela J ; Roth, Jerome A. / Effect of short-term exposure to hexachlorophene on rat brain marker enzymes. In: Toxicological Sciences. 1988 ; Vol. 11, No. 1. pp. 519-527.
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abstract = "Effect of Short-Term Exposure to Hexachlorophene on Rat Brain Cell Specific Marker Enzymes.KUNG, M-P., NICKERSON, P. A., SANSONE, F. M., OLSON, J. R., KOSTYNIAK, P. J., ADOLF, M. A., LIEN, P. J., AND ROTH, J. A. (1988). Fundam. Appl Toxicol 11, 519-527. Seven cell specific marker enzymes in brain and optic nerve and morphological evaluation by light microscopy were used to characterize the neurotoxicity associated with exposure of rats to hexachlorophene (HCP, 40 mg/kg/day, po, for 9 days). In vitro exposure to HCP at concentrations up to 100mm had no direct inhibitory effect on the marker enzymes, validating their use in evaluating brain function in vivo. Rats exhibited a reduction in body weight gain, weakness, and ataxia of the hind limbs by the ninth day of HCP exposure. At 24 hr following the last day of exposure to HCP, the activities of the three neuron specific enzymes, glutamic acid decarboxylase, tyrosine hydroxylase, and choline acetyltransferase, in rat brain were unchanged from 3 those of the vehicle-treated control group. Of the two astroglial enzyme markers measured, a small but significant increase was observed in the activity of nonneuronal enolase in the cerebellum and glutamine synthetase in the hippocampus of HCP-treated rats. The optic nerve appeared to be the most sensitive tissue in that the activity of both the astroglial marker, nonneuronal enolase, and the myelin marker, 2',3'-cyclic nuceleotide phosphohydrolase, was significantly decreased following HCP exposure. This decrease in enzyme activity is consistent with the histo-4 logical observations demonstrating extensive vacuolization and edema in the optic nerve after exposure to HCP.",
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