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 language | English (US) |
|---|---|
| Pages (from-to) | 519-527 |
| Number of pages | 9 |
| Journal | Toxicological Sciences |
| Volume | 11 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1988 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Molecular Biology
- Embryology
- Cell Biology
- Genetics
- Developmental Biology
- Toxicology
Cite this
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 journal › Article
}
TY - JOUR
T1 - Effect of short-term exposure to hexachlorophene on rat brain marker enzymes
AU - Kung, MEI PING
AU - Nickerson, Petera
AU - Sansone, Frances M.
AU - Olson, James R.
AU - Kostyniak, Paul J.
AU - Adolf, Maureen A.
AU - Lein, Pamela J
AU - Roth, Jerome A.
PY - 1988
Y1 - 1988
N2 - 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.
AB - 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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UR - http://www.scopus.com/inward/citedby.url?scp=77957180896&partnerID=8YFLogxK
U2 - 10.1093/toxsci/11.1.519
DO - 10.1093/toxsci/11.1.519
M3 - Article
C2 - 2906023
AN - SCOPUS:77957180896
VL - 11
SP - 519
EP - 527
JO - Toxicological Sciences
JF - Toxicological Sciences
SN - 1096-6080
IS - 1
ER -