Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
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Drug
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Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: EC:3.1.4.37 (
CNPase
)
539
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The activity of 2', 3'-cyclic nucleotide 3'-phosphohydrolase (CNP,
EC 3.1.4.37
), a myelin-associated enzyme, was monitored in brain, spinal cord, and sciatic nerve homogenates from tri-o-tolyl phosphate (TOTP) and tri-m-tolyl phosphate (TMTP) treated hens. Atropinized adult White Leghorn hens were orally dosed with TOTP (200 mg/kg) or with TMTP (200 mg/kg). The treated birds were monitored daily for development of delayed neurotoxicity, and CNP activity was measured via spectrophotometry at the time of maximal locomotor impairment (27-35 days post dosing). The TOTP-treated birds manifested locomotor deficit by 15 days postdosing and exhibited T2-T4
ataxia
at maximal locomotor impairment. The hens administered TMTP exhibited no signs of delayed neurotoxicity. CNP activity of sciatic nerve preparations from TOTP-dosed hens was significantly inhibited (p less than 0.05) at the time of maximal locomotor impairment. There was also a significant correlation between decreased CNP activity and the degree of
ataxia
at the time of maximal locomotor impairment. This decrease in sciatic nerve CNP activity was most likely associated with nerve fiber degeneration. The level of CNP activity in spinal cord and brain homogenates from TOTP-dosed birds was not markedly altered. TMTP-treated birds exhibited no change in neural tissue CNP activity. The results suggest that the criterion of decreased CNP activity may serve as a useful biochemical adjunct to established clinical, biochemical, and morphological methods in the assessment of chemically-induced neuropathies.
...
PMID:Effect of acute tri-o-tolyl phosphate exposure on 2', 3'-cyclic nucleotide 3'-phosphohydrolase activity in hen neural tissues. 284 76
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 100 microM 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 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 nucleotide phosphohydrolase
, was significantly decreased following HCP exposure. This decrease in enzyme activity is consistent with the histological observations demonstrating extensive vacuolization and edema in the optic nerve after exposure to HCP.
...
PMID:Effect of short-term exposure to hexachlorophene on rat brain cell specific marker enzymes. 290 23