Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.16.2 (
PCP
)
3,761
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Morphine elicited a dose-related increase in the duration of phencyclidine (
PCP
)-induced motor incoordination. In the open field behavioral observations, morphine enhanced the
PCP
-induced decrease in the number of ambulation and rearing. Morphine potentiated the
PCP
-induced decrease in body temperature. The LD50 of
PCP
was significantly decreased in the presence of morphine. An opiate antagonist, naloxone, antagonized the morphine-induced effects without influencing the pharmacological actions of
PCP
itself. The levels of hepatic microsomal cytochrome P-450 and cytochrome b5 and the activities of
NADPH dehydrogenase
and NADPH cytochrome c reductase were unaffected by morphine treatment. The half-lives of
PCP
in serum and brain were increased by the concurrent administration of morphine. The ratio of the liver weight to body weight and aniline hydroxylase activity in hepatic microsomal fraction were decreased in the morphine-treated group compared with the control group; this is indicative of a possible reduction in the oxidative metabolism of
PCP
. The results indicate that acute administration of morphine enhances a variety of pharmacological effects of
PCP
; an inhibition of
PCP
disposition by morphine may be a mechanism involved in this process.
...
PMID:Effect of morphine on the responses to and disposition of phencyclidine in mice. I. Enhancement of phencyclidine effects by acute morphine administration. 684 96
We investigated whether ginsenoside Re (Re) modulates phencyclidine (
PCP
)-induced sociability deficits and recognition memory impairments to extend our recent finding. We examined the role of GPx-1 gene in the pharmacological activity of Re against mitochondrial dysfunction induced by
PCP
in the dorsolateral cortex of mice. Since mitochondrial oxidative stress activates
NADPH oxidase
(PHOX), we applied PHOX inhibitor apocynin for evaluating interactive modulation between GPx-1 and PHOX against
PCP
neurotoxicity. Sociability deficits and recognition memory impairments induced by
PCP
were more pronounced in GPx-1 knockout (KO) than in wild type (WT) mice.
PCP
-induced mitochondrial oxidative stress, mitochondrial dysfunction, and membrane translocation of p47phox were more evident in GPx-1 KO than in WT. Re treatment significantly attenuated
PCP
-induced neurotoxic changes. Re also significantly attenuated
PCP
-induced sociability deficits and recognition memory impairments. The attenuation by Re was comparable to that by apocynin. The attenuation was more obvious in GPx-1 KO than in WT. Importantly, apocynin did not show any additional positive effects on the neuroprotective activity of Re, indicating that PHOX is a molecular target for therapeutic activity of Re. Our results suggest that Re requires interactive modulation between GPx activity and PHOX (p47phox) to exhibit neuroprotective potentials against
PCP
insult.
...
PMID:Ginsenoside Re protects against phencyclidine-induced behavioral changes and mitochondrial dysfunction via interactive modulation of glutathione peroxidase-1 and NADPH oxidase in the dorsolateral cortex of mice. 2903 73
