Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the group of 107 patients poisoned by carbon monoxide (18 patients), ethanol (10), barbiturates (18), glutehimide (10), tranquilizers (19), organic solvents (10),salicylates (3), organochlorines (8), and sulfonamides (5)--the activities of 8 serum enzymes were determined for 6 consecutive days of treatment, the enzymes being as follows: aminotransferases, cholinesterase, alkaline phosphatase, lactate, alpha-hydroxybutyrate, glutamate, and sorbitol dehydrogenase. The antipyrine half-life was also assayed. It has been shown that the poisonings by particular groups of poisons do not bring about characteristic changes in the activity of enzymes that might be of any diagnostic value. The intensity of changes was connected withe depth and duration of toxic coma. Most frequently an increase ensued in the activity of AspAt and AlAt in the third 24-hrs period, and an increase in the activity of SDH in the first 24-hrs period. In the group under examination there were 26 drug abusers in whom a shortening of the antipyrine half-life was discovered. They were less responsive to toxic doses of drugs, and the enzymatic changes in them were less distinct. No changes in the activity of tested enzymes, which are characteristic of toxicomania, were found.
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PMID:The usefulness of the enzymatic tests in acute poisonings. 124 89

Benzodiazepines (BDZ) interact with specific receptors (R), whose activation improves Cl- -channel gating by the GABA receptor (GABA-R). Neurones, whose GABAergic input has a certain level of activity, will be more inhibited in the presence of BDZ (primary target neurones for BDZ). Secondarily, neurones dependent on the activity of primary target neurones will also be effected. Drugs that interact with GABAergic functions (except the BDZ-R) or with the function of primary or secondary target neurones may inhibit some or all BDZ effects; these are nonspecific BDZ antagonists (e.g. GABA-antagonists, cholinesterase inhibitors, naloxone, methylxanthines). Specific BDZ antagonists inhibit the action of BDZ by blocking competitively the BDZ-R. Ro 15-1788 is the best investigated specific BDZ antagonist. Virtually devoid of any pharmacological action by itself, the compound blocks all typical effects of BDZ. It is well tolerated also in man and will find application in anaesthesiology to shorten the sedative and muscle relaxant effect of BDZ and in emergency services to reverse comatose states after BDZ overdosage. Recently drugs have been found that produce effects opposite to the BDZ tranquilizers by inducing a conformation of the BDZ-R which depresses GABA-mediated Cl- -channel gating. The effects of these inverse agonists (e.g. proconvulsant , convulsant, anxiogenic) are blocked by pure competitive BDZ-R blockers, such as Ro 15-1788.
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PMID:Antagonists of benzodiazepines. 614 9

Tissue transglutaminase (tTG) is a marker for apoptosis, and its protein level is known to be increased in post-mortem Alzheimer's and Huntington's disease brains. tTG is increased in the cerebrospinal fluid of patients with Alzheimer's disease. However, the influence of psychotropic medication on acute cell death has not been studied so far in vivo, although some experiments performed in vitro suggest that antipsychotic drugs are neurotoxic. The protein level of tTG was examined in the cerebrospinal fluid obtained from 29 patients under neuroleptic medication in the last 24 h before lumbar puncture (eight patients diagnosed with Alzheimer's disease and 21 patients with other neurological diseases), and compared with those from 55 patients without antipsychotic medication (25 Alzheimer's patients and 30 others). In addition, the influence of several other psychotropic drugs on apoptosis was analysed. A significant influence (P<0.01) of antipsychotic drugs for both the Alzheimer's and the non-Alzheimer's group was found with respect to tTG protein levels in cerebrospinal fluid. By contrast to the male subgroups, the female groups showed a strong influence of neuroleptics on cerebral cell death. Surprisingly, atypical antipsychotics did not differ from typical neuroleptics in neurotoxicity. By contrast, no influence of antidepressants, cholinesterase-inhibitors, nootropics, tranquilizers and tramadol on cerebral cell death was found. The results suggest that typical and atypical antipsychotic drugs may induce cerebral cell death, especially in female patients. Subjects with Alzheimer's disease might be even more vulnerable to any antipsychotic. Therefore, subsequent research should aim to identify atypical neuroleptics without neurotoxicity. A limit on the use of first- and second-generation antipsychotics in elderly patients is proposed. Finally, the possible connection between the observed increased cerebral cell death and tardive dyskinesia, the most threatening side-effect in antipsychotic therapy, is discussed.
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PMID:The influence of psychotropic drugs on cerebral cell death: female neurovulnerability to antipsychotics. 1581 64