Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.25 (triphosphatase)
 1,529 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Opioid agonists of the mu, kappa and delta types stimulated low-Km guanosine triphosphatase (GTPase) in membranes, from the brain of the rat by up to 34%, with potencies the rank order of which corresponded to the respective binding affinities to opioid receptor. In general, kappa ligands stimulated GTPase to a lesser degree than mu or delta opiates. The coupling of a given type of opioid receptor to GTPase was resolved by direct or protective alkylation of the other receptors. Treatment of the membranes with beta-funaltrexamine abolished the stimulation of GTPase by sufentanil and levorphanol (mu), but not by bremazocine (kappa) or DSLET (delta). On the other hand, prior incubation with Superfit, an alkylating agent with selectivity for the delta opioid receptor, specifically eliminated the effect of DSLET. Partial alkylation by increasing concentrations of Superfit gradually reduced the extent of stimulation of GTPase by DSLET. The successive treatment of membranes with Superfit and beta-funaltrexamine blocked the actions of DSLET, sufentanil and levorphanol, but had no effect on the stimulation of the GTPase by bremazocine. Selective coupling of an opioid receptor to GTPase was also obtained after incubation of membranes with beta-chlornaltrexamine in the presence of protective concentrations of mu, kappa or delta opioid ligands. Alkylation resolved the coupling of the non-selective opiate etorphine: the sum of stimulation of GTPase in the receptor-selective membranes equalled maximal stimulation of enzyme in untreated membranes. Naloxone blocked the stimulation of GTPase by mu, kappa or delta agonists, but ICI-174,864 specifically inhibited the effect of DSLET.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Coupling of multiple opioid receptors to GTPase following selective receptor alkylation in brain membranes. 283 May 55

Endorphins have been implicated in the pathophysiology of spinal cord injury. The effect of naloxone on the sodium- and potassium-activated and magnesium-dependent adenosine-5'-triphosphatase (Na(+)-K+/Mg+2 ATPase, EC.3.6.1.3.) activity, lipid peroxidation, and early ultrastructural findings were studied in rats at the early stage of spinal cord injury, produced with an aneurysm clip on the T2-T7 segments. The rats were divided into four groups. The 10 rats in Group I, which had no injury and received no medication, were used for determining Na(+)-K+/Mg+2 ATPase activity, the extent of lipid peroxidation (by measuring the level of thiobarbituric acid-reactive substances as malondialdehyde), and normal ultrastructural findings. On the 15 rats in Group II, without spinal cord injury, only laminectomy was performed to determine the effect of surgery on the biochemical indices and findings. In the 15 rats in Group III, physiological saline was administered intraperitoneally in an amount equivalent to that of the naloxone administered immediately after spinal cord injury. In the 15 rats in Group IV, 0.5 mg of naloxone was administered intraperitoneally as a single dose immediately after injury and again 60 minutes after injury. The Na(+)-K+/Mg+2 ATPase activity was promptly reduced after spinal cord injury and remained in a lower level than the levels of Groups I and II during 120 minutes after injury. Naloxone treatment, immediately after trauma, attenuated the inactivation of Na(+)-K+/Mg+2 ATPase. On the other hand, there was a significant difference in the malondialdehyde content between animals in Groups I and III. Naloxone treatment reduced the malondialdehyde content in Group IV.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of naloxone on sodium- and potassium-activated and magnesium-dependent adenosine-5'-triphosphatase activity and lipid peroxidation and early ultrastructural findings after experimental spinal cord injury. 759 12