Cysteine oxidase (cysteine dioxygenase, EC 1.13.11.20) was purified approximately 1000-fold from rat liver. The purified enzyme (protein-B) was obtained as an inactive form, which was activated by anaerobic preincubation with L-cysteine. The active form of protein-B was inactivated during aerobic incubation to produce cysteine sulfinate. This inactivation of protein-B was protected by a distinct protein in rat liver cytoplasm, namely stabilizing protein (protein-A). The Ka and Km values for L-cysteine were 0.8-10(-3) M and 1.3-10(-3) M respectively. The enzyme was strongly inhibited by Cu+ and/or Fe2+ chelating agents but not by Cu2+ chelating agent. The optimum pH of enzyme reaction was 8.5-9.5 while that of enzyme activation was 6.8-9.5, with a broad peak.

Animals↗

PubMed1976

The role of metal ions in the activation of arginase.

The role of metal ions as activators of arginase hydrolyzing arginine were studied. The metal ion is assumed to form a complex with arginine and to promote the enzymatic reaction. The activating ability of the metal ion appears to be governed by the chelating ability and/or the coordination numbers which determine whether the metal ion combines with the enzyme or the substrate (or both substrate and enzyme) and factors which influence the configuration of the resulting complexes.

Animals↗

PubMed1976

Multiple factor analysis of the action of local anesthetics.

The pH jump data of Bianchi and Strobel [(1968) Trans. N.Y. Acad. Sci. Ser. II, 30, 1082-1092] on desheathed frog sciatic nerve are fitted to rate equations. A general quantitation of synergism, summation, and antagonism of anesthetics and of excitation is given.

Action Potentials↗

PubMed1976

Nuclear magnetic resonance studies of the interaction of general anesthetics with 1,2-dihexadecyl-sn-glycero-3-phosphorylcholine bilayer.

Sonicated 1,2-dihexadecyl-sn-glycero-3-phosphorylcholine forms liposomes. Studies by Fourier transform proton magnetic resonance of the interaction of these bilayers with some general anesthetics, i.e., chloroform, halothane, methoxyflurane, and enflurane, show that the addition of a general anesthetic to the liposomes and raising the temperature have a similar effect in cuasing the fluidization of the bilayer. General anesthetics act on the hydrophilic site (choline group) in clinical concentrations and then diffuse into the hydrophobic region with the addition of larger amount of anesthetics. There is evidence that the lecithin choline groups are involved in the interaction with protein and that the general anesthetics change the conformation of some polypeptides and proteins. We conclude that the general anesthetics, by increasing the motion of positively charged choline groups and negatively charged groups in protein, weaken the Coulomb-type interaction and cause the liprotein conformational changes.

Anesthetics↗

PubMed1976

Molecular mechanism of inhibition of firefly luminescence by local anesthetics.

The kinetics of the action of local anesthetics upon firefly luciferin and luciferase systems is presented. Clinical concentrations of local anesthetics inhibited this ATP-induced luminescence in a dose-dependent manner. From the effects of temperature and pH upon the inhibitory action of the local anesthetics, it is concluded that hydrophobic ligand-enzyme interaction is the predominant cause of the inhibition, but hydrophilic interaction also contributes to the inhibition to a lesser degree. A molecular theory of anesthesia is outlined which postulates that release of electrostricted water molecules from the hydrophilic parts of the enzyme due to the protein conformational changes induced by anesthetics is the cause of the decreased luminescence. A similar mechanism is expected to occur at the cell membrane, which probably dehydrates the sodium channel and suppresses the conductance of this ion across the membrane. These events lead to a volume expansion of the total system, and the system becomes reactive to a pressure which reverses the anesthesia by shifting the equilibrium to the nonanesthetized original volume. The pressure antagonism of anesthesia can be explained by this overall volume expansion and not by a mere swelling of the cell membrane.

Anesthetics, Local↗

PubMed1976

Combined effects of dissociable and undissociable local anesthetics upon ATP-induced firefly bioluminescence.

Combined effects of two drugs present simultaneously are usually expressed as summation, synergism or potentiation, and antagonism. When the sum of the effects of each drug present separately equals the combined effect of the two drugs present simultaneously, the action is called additive or summation. However, the expected value of the sum of each effect of drugs present alone has not been well defined. In this report, the thearetical value of the expected sum of each effect of two inhibitors is given and a graphical method is presented to visualize summation, synergism, and antagonism. The inhibitory effects of a dissociable local anesthetic, tetracaine, and an undissociable local anesthetic, benzyl alcohol, upon a soluble firefly luminescent system were analyzed according to the above theory. The results clearly indicate that the action of these two classes of local anesthetics is pure additive or summation.

Adenosine Triphosphate↗

PubMed1975

Effect of polyamines on phosphorylation of non-histone chromatin proteins from hog liver.

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Animals↗

PubMed1975

Cysteine metabolism in vivo of vitamin B6-deficient rats.

The expirations of 14CO2 from DL-[1-14C]-, DL-[3-14C]- and L-[U-14C] cysteine used as isotopic tracers were estimated in order to determine the in vivo metabolic distribution of L-cysteine in pyridoxine deficient rats. The expired 14CO2 from L-[U-14C] cysteine was increased by pyridoxine deficiency. The loading of non-physiological dose of L-cysteine resulted in remarkable increase in the expiration of 14CO2 from each tracer in deficient rats as well as in controls. The in vivo metabolic distributions of L-cysteine were calculated from the expired 14CO2 from these isotopic tracers. The in vivo metabolic distribution of L-cysteine calculated showed that the remarkable lesion in taurine pathway occurred in pyridoxine deficient rats, and when non-physiological dose of L-cysteine was loaded the catabolism of L-cysteine of controls was markedly increased in either pyruvate or taurine pathway, whereas the L-cysteine catabolism in deficient rats was increased only in pyruvate but not in taurine pathway. The urinary excretions of 35S-labeled metabolites such as sulfate or taurine were also examined in deficient and control rats.

Animals↗

PubMed1975