Acceleratory Effect Research Articles

Formation and properties of a synthetic bone composite: Hydroxyapatite–collagen

Composites composed of microcrystalline calcium-deficient hydroxyapatite (HAp) and collagen were formed at 38 degrees C via an acid-base reaction between calcium phosphate precursors in the presence of a collagen matrix. Formation of composites having HAp:collagen weight ratios of 4.5:1, 11:1, and 22:1, along with that of pure mineral were investigated. Isothermal calorimetry and X-ray diffraction indicated complete reaction within 5 h resulting in hardened monoliths. The rate of HAp formation increased with an increase in the proportion of collagen present. Electron microscopy indicated that the acceleratory effect of collagen was associated with the provision of nucleation sites for HAp crystallization. Analysis of the solution chemistry also showed that collagen affected the calcium and phosphate concentrations and the pH. While collagen was shown to effect the kinetics of HAp formation, the rate limiting step, as shown by X-ray diffraction and solution chemistry, was the dissolution of the acidic calcium phosphate precursor, CaHPO4. Preliminary mechanical data indicated that the Young's modulus, yield strength, and work to fracture were at the lower end of the range of those values reported for bone. The porosities observed in these composites suggest that they might be osteoinductive while their compositions should allow their eventual resorption. Thus, microstructure, kinetics, and mechanical data suggest that these composites might be suitable as bone substitutes which form in vivo.

Stimulatory effect of calcium on metabolism and its sensitivity to pH in kidney mitochondria.

The relationship between mitochondrial matrix free Ca2+ concentration ([Ca2+]m) and pH was evaluated by incubating isolated rat kidney mitochondria with different extramitochondrial Ca2+ concentrations ([Ca2+]e) at medium pH (pHe) 7.0 and 7.4. [Ca2+]m was monitored using the fluorescent signal from mitochondria loaded with the Ca2+ indicator fura 2. The changes in [Ca2+]m were compared with alpha-ketoglutarate dehydrogenase (alpha-KGDH) flux, measured as O2 consumption (nmol.min-1.mg protein-1) from 185 microM alpha-ketoglutarate (alpha-KG). The apparent dissociation constant of the matrix fluorescent probe for Ca2+ was determined in each experiment and was 323 +/- 45 nM (n = 14). When mitochondria were exposed to [Ca2+]e below 160 nM, [Ca2+]m was greater at pHe 7.0 than at pHe 7.4. However, above 160 nM [Ca2+]e, [Ca2+]m plateaued at pHe 7.0 but rose progressively at pHe 7.4. Increasing [Ca2+]m by consecutive additions of Ca2+ to the medium had a significantly more pronounced acceleratory effect on alpha-KG oxidation at pHe 7.0 than at pHe 7.4. Kinetic analysis of alpha-KGDH revealed a 45% decrease in the Michaelis constant (Km) for alpha-KG at pHe 7.0, but the Km was unchanged at pHe 7.4 with elevation of [Ca2+]m from 32 to 751 nM. Maximal velocity (Vmax) increased significantly at both pHe values. Half-maximal alpha-KG oxidation occurred at [Ca2+]m of 76 +/- 11 nM and 105 +/- 31 nM at pHe 7.0 and 7.4, respectively. These studies demonstrate a direct, pH-sensitive correlation between [Ca2+]e and [Ca2+]m; [Ca2+]m changed over a range that may regulate alpha-KGDH flux in intact kidney mitochondria.(ABSTRACT TRUNCATED AT 250 WORDS)

Kinetics of Hemoglobin S Polymerization and Gelation Under Shear: I. Shape of the Viscosity Progress Curve and Dependence of Delay Time and Reaction Rate on Shear Rate and Temperature

Abstract Polymerization and gelation of deoxyhemoglobin S makes red blood cells (RBCs) rigid and is the immediate basis of pathogenesis in sickle cell disease. Hence, characterization of hemoglobin S viscosity and its time- dependent development as RBCs pass through the microvasculature is important in understanding pathogenesis. Because RBCs and the intraerythrocytic milieu in vivo are subject to shear, the shear dependence of polymerization kinetics is also important. In steady- state cone-plate viscometry we find: (1) gelation under shear progresses exponentially with time; (2) shear markedly increases exponential rate and (3) shortens delay time independent of when in the delay time it is applied; (4) shear greatly decreases the temperature dependence of the exponential rate and delay time; (5) simultaneous with its acceleratory effect on polymerization, shear breaks down gel structure. We conclude that shear acts to accelerate gelation by breaking fibers and creating new growing ends, a process that occurs in addition to the homogeneous and heterogeneous nucleation of new fibers that occurs in the absence of shear. Fibers that break are part of a gel network rather than in free solution. The shear dependence of gelation rates means that the critical clinical issue, whether the delay time is long enough and gelation slow enough to permit deoxygenated cells to pass through the microvasculature before they rigidify, depends on in vivo shear rates as well as on degree of unsaturation and hemoglobin concentration.

Kinetics of hemoglobin S polymerization and gelation under shear: I. Shape of the viscosity progress curve and dependence of delay time and reaction rate on shear rate and temperature

Polymerization and gelation of deoxyhemoglobin S makes red blood cells (RBCs) rigid and is the immediate basis of pathogenesis in sickle cell disease. Hence, characterization of hemoglobin S viscosity and its time-dependent development as RBCs pass through the microvasculature is important in understanding pathogenesis. Because RBCs and the intraerythrocytic milieu in vivo are subject to shear, the shear dependence of polymerization kinetics is also important. In steady-state cone-plate viscometry we find: (1) gelation under shear progresses exponentially with time; (2) shear markedly increases exponential rate and (3) shortens delay time independent of when in the delay time it is applied; (4) shear greatly decreases the temperature dependence of the exponential rate and delay time; (5) simultaneous with its acceleratory effect on polymerization, shear breaks down gel structure. We conclude that shear acts to accelerate gelation by breaking fibers and creating new growing ends, a process that occurs in addition to the homogeneous and heterogeneous nucleation of new fibers that occurs in the absence of shear. Fibers that break are part of a gel network rather than in free solution. The shear dependence of gelation rates means that the critical clinical issue, whether the delay time is long enough and gelation slow enough to permit deoxygenated cells to pass through the microvasculature before they rigidify, depends on in vivo shear rates as well as on degree of unsaturation and hemoglobin concentration.

Evidence for an effect of phospholamban on the regulatory role of ATP in calcium uptake by the calcium pump of the cardiac sarcoplasmic reticulum.

The purpose of this study was to investigate the functional relationship between phospholamban and the nucleotide site of the calcium pump protein of the cardiac sarcoplasmic reticulum. We used control and trypsin-treated cardiac microsomes in which cleavage of the inhibitory cytoplasmic domain of phospholamban is associated with an activation of the calcium pump similar to that produced by protein kinase A catalyzed phospholamban phosphorylation. Phenylglyoxal was shown to inactivate the calcium pump in a pseudo-first-order reaction by binding to a single Arg at the nucleotide binding site. No differences upon trypsin treatment of microsomes were observed in the kinetics of phenylglyoxal inactivation or the ability of millimolar ATP to protect against inactivation. In subsequent kinetic studies, Ca-uptake rates measured at saturating Ca2+ and 5 microM-1 mM MgATP2- were increased 15-32% by trypsin treatment in each of three different microsome preparations. Double-reciprocal plots of the data showed marked downward curvature indicating an acceleratory effect associated with ligand binding to a lower affinity site. At 0.32 microM Ca2+, Ca-uptake rates were lower than at 11 microM Ca2+ but were stimulated to a greater extent by trypsin treatment; control microsomes showed reduced evidence of apparent negative cooperativity. At 0-2 microM MgATP2- and saturating Ca2+, there was a 50% increase in Vmax(app) when the Hill coefficient (N) was 1. At 0-10 microM MgATP2-, second-site binding was evident. At both 0-10 microM and 5 microM-1 mM MgATP2-, trypsin-treated microsomes showed greater activation of Ca uptake attributable to second-site binding than did control microsomes.(ABSTRACT TRUNCATED AT 250 WORDS)

The acceleratory effect of thrombin on fibrin clot assembly

Inhibition of thrombin proteolysis of fibrinogen with D-phenylalanyl-L-propyl-L-arginine chloromethyl ketone (PPACK) results in irreversible inactivation of the thrombin catalytic site, but the PPACK-inhibited thrombin, through its exosite, retains its ability to bind to fibrinogen or fibrin. Hirudin inactivates thrombin at the catalytic site and also inhibits thrombin exosite binding to fibrin or fibrinogen. PPACK or hirudin was added to a clotting mixture of fibrinogen and active thrombin (enzyme:substrate ratio, 1:400 and 1:800) prior to the onset of gelation. Subsequent fibrin assembly was evaluated by turbidity measurements at 350 nm and by determining the fibrin and fibrinogen content of the clots that ultimately formed. Polymerization rates and the fibrin/fibrinogen content of the clots that formed were greater in the PPACK-inhibited system than in the hirudin-inhibited system. Lowering the ionic strength from 0.14 to 0.09 amplified these differences. The results suggest that in addition to its well-recognized role in the proteolytic conversion of fibrinogen to fibrin, thrombin functions as a cofactor in the fibrin assembly process.

Effect of S-adenosylmethionine on methylation of inorganic arsenic.

We studied the role of S-adenosylmethionine (SAM) as a methyl group donor in the methylation of inorganic arsenic in mammalians. The SAM and S-adenosylhomocysteine (SAH) levels in the livers of untreated hamsters were 74.3 +/- 8.2 and 40.0 +/- 6.4 nmol/g, respectively. The SAM level was 63.9 +/- 6.5 nmol/g following oral administration of 1.5 mg/kg of arsenic trioxide, which was 14% lower than the control level (t-test, p less than 0.05). This fall of the SAM level in the liver presumably derived from the SAM having acted as a methyl group donor. Oral administration of 1.5 mg/kg of arsenic trioxide once only to hamsters pretreated intraperitoneally with 2.0 mg/kg of SAM once only gave the following arsenic levels in the liver and urine. The dimethylated arsenic (DMA) levels in the livers of hamsters treated with SAM plus arsenic trioxide were significantly high, that is, 2 times as high as the control value at 6 hours, and 1.5 times as high as the control value at 24 hours after the administration of arsenic trioxide. The urinary DMA excretion rate was significantly higher, that is, higher by 36%, than the control value. The urinary DMA excretion rate following pretreatment with SAM was not dose-dependent. Pretreatment with methionine failed to exert any significant acceleratory effect on the methylation of arsenic trioxide. The decreasing pattern of the SAM level in the liver following administration of arsenic trioxide and the DMA behavior in the liver and urine following administration of SAM and arsenic trioxide revealed that SAM accelerated the methylation of inorganic arsenic. In other words, it appeared that SAM could be a very potent methyl group donor to inorganic arsenic.

Effect of exogenous collagen I on tissue repair in the rabbit ear and regeneration of the rat liver.

Collagen type I from rat tail was tested for its effect on wound healing of 6 male rabbits and on the regeneration of liver after partial hepatectomy in 15 male rats. It had a negligible effect on the rate of wound healing and a statistically significant acceleratory effect on regeneration of the rat liver.

Reactivity of the ternary fuse head system lead 2,4-dinitrophenolate-lead dioxide-aluminium

The reactivity of the ternary system lead 2,4-dinitrophenolate-lead dioxide-aluminium has been studied in comparison with the binary system lead 2,4-dinitrophenolate-lead dioxide using differential scanning calorimetry. It was observed that the heat evolved per unit mass of LDNP increased with increasing lead dioxide content for both the binary and the ternary systems. Aluminium imparts an acceleratory effect on the reaction between lead 2,4-dinitrophenolate and lead dioxide without altering the decomposition pattern. Fourier transform IR spectra of undecomposed material were compared with those of the residue and the results were correlated with the thermal analysis data.

Inactivation of Human Antithrombin by Neutrophil Elastase: Kinetics of the heparin-dependent reaction

Human neutrophil elastase catalyzes the inactivation of antithrombin by a specific and limited proteinolytic cleavage. This inactivation reaction is greatly accelerated by an active anticoagulant heparin subfraction with high binding affinity for antithrombin. A potentially complex reaction mechanism is suggested by the binding of both neutrophil elastase and antithrombin to heparin. The in vitro kinetic behavior of this system was examined under two different conditions: 1) at a constant antithrombin concentration in which the active anticoagulant heparin was varied from catalytic to saturating levels; and 2) at a fixed, saturating heparin concentration and variable antithrombin levels. Under conditions of excess heparin, the inactivation could be continuously monitored by a decrease in the ultraviolet fluorescence emission of the inhibitor. A Km of approximately 1 microM for the heparin-antithrombin complex and a turnover number of approximately 200/min was estimated from these analyses. Maximum acceleratory effects of heparin on the inactivation of antithrombin occur at heparin concentrations significantly lower than those required to saturate antithrombin. The divergence in acceleratory effect and antithrombin binding contrasts with the anticoagulant functioning of heparin in promoting the formation of covalent antithrombin-enzyme complexes and is likely to derive from the fact that neutrophil elastase is not consumed in the inactivation reaction. A size dependence was observed for the heparin effect since an anticoagulantly active octasaccharide fragment of heparin, with avid antithrombin binding activity, was without effect on the inactivation of antithrombin by neutrophil elastase. Despite the completely nonfunctional nature of elastase-cleaved antithrombin and the altered physical properties of the inhibitor as indicated by fluorescence and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the inactivated inhibitor exhibited a circulating half-life in rabbits that was indistinguishable from native antithrombin. These results point to an unexpected and apparently contradictory function for heparin which may relate to the properties of the vascular endothelium in pathological situations.

The function of the cardiac branch of the vagus and the location of its preganglionic neurons in the rainbow trout Salmo gairdneri.

The function of cholinergic vagal innervation and the locality of its preganglionic neurons were investigated using in situ preparations of the rainbow trout heart.The cardiac-visceral branches of the vagus were identified by vagal stimulation. The stimulation induced intense bradycardia with frequencies between 10 and 100Hz, while tachycardia was never produced even after atropinization, indicating that only the cholinergic vagus nerves were stimulated in the study. Subsequent beta-adrenoceptor blockade by propranolol intensified the stimulation-induced cardiac inhibition. It is suggested that the serum catecholamine levels in the preparations were kept high by secretion from chromaffin tissues and they produced a chronotropic acceleratory effect to the heart during the experiment.A group of preganglionic neurons of the cardiac-visceral trunk of the vagus were identified in the vagal motor nucleus of the medulla by retrograde labeling with HRP. They formed a longitudinal column within the nucleus at the level around the obex.

Effects of gas-phase mass transport in the pyrotechnic system red lead-silicon-potassium perchlorate

The acceleratory effect of potassium perchlorate on the reactivity of the red lead-silicon system has been studied by employing DTA and DSC. Supporting investigations on pure potassium perchlorate and the binary system red lead-potassium perchlorate suggest that the complex decomposition kinetics of potassium perchlorate drastically influences the oxidation of silicon. Further, the ternary system also undergoes a transition from exothermic smooth decomposition to ignition at a certain critical mass, as noted in the red lead-silicon and iron(III) oxide system. The criticality should be a result of the rise in temperature expressed as a perturbation of the steady-state energy conservation conditions, as postulated by Gray.

Acceleration of reproductive development in female Djungarian hamsters by adult males

Housing young female Djungarian hamsters (Phodopus campbelli) with an adult male accelerates uterine and ovarian development and there is a strong relationship between uterine weight and ovarian measures (e.g., follicular size). Uterine weights of females housed with an adult male for 10 days following weaning are comparable to values from females housed alone for 25 days. Removal of endogenous androgens by castration eliminated the capacity of adult males to accelerate reproductive development in young females and treatment of castrated males with exogenous androgens maintained the production of the acceleratory chemosignal. When adult male urine and ventral gland sebum were examined as possible sources for the acceleratory chemosignal, only male urine had an acceleratory effect on reproductive development. Thus, female Djungarian hamsters respond with accelerated reproductive development to androgen-dependent chemosignals in the urine of adult males. These mechanisms are similar to those found in several other rodents but contrast with the lack of such effects in the golden hamster (Mesocricetus auratus).

Acceleration and delay of sexual maturation in female house mice (Mus domesticus) by urinary chemosignals: mixing urine sources in unequal proportions.

Urine from male mice, from estrous female mice, and from pregnant or lactating female mice accelerate first vaginal estrus in females, whereas urine from grouped female mice delays first estrus. Nine experiments were used to test the effects of treatment of young female mice with urinary chemosignals that influence the onset of first estrus using unequal proportions of urine from the different sources. At ratios of 10-20 parts acceleratory chemosignal to 1 part delay chemosignal the acceleratory effect overrides the delay chemosignal, and the mice attain first estrus at earlier ages than controls. Ratios of about 4 to 1 up to 7 to 1 result in mean ages for puberty that are not accelerated or delayed relative to controls. Over a modest range of actual dose amounts of urine, the ratio effects are the same regardless of the actual quantities of urine employed in treating test females.

Intermittent stimulation and acceleration of puberty by urinary chemosignals in female mice (Mus musculus domesticus).

A sequence of 17 experiments was used to test the effects of intermittent stimulation with urinary chemosignals on the age of puberty in young female mice. The three chemosignals tested all accelerate the age of sexual maturation: urine from adult males, urine from females in estrus, and urine from females that are pregnant or lactating. The basic technique involved presenting the prepubertal females with 'Nestlets' on which the urine was placed. The 'Nestlets' were placed in the cages of the test females for a 15-min period, removed for a variable period, and then replaced in the cage for 15 min. In this manner it was possible to vary the number of exposures, the total length of exposure, and the total time period over which the exposures occurred. Control procedures, involving exposures of young females to cotton squares with water rather than urine placed upon them, resulted in no alterations in puberty relative to untreated females. For mice exposed to the urine-treated cotton squares, acceleration of puberty occurred with less total stimulus-exposure time when the stimulus was presented in short exposures over a number of hours than in previous investigations when the exposure to the urinary chemosignal occurred in a single block of time of one or two hours. For each of the three acceleratory chemosignals, there was a diminution of acceleratory effect when the ratio of total stimulus-exposure time to total exposure time grew smaller. This diminution was more pronounced for urine from pregnant or lactating females than for urine from males or from females in estrus.(ABSTRACT TRUNCATED AT 250 WORDS)

Contributions of superoxide, hydrogen peroxide, and transition metal ions to auto-oxidation of the favism-inducing pyrimidine aglycone, divicine, and its reactions with haemoglobin

The influence of O 2 −, H 2O 2 and metal ions on the auto-oxidation of divicine, a pyrimidine aglycone, was studied. In air at pH 7.4, the hydroquinonic form oxidized within a few minutes. Superoxide dismutase (SOD) markedly decreased the initial rate, giving a lag phase followed by rapid oxidation. Although catalase or diethylenetriamine-penta-acetic acid (DTPA) alone had little effect, each in the presence of SOD further slowed the initial rate and increased the lag. H 2O 2 decreased the lag time, as did Cu 2+, FE 2+ or haemoglobin. GSH substantially increased the lag phase, but it eventually reacted with the divicine to form a 305 nm-absorbing adduct. These results indicate that an O 2 −-dependent mechanism of divicine auto-oxidation normally predominates. Auto-oxidation can also occur by a mechanism involving H 2O 2 and transition metal ions or haemoglobin, and if both these reactions are prevented by SOD and DTPA or catalase, a third mechanism, requiring build-up of an autocatalytic intermediate, becomes operative. Oxyhaemoglobin did not react directly with divicine, but reacted with the H 2O 2 produced by divicine auto-oxidation to give mainly an oxidized derivative presumed to be ferrylhaemoglobin. Divicine was shown to reduce ferylhaemoglobin to methaemoglobin, and this reaction was probably responsible for the acceleratory effect of haemoglobin on divicine oxidation. These results indicate that O 2 rather than oxyhaemoglobin is likely to initiate divicine oxidation in the erythrocyte. Haemolytic crises, which are thought to result from this oxidation, occur only sporadically in glucose-6-phosphate dehydrogenase deficient individuals following ingestion of fava beans. A characteristic of the crises is acute depletion of erythrocyte GSH, and the vulnerability of these cells could relate to the ability of GSH, in combination with SOD, to protect against the autocatalytic mechanism of divicine auto-oxidation. Our demonstration of a variety of auto-oxidation pathways also suggests possible areas of individual variation.

The kinetics of inhibition of thrombin by antithrombin in the presence of components of the hemostatic system

AbstractThe inhibition of human thrombin by antithrombin has been measured in pure systems in the presence of other components of the hemostatic system that might affect the kinetics of the reaction. These included fibrinogen, calcium ions, phospholipid, prothrombin, platelets (both adenosine diphosphate [ADP]-stimulated and -unstimulated), and platelet extracts. Inhibition rates were measured in each case by a discontinuous amidolytic assay over a range of antithrombin concentrations, from 0 to 4.5 mumol/L. Under all conditions, rates of inhibition were proportional to antithrombin concentration. Calcium ions at 5 mmol/L caused a small (20%) reduction in rate, but phospholipid and prothrombin had no additional effect. In contrast, both fibrinogen and platelets significantly changed the rate of inhibition. In the presence of calcium, fibrinogen at concentrations from 0 to 12 mumol/L reduced the rate of inhibition in a competitive manner, giving an apparent Kd for fibrinogen of 6.0 mumol/L. As the plasma fibrinogen level is about 8 mumol/L, one may therefore predict that variations in fibrinogen level will have a significant effect on the rate of thrombin inhibition in plasma. More unexpected was the observation that platelets increase the rate of inhibition: unstimulated platelets increased the rate constant by 40%, and ADP- stimulated platelets increased it by 55%. However, this acceleratory effect could not be mimicked with either a KCI extract or a Triton extract of platelets, and its cause remains unknown. In sum, it has been shown that the rate of inhibition of thrombin can be modulated in at least three ways-antithrombin concentration, fibrinogen concentration, and platelets; each of which can vary independently in vivo. It is well known that defects of the first lead to an increased risk of thrombosis, and it is proposed that this may be substantially caused by changes in the kinetics of inhibition such as those described. Additionally, it is suggested that changes in inhibition rate caused by other components may also be significant, for the same reason, in modulating the clotting system in vivo.

The kinetics of inhibition of thrombin by antithrombin in the presence of components of the hemostatic system

The inhibition of human thrombin by antithrombin has been measured in pure systems in the presence of other components of the hemostatic system that might affect the kinetics of the reaction. These included fibrinogen, calcium ions, phospholipid, prothrombin, platelets (both adenosine diphosphate [ADP]-stimulated and -unstimulated), and platelet extracts. Inhibition rates were measured in each case by a discontinuous amidolytic assay over a range of antithrombin concentrations, from 0 to 4.5 mumol/L. Under all conditions, rates of inhibition were proportional to antithrombin concentration. Calcium ions at 5 mmol/L caused a small (20%) reduction in rate, but phospholipid and prothrombin had no additional effect. In contrast, both fibrinogen and platelets significantly changed the rate of inhibition. In the presence of calcium, fibrinogen at concentrations from 0 to 12 mumol/L reduced the rate of inhibition in a competitive manner, giving an apparent Kd for fibrinogen of 6.0 mumol/L. As the plasma fibrinogen level is about 8 mumol/L, one may therefore predict that variations in fibrinogen level will have a significant effect on the rate of thrombin inhibition in plasma. More unexpected was the observation that platelets increase the rate of inhibition: unstimulated platelets increased the rate constant by 40%, and ADP- stimulated platelets increased it by 55%. However, this acceleratory effect could not be mimicked with either a KCI extract or a Triton extract of platelets, and its cause remains unknown. In sum, it has been shown that the rate of inhibition of thrombin can be modulated in at least three ways-antithrombin concentration, fibrinogen concentration, and platelets; each of which can vary independently in vivo. It is well known that defects of the first lead to an increased risk of thrombosis, and it is proposed that this may be substantially caused by changes in the kinetics of inhibition such as those described. Additionally, it is suggested that changes in inhibition rate caused by other components may also be significant, for the same reason, in modulating the clotting system in vivo.

The influence of the solvent on organic reactivity. Part 5. Kinetics of the reaction of diazodiphenylmethane with benzoic acid in branched-chain alkanols and in electronegatively substituted alcohols

Rate coefficients at 30.0 °C are presented for the reaction of diazodiphenylmethane and benzoic acid in five branched-chain alkanols and in nine electronegatively substituted alcohols. As in earlier work, correlation analysis of log k values involves multiple regression on the σ* value of the group R1 in the alcohol R1OH, the Kirkwood function of dielectric constant f(Iµ)=(Iµ– 1)/(2Iµ+ 1), and nγH, the number of hydrogen atoms in the γ-position of the alcohol. The results for branched-chain alcohols provide further examples of the acceleratory effect of γ-hydrogen atoms. A correlation equation based on 27 alkanols and phenyl-substituted alcohols, for which σ* lies between –0.325 and +0.215, can be applied with reasonable success to seven electronegatively substituted alcohols, for which σ* lies in the range 0.07–0.92. 2-Methoxy- and 2-phenoxy-ethanol show marked deviations. Correlation equations properly incorporating the data for the electronegatively substituted alcohols are finally presented.

Inhibition of the antimetamorphic action of prolactin in larval Ambystoma tigrinum by lysine vasopressin, arginine vasotocin, and aldosterone.

Abstract In an earlier study it was reported that oxytocin was able to block the antimetamorphic action of prolactin (PRL) in larval tiger salamanders, Ambystoma tigrinum ( Platt and LiCause, 1980 ). In this study, we have examined the effects of lysine vasopressin (LVP), arginine vasotocin (AVT), and aldosterone on induced metamorphosis in larval A. tigrinum and on the inhibition of this process by PRL. Both LVP and AVT were found to interfere with the inhibition of gill resorption, tail fin regression, and body weight loss by PRL. An anti-PRL effect of aldosterone was observed but appeared to be limited to the gill. AVT alone had a significant acceleratory effect on body weight loss during metamorphosis. A “water balance” response was observed in only one case. Twenty-four hours after treatment with LVP and PRL, this group of animals did show a significant increase in body weight. These results are discussed with regard to the problem posed by neurohypophysial hormone contamination of PRL preparations and in context with our hypothesis that the antimetamorphic action of PRL is at least partially osmoregulatory in nature.