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Relationships among mechanisms in psychosocial treatments for chronic pain: mechanism to mechanism lagged effects and relationships with outcomes.

Results suggest that psychosocial treatments for chronic pain work via several mechanisms, and that they often do so to similar degrees and in similar ways. Extant research, however, has focused on individual and/or independent effects of mechanisms on outcomes. Whether successful outcomes are also partly because of sequential and meaningful relationships among and between mechanisms-mechanism-to-mechanism effects-has not been examined. Secondary analyses were conducted of an RCT that compared cognitive therapy, mindfulness-based stress reduction, and behavior therapy to treatment as usual in a sample (N = 521) of people with chronic low back pain. Results of hierarchical linear modeling revealed that (1) Treatment Condition × Mechanism interactions predicting changes in other mechanisms were nonsignificant; (2) lagged prior session mechanism changes predicted next session changes in another mechanism; (3) lagged relationships between pain catastrophizing and pain self-efficacy were reciprocal, whereas links between lagged pain catastrophizing and mindfulness changes and lagged pain catastrophizing changes and behavioral activation changes were unidirectional; and (4) individual differences in the strengths of mechanism-to-mechanism relationships predicted pre- to post-treatment changes in outcomes. Results reveal heretofore hidden therapeutic processes that cognitive therapy, mindfulness-based stress reduction, and behavior therapy may share. Namely, that mechanism-to-mechanism lagged effects do indeed emerge beyond mechanism-to-outcome effects. Findings show not only that mechanisms may change in definable sequences relative to each other but that individual differences in the strengths of mechanism-to-mechanism relationships may themselves be predictive of outcomes.

Humans

Cytolytic mechanisms of activated macrophages. Tumor necrosis factor and L-arginine-dependent mechanisms act synergistically as the major cytolytic mechanisms of activated macrophages.

We examined the cytolytic mechanisms of activated macrophages by using proteose peptone- or thioglycollate broth-induced mouse peritoneal macrophages or mouse macrophage hybridomas as effector cells, L.P3 cells, a clone of L929 cells, and P815 cells as target cells, and IFN-gamma and LPS as activators. It was determined that TNF is the main cytolytic molecule against L.P3 cells from the following results: 1) activated macrophages can produce TNF; 2) TNF shows cytotoxic activity against L.P3 cells; 3) the addition of anti-TNF antibody inhibited most of the cytolytic activity of activated macrophages against L.P3 cells. On the other hand, it was concluded that the main cytolytic mechanism against P815 cells is the production of NO2-/NO3- from L-arginine, from the following results: 1) activated macrophages can produce NO2-; 2) NaNO2 shows high cytotoxic activity against P815 cells; 3) the depletion of L-arginine from the medium inhibited most of the cytolytic activity of activated macrophages against P815 cells and NO2- production by activated macrophages. In this study, however, cytostatic effects of L-arginine-dependent effector mechanism were not studied. Thus, these results show that activated macrophages can express at least two cytolytic mechanisms independently, namely, the one that appears to be mediated by the L-arginine-dependent effector mechanism and the second that appears to be mediated directly by TNF. Furthermore, it was demonstrated that TNF and L-arginine-dependent NO2- production act synergistically as killing mechanisms of activated macrophages. These mechanisms can explain the cytolytic activity of activated macrophages against a variety of target cells.

Animals

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XIV. Mutational and non-mutational mechanisms as subsets of a more general mechanism. Part C. A defined cancer mutation.

The results of applying a mechanism of ethionine-induced embryonic gene derepressions to explain similar features found in hereditary tyrosinemia have been extended to a well defined cancer mutation. In all three cases, the described mechanism is compatible with the explanation for the etiology of embryonic like phenotypic expressions in cells and potentially for the carcinogenic process. The essence of the formulated process for a human bladder carcinoma mutation in the ras gene for a protein phosphokinase states that a specific proto-oncogene is mutated to an oncogene by various known processes. The protein phosphokinase that has an altered specificity resulting in anomalous phosphorylation of important regulating proteins by a non-mutation mechanism, i.e. by ethionine, would produce the same effect in a hypomethylated state of deoxyribonucleic acid causing an embryonic type protein phosphokinase gene to become activated. These embryonic oncogenes are supersensitive to methylation control mechanisms--thus the link between non-mutation and mutation type mechanisms.

Carcinogens

Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XIII. Mutational and non-mutational mechanisms as subsets of a more general mechanism. Part B--hereditary tyrosinemia.

In this mini-series three different examples of the etiology for the induction of alpha-fetoprotein and hepatocarcinogenesis have been chosen. The first paper describes the mechanism using the non-mutagen, ethionine. In this paper the mechanism is derived by virtue of a mutation that causes a deficiency in fumarylacetoacetate fumarylhydrolase activity with subsequent accumulation of fumarylacetoacetate that is an inhibitor of ATP: L-methionine S-adenosyltransferase. It is hypothesized that the chronically low levels of active methyl groups disallows base-pairing by the adenine moiety of S-adenosyl-L-methionine and the repressed conformation of the alpha-fetoprotein gene is altered and subsequent transcription takes place. The same or similar process occurs with the subset of genes (embryonically repressed) that as a special group of active genes gives embryonic features to a quasi-differentiated stem cell causing "dysdifferentiation" to a neoplastic state.

Amino Acid Metabolism, Inborn Errors

Contributions of glomerular and tubular mechanisms to antidiuresis in conscious domestic fowl.

Recently developed radioimmunoassay (RIA techniques were employed in a quantitative investigation of the renal actions of the avian antidiuretic hormone arginine vasotocin (AVT) in the conscious domestic fowl. Constant intravenous infusion of AVT at doses of 0.125-1.00 ng . kg-1 . min-1 was used to produce plasma AVT (PAVT) concentrations (verified by RIA) over the entire range of physiological PAVT levels in the domestic fowl. Comparison of the dose-response relationships between PAVT and glomerular and tubular mechanisms of antidiuresis revealed that tubular mechanisms are of primary importance and glomerular mechanisms of secondary importance in the conservation of water by the avian kidney. The greatest proportion of the total AVT-induced reduction in renal water excretion occurred at low physiological PAVT levels (less than 5 microU/ml), prior to any significant reduction in glomerular filtration rate (GFR), and appeared to be the exclusive result of tubular mechanisms of antidiuresis. At high PAVT levels (5-16 microU/ml), glomerular and tubular mechanisms overlapped, and their effects on water conservation could not be separated. Although GFR was reduced by nearly 30% at the highest dose of AVT, only minor additional amounts of water were conserved by the combined actions of glomerular and tubular mechanisms. The glomerular mechanisms appear to have only a minor secondary effect on water-conserving ability of the avian kidney.

Animals

Light-adaptation properties of the ultraviolet-sensitive cone mechanism in comparison to the other receptor mechanisms of goldfish.

The light-adaptation properties of goldfish photoreceptor mechanisms were examined using Stiles' two-color threshold technique. Threshold vs. background intensity (TVI) curves were determined for isolated cone and rod mechanisms using the heart-rate conditioning technique. The principal aim of this study was to compare the light-adaptation properties of the ultraviolet (UV)-sensitive cone mechanism to the other receptor mechanisms of goldfish. This examination revealed several striking functional differences: (1) The UV-sensitive cone mechanism threshold vs. background intensity (TVI) exhibited a slope of 0.65 (compared to the approximate 1.0 for the other cone mechanisms on a log/log plot) and thus was not in accordance with Weber's law. This may in part be related to the intrusion of the blue-sensitive mechanism at the upper radiance range. (2) The operation of the UV-sensitive cone mechanism was limited to intermediate intensities (i.e. not very dim or bright). (3) The UV-sensitive cone mechanism exhibited a Weber fraction or luminance contrast threshold of 0.316 that was approximately six times larger than the other cone mechanisms but comparable to the rod mechanism. This indicates that the UV-sensitive cone mechanism performs relatively poorly in terms of brightness contrast detection.

Adaptation, Ocular

Skeletal structural adaptations to mechanical usage (SATMU): 4. Mechanical influences on intact fibrous tissues.

This paper proposes that the growth in length of living fibrous tissue structures (tendon, ligament, fascia) responds primarily to circulating systemic rather than mechanical factors. However, growth of the thickness of those structures responds primarily to their mechanical tension loads in the special sense that, when the tissue's typical peak mechanical strains exceed a threshold value, its cells begin to add new collagen to increase its thickness, strength, and tension stiffness. When subsequent peak strains reduce to the threshold value, then further additions of collagen stop. That process defines mechanically controlled modeling of fibrous tissues. The collagen in these tissues can also develop mechanical microdamage (MDx) under repeated tension load-deload cycles. Special maintenance mechanisms normally repair that MDx to prevent accumulations that would threaten structural integrity. As a result, spontaneous complete ruptures of these structures can happen when MDx production exceeds its repair. These maintenance mechanisms also prevent gradual stretching under continuous tension loads, a process the author suggests calling creep compensation. When the creep compensation mechanism becomes incompetent, structures can stretch under continuous loads; when it becomes overactive, contractures can occur. The above meld of fact and inference provides the kernel of a general theory for the responses of the architecture and mechanical competence of intact fibrous tissues to mechanical usage.

Adaptation, Physiological

Effect of spontaneous and mechanical breathing on dynamic lung mechanics in hyaline membrane disease.

We measured then compared the dynamic lung mechanics of spontaneous breaths and mechanical breaths in 9 mechanically ventilated neonates with hyaline membrane disease. All were receiving intermittent mandatory ventilation. All breathed spontaneously between ventilator breaths. Tidal volume, transpulmonary pressure, dynamic lung compliance, airways resistance, and peak inspiratory and peak expiratory gas flows were determined for both the mechanical and the spontaneous breaths. The mechanical breaths consistently had larger tidal volumes, higher transpulmonary pressures, higher airway resistance, and lower lung compliance values (P less than 0.05). Peak inspiratory and expiratory gas flows were also higher (P less than 0.01) during mechanical breathing. The spontaneous breaths generated by patients and the mechanical breaths generated by mechanical ventilators are different. The lung mechanics measurements of these two different types of breathing should be collected, analyzed, and reported separately.

Humans

Interactions between non-symmetric mechanical vector forces in the body and the autonomic nervous system: basic requirements for any mechanical technique to engender long-term improvements in autonomic function as well as in the functional efficiency of the respiratory, cardiovascular, and brain systems.

There are known anatomical asymmetries in the respiratory, cardiovascular, and nervous system. The coupling mechanisms between each of these systems--lungs-heart, heart-brain, and lungs-brain--are also asymmetrical. There is a growing body of literature indicating that mechanical pressure asymmetrically applied to certain areas of the human body produces changes in the balance of autonomic parameters. These findings implicitly indicate that not only magnitude but also the direction and point of application of the force play a role in its influence upon the autonomic nervous system. Therefore, we suggest that asymmetrical vector forces resulting from the mechanical activity of the lungs, heart and blood moving throughout the circulatory system, will also produce a lateralization effect in autonomic balance. We postulate the existence of negative feedback loops between brain autonomic control and mechanical functions in the body as a fundamental part of the body's homeostatic mechanisms. It follows that any mechanical assist to the respiratory or cardiovascular system will be significantly reduced or even eliminated if these homeostatic mechanisms are not taken into account. Our hypothesis predicts that a long-term improvement in autonomic balance as well as in respiratory, cardiovascular, and brain function can be achieved if mechanical forces are applied to the body with the aim of reducing existing imbalances of mechanical force vectors. This technique implies continually controlling for precise timings resulting from physiological periodical forces as well as factors derived from anatomical and coupling asymmetries in the respiratory, cardiovascular, and nervous systems.

Autonomic Nervous System

Partitioning of respiratory mechanics in mechanically ventilated patients.

In ten mechanically ventilated patients, six with chronic obstructive pulmonary disease (COPD) and four with pulmonary edema, we have partitioned the total respiratory system mechanics into the lung (l) and chest wall (w) mechanics using the esophageal balloon technique together with the airway occlusion technique during constant-flow inflation (J. Appl. Physiol. 58: 1840-1848, 1985). Intrinsic positive end-expiratory pressure (PEEPi) was present in eight patients (range 1.1-9.8 cmH2O) and was due mainly to PEEPi,L (80%), with a minor contribution from PEEPi,w (20%), on the average. The increase in respiratory elastance and resistance was determined mainly by abnormalities in lung elastance and resistance. Chest wall elastance was slightly abnormal (7.3 +/- 2.2 cmH2O/l), and chest wall resistance contributed only 10%, on the average, to the total. The work performed by the ventilator to inflate the lung (WL) averaged 2.04 +/- 0.59 and 1.25 +/- 0.21 J/l in COPD and pulmonary edema patients, respectively, whereas Ww was approximately 0.4 J/l in both groups, i.e., close to normal values. We conclude that, in mechanically ventilated patients, abnormalities in total respiratory system mechanics essentially reflect alterations in lung mechanics. However, abnormalities in chest wall mechanics can be relevant in some COPD patients with a high degree of pulmonary hyperinflation.

Aged

A comparison of the mechanisms of alpha-adrenergic inhibition of thyrotropin-stimulated adenosine 3',5'-monophosphate in cat, rat, mouse, hamster, beef, and pig tissues with the stimulatory effect of epinephrine on beef thyroid iodination: evidence for multiple, species-specific adrenergic mechanisms.

Epinephrine was shown to inhibit TSH-stimulated cAMP formation in cat and pig thyroid slices and isolated rat and hamster thyroid lobes. In contrast, no such inhibitory action could be demonstrated in sheep or beef thyroid slices or mouse thyroid-trachea preparations. The inhibitory effect of epinephrine on TSH-stimulated cAMP formation in pig thyroid slices was blocked by 10 microM yohimbine, but not by 10 microM prazosin, suggestive of mediation through an alpha 2-catecholamine receptor mechanism. In cat thyroid slices, the inhibitory effect of epinephrine was blocked by both yohimbine and prazosin, suggestive of a mixed alpha-adrenoceptor mechanism. Meclofenamate and indomethacin attenuated the epinephrine response in cat, but not pig, thyroid slices, but other prostaglandin inhibitors were ineffective. Beef thyroid slices responded to epinephrine with an increase in iodide organification that is mediated through an alpha-adrenergic mechanism not blocked by propranolol. This stimulatory effect of epinephrine was abolished by both 10 microM prazosin and 10 microM yohimbine. In contrast to the inhibitory effect of the catecholamines on TSH-stimulated cAMP formation in cats, the stimulatory response of beef iodide organification to epinephrine was not modified by meclofenamate, indomethacin, or verapamil. These findings suggest that the receptor mechanisms mediating the inhibitory effect of catecholamines on cat thyroid and the stimulatory effect of catecholamines in beef thyroid slices may well be mediated by separate and as yet undefined receptor mechanisms. In contrast, the inhibitory effect of epinephrine on TSH-stimulated cAMP formation in pigs is most likely mediated through an alpha 2-adrenoceptor mechanism. These findings further document the multiplicity of catecholamine actions on thyroid function as well as the diversity observed among various species.

Adenosine Monophosphate

Comparison of standard weaning parameters and the mechanical work of breathing in mechanically ventilated patients.

Standard bedside criteria of respiratory mechanical capability and the mechanical work of spontaneous breathing were measured in 17 mechanically ventilated patients. Eleven patients were extubated within 24 hs of study and required only a brief period of mechanical ventilation (group 1). Group 2 consisted of six patients requiring more prolonged ventilator support. Group 1 patients met three of four bedside criteria; seven patients met all four. Five of six patients in group 2 also satisfied three of four standard criteria while ventilator-dependent, whereas only two patients satisfied all four when successfully weaning. As group 2 patients progressed from unsuccessful to successful weaning there was no consistent improvement in bedside criteria; however, measures of work did significantly improve. Hence, satisfaction of bedside mechanical weaning criteria is associated with weaning success in patients requiring brief mechanical ventilation. In patients requiring prolonged ventilation, work may be a better indicator of successful weaning.

Aged

Doxofylline and respiratory mechanics. Short-term effects in mechanically ventilated patients with airflow obstruction and respiratory failure.

To assess the short-term effects of a methylxanthine (doxofylline) on respiratory mechanics in mechanically ventilated patients with airway obstruction and respiratory failure, nine consecutive patients were examined within three days from the onset of mechanical ventilation. Flow, changes in pulmonary volume, and Paw were measured using a ventilator (Servo 900C). End-expiratory and end-inspiratory airway occlusion was performed to measure PEEPi, Cstrs, Rrsmax, and Rrsmin. Measurements were performed before and at 5, 15, and 30 minutes after an intravenous loading dose of doxofylline (5 to 6 mg/kg). We found that doxofylline determined, on the average, a marked decrease in respiratory resistance (Rrsmax and Rrsmin, -27.2 percent and -36.5 percent, respectively) without significant changes in Cstrs and Pmax. The PEEPi, reflecting pulmonary dynamic hyperinflation, was also significantly decreased by doxofylline (-41 percent, on the average). The Pmax was not reliable for evaluation of a single patient, since changes in the elastic pressure can offset changes in the resistive one. No patient experienced significant side effects due to doxofylline. We conclude that (1) the effects of therapy can be assessed noninvasively at bedside in critically ill patients; (2) doxofylline is a rapid and efficient bronchodilator in mechanically ventilated patients with ARF and airflow obstruction; and (3) the decrease in the respiratory resistance and PEEPi, associated with an improved mechanical efficiency of the respiratory muscles at a lower pulmonary volume, can provide better conditions for the patient-ventilator interaction and for weaning.

Bronchodilator Agents

Pulmonary mechanics in preterm neonates with respiratory failure treated with high-frequency oscillatory ventilation compared with conventional mechanical ventilation.

Pulmonary mechanics were measured in 43 preterm neonates (mean +/- SD values of birth weight 1.2 +/- 0.3 kg, gestational age 30 +/- 2 weeks) with respiratory failure who were concurrently randomly assigned to receive conventional mechanical ventilation (n = 22) or high-frequency ventilation (n = 21). The incidence of bronchopulmonary dysplasia was comparable in the two groups (high-frequency ventilation 57%, conventional ventilation 50%). Pulmonary functions were determined at 0.5, 1.0, 2.0, and 4.0 weeks postnatal ages. Data were collected while subjects were in a nonsedated state during spontaneous breathing. These sequential data show similar patterns of change in pulmonary mechanics during high-frequency ventilation and conventional mechanical ventilation irrespective of gestational age, birth weight stratification, or bronchopulmonary dysplasia. There was no significant difference in the pulmonary functions with either mode of ventilation during the acute phase (less than or equal to 4 weeks) of respiratory disease. When evaluated by the clinical diagnosis of bronchopulmonary dysplasia, the pulmonary data suggested a less severe dysfunction in the high-frequency oscillatory ventilation-treated bronchopulmonary dysplasia group compared with the conventional mechanical ventilation-treated group. These results indicate that high-frequency oscillatory ventilation in preterm neonates does not reduce the risk of acute lung injury; however, the magnitude of the pulmonary dysfunction in the first 2 weeks of life merits a reevaluation.

Bronchopulmonary Dysplasia

Increased vulnerability of the mildly traumatized rat brain to cerebral ischemia: the use of controlled secondary ischemia as a research tool to identify common or different mechanisms contributing to mechanical and ischemic brain injury.

Fasted Wistar rats were subjected to either a mild mechanical injury, 6 min of transient forebrain ischemia, or a mild mechanical injury followed 1 h later by 6 min of forebrain ischemia. EEG and evoked potentials were assessed intermittently and morphological analyses were performed after 7 days postinjury survival. In all groups complete qualitative recovery of electrical activity and general behavior was observed with 7-day survival. However, rats subjected to combined concussion and ischemia displayed EEG spike activity and a delayed return of EEG and evoked potentials during acute recovery not evident in other groups. No overt neuronal cell loss was seen in trauma alone and was minimal or absent in ischemia alone. However, extensive bilateral CA1 and subicular pyramidal cell loss was found in the septal and mid-dorsal hippocampi in the combined trauma and ischemia group. In contrast, no overt axonal injury was found in any group. We conclude that even mild mechanical injury can potentiate selective ischemic hippocampal neuronal necrosis in the absence of overt axonal injury. This potentiation also occurs in conjunction with more generalized electrophysiological disturbances such as EEG evidence of postischemic neuronal hyperactivity suggesting that mild concussion may also decrease the threshold for post-ischemic neuronal excitation. These results suggest the potential of this model for examining common or different injury mechanisms in mechanical and ischemic brain injury.

Animals

An energy 'sources' and 'fractions' approach to the mechanical energy expenditure problem--III. Mechanical energy expenditure reduction during one link motion.

Mechanical energy economy and transformation during one link motion are analyzed on the basis of the theory developed in the previous publications (parts I and II of this series, J. Biomechanics 19, 287-300). The 'compensation coefficient' characterizing mechanical energy economy is introduced. The attempts to estimate MEE using only energy curves and neglecting the powers of real sources of energy implicitly lead to replacement of real force and moment systems by the systems reduced to the centers of mass. But such an unintentional substitution of imaginary sources for real ones, specifically, the reduction of forces acting on the link to the equivalent system, changes estimates of mechanical energy expenditure (MEE). That is why the methods of calculating MEE economy based on the determination of so-called 'quasi-mechanical' work (the sum of the kinetic and potential energy increases per one cycle of motion) are not correct. There are two mechanisms to reduce the MEE using the antiphase fluctuations (corresponding to energy transformations) of the (a) rotational and translational fractions of the total energy (at the expense of the F-sources); (b) potential and kinetic energies (at the expense of the mg-source).

Biomechanical Phenomena

Mechanical restitution in isolated mammalian myocardium: species differences and underlying mechanisms.

Ventricular myocardium was obtained from guinea-pig, ferret and human hearts. In each case small strips were mounted isometrically in a tissue bath and superfused with a physiological saline at 37 degrees C. The preparations were stimulated at 1 Hz and ectopic stimuli of different preceding intervals were given. The relationship between the force produced by the ectopic contraction and the duration of the preceding interval was plotted to form mechanical restitution curves (MRC). In the guinea-pig the MRC is described by a rapid recovery phase with an exponential time constant of 220 +/- 22.7 ms (mean +/- S.E.M.) followed by a decay (28.5 +/- 8.4 s). In ferret and man the rising phase is described by two exponentials (192.5 +/- 43.2 ms and 4.4 +/- 1.5 s in the ferret; 259.7 +/- 45.2 ms and 3.0 +/- 1.0 s in man). The decay phase is slower in ferret (22 +/- 156 s, P less than 0.02) and man (177 +/- 70 s, P less than 0.002) than in guinea-pig. There was no significant difference between the time constants of the rapid recovery phase of mechanical restitution in each species. The time constant of the rapid recovery phase (tau 1) was abbreviated by ryanodine, ouabain and adrenaline in human myocardium and by ryanodine alone in guinea-pig. Verapamil increased tau 1 in both species. The decay time constant (tau 3) was prolonged by ouabain, verapamil and by increasing extracellular [Ca2+] in human myocardium and by ouabain and verapamil in guinea-pig. The recovery of the second inward current in human myocardium was not correlated to the recovery of mechanical function. It is suggested that tau 1 is dependent on the recycling of Ca2+ within the cell as well as the reactivation of the second inward current. The decay phase, tau 3, is dependent on the rate of Ca2+ efflux from the cell, possibly via a Na+/Ca2+ exchange mechanism. The mechanisms underlying the slow recovery time constant, tau 2, are unclear but it is important to calculate tau 2 for the proper evaluation of tau 1.

Animals

Mechanism of dioxygen formation catalyzed by vanadium bromoperoxidase from Macrocystis pyrifera and Fucus distichus: steady state kinetic analysis and comparison to the mechanism of V-BrPO from Ascophyllum nodosum.

Vanadium bromoperoxidase (V-BrPO) catalyzes the oxidation of bromide by hydrogen peroxide, which results in the bromation of appropriate organic substrates or the formation of dioxygen, in the absence of an organic substrate and under certain other conditions. The mechanism of the bromide-assisted disproportionation of hydrogen peroxide catalyzed by V-BrPO, which is the reaction that forms dioxygen, has been investigated for V-BrPO isolated from two new marine algal sources, Macrocystis pyrifera and Fucus distichus. The steady state kinetic studies have been performed under conditions of 0.02-40 mM H2O2, 1-500 mM Br- and pH 4.0-8.0. The rate data is consistent with a substrate-inhibited bi bi ping pong mechanism, in which the substrate bromide, is also an inhibitor by a noncompetitive-type mechanism. Bromide inhibits V-BrPO from M. pyrifera most strongly at pH 5.0-5.5 and V-BrPO from F. distichus most strongly at pH 5.5-6.0. The steady state mechanism of the Macrocystis and the Fucus enzymes are compared to the mechanism of the bromide-assisted disproportionation of hydrogen peroxide catalyzed by V-BrPO from Ascophyllum nodosum. In addition, the substrate hydrogen peroxide can also inhibit V-BrPO.

Catalysis