Histamine-forming Capacity Research Articles

Prevalence of Histamine-Forming Bacteria in Two Kinds of Salted Fish at Town Markets of Guangdong Province of South China

Histamine-forming bacteria (HFB) were isolated from the 70 salted fish samples bought from town markets of Guangdong Province of south China. In addition, the histamine-forming ability of HFB was analyzed. There were 31 strains of HFB isolated from 36 salted fish pickled overnight. They were identified as six bacteria species: Vibrio alginolyticus, Vibrio rumoiensis, Staphylococcus saprophyticus, Staphylococcus xylosus, Lactococcus lactis, and Morganella morganii. The rate of confirmation of V. alginolyticus was highest (23 of 31), exceeding 200 mg/kg histamine. In particular, M. morganii produced a histamine amount that exceeded 2,000 mg/kg, although it was only one isolate in this study. In addition, five bacteria species of HFB were isolated from 34 dried salted fish. Among them, S. saprophyticus was dominant in the dried salted fish but produced histamines below 200 mg/kg. However, Enterobacter aerogenes from dried salted fish formed a histamine amount exceeding 200 mg/kg. The study showed that the dominant strain of HFB was different in two kinds of salted fish. Both kinds of salted fish contained HFB whose histamine-forming capacity exceeded 200 mg/kg. As a result, the safety of salted fish should be of concern, especially salted fish pickled overnight.

Precooking as a Control for Histamine Formation during the Processing of Tuna: An Industrial Process Validation

An experiment to validate the precooking of tuna as a control for histamine formation was carried out at a commercial tuna factory in Fiji. Albacore tuna (Thunnus alalunga) were brought on board long-line catcher vessels alive, immediately chilled but never frozen, and delivered to an on-shore facility within 3 to 13 days. These fish were then allowed to spoil at 25 to 30°C for 21 to 25 h to induce high levels of histamine (>50 ppm), as a simulation of "worst-case" postharvest conditions, and subsequently frozen. These spoiled fish later were thawed normally and then precooked at a commercial tuna processing facility to a target maximum core temperature of 60°C. These tuna were then held at ambient temperatures of 19 to 37°C for up to 30 h, and samples were collected every 6 h for histamine analysis. After precooking, no further histamine formation was observed for 12 to 18 h, indicating that a conservative minimum core temperature of 60°C pauses subsequent histamine formation for 12 to 18 h. Using the maximum core temperature of 60°C provided a challenge study to validate a recommended minimum core temperature of 60°C, and 12 to 18 h was sufficient to convert precooked tuna into frozen loins or canned tuna. This industrial-scale process validation study provides support at a high confidence level for the preventive histamine control associated with precooking. This study was conducted with tuna deliberately allowed to spoil to induce high concentrations of histamine and histamine-forming capacity and to fail standard organoleptic evaluations, and the critical limits for precooking were validated. Thus, these limits can be used in a hazard analysis critical control point plan in which precooking is identified as a critical control point.

Histidine decarboxylase in experimental tumours.

Abstract Histidine decarboxylase activity has been demonstrated in some experimental tumours by direct enzyme assay. The kinetic properties of semi-purified preparations of the histamine-forming enzyme from Rous rat sarcoma and Walker rat mammary carcinoma were similar to those of the “specific” histidine decarboxylase of the foetal rat. Transplants from a malignant hamster melanoma had no “specific” histidine decarboxylase but high dopa decarboxylase activity. The lack of histidine decarboxylase in this tumour seems to indicate that a high histamine-forming capacity is not indispensable for tumour growth.

Ischemia mobilizes histamine but not pancreastatin from ECL cells of rat stomach: evidence for a cytosolic histamine compartment

Histamine in the rat stomach resides in enterochromaffin-like (ECL) cells and mast cells. The ECL cells are peptide-hormone-producing endocrine cells known to release histamine and chromogranin-A-derived peptides (such as pancreastatin) in response to gastrin. Ischemia (induced by clamping of the celiac artery or by gastric submucosal microinfusion of the vasoconstrictor endothelin) mobilizes large amounts of ECL-cell histamine in a burst-like manner. This report examines the ECL-cell response to ischemia and compares it with that induced by gastrin in rats. Arterial clamping (30 min) and gastric submucosal microinfusion (3 h) of endothelin, vasopressin, or adrenaline caused ischemia, manifested as a raised lactate/pyruvate ratio and mucosal damage. Whereas microinfusion of gastrin released both histamine and pancreastatin, ischemia mobilized histamine only. The mucosal concentrations of histamine and pancreastatin, the number and immunostaining intensity of the ECL cells, and the ultrastructure of the ECL cells were unchanged following ischemia. The long-term effects of ischemia and reperfusion (60-90 min) on gastric mucosa were examined in rats treated with the proton pump inhibitor omeprazole for 4 days. The activity of the ECL cells was suppressed (reflected in low histamine-forming capacity) but returned to normal within 1 week, illustrating the ability of the ECL cells to recover. We suggest that ischemia mobilizes cytosolic ECL-cell histamine without affecting the storage of histamine (and pancreastatin) in the secretory organelles and without causing lasting ECL-cell impairment.

Histamine forming capacity (HFC) and its modulation by H3 receptor ligands in a model of bronchial hyper-responsiveness

The histamine forming capacity (HFC) of acutely challenged airways from sensitised guinea pigs was investigated. After exposure to nebulised bovine serum albumin (BSA) or normal saline, animals were sacrificed, the pulmonary HFC determined and concurrent in vitro histamine log concentration response curves were constructed for parenchymal strips and tracheal muscle, the latter was field stimulated to record neurogenic responses. Exposure to BSA increased the HFC above controls for 24 hours (p < 0.001) and log concentration response curves for the parenchymal strips were shifted slightly to the left with an increased maximum response. This change appeared 3 hours after exposure and remained elevated at 24 hours. Similar changes did not occur with the trachea. Pre-treatment with thioperamide augmented (p < 0.02) HFC and this increase was inhibited by alpha-methylhistamine (p < 0.05). A possible relationship may exist between increased responsiveness of lower airways to exogenous histamine and a raised endogenous formation, regulated by the H3 receptor.

Platelet Histamine: Characterization of the Proaggregatory Effect of Histamine in Human Platelets.

Minute amounts of histamine and a discrete histamine-forming capacity was present in quiescent human platelets. Aggregation of human platelets induced by thrombin was concomitant with the release of histamine. In platelets obtained from actively sensitized guinea pig, the exposure to the specific antigen results in aggregation and histamine release which was not reproduced by the exposure to an unspecific protein or in platelets taken from unsensitized animals. The present results lend further support to positioning platelets among the inflammatory cells.

Enhanced carnosine (β-alanyl-L-histidine) breakdown and histamine metabolism following treatment with compound [formula omitted

We have previously suggested that carnosine may serve as a reservoir for histidine to be used as a source of histamine in the trauma response of rats. In this study we report the effect of stimulation of histamine-forming capacity by compound 48 80 on muscle carnosinase (C'ASE) and histidine decarboxylase (HDC) activities as well as on muscle carnosine and histamine concentrations. Male rats (180 g) were injected i.p. with 5 mg/kg bw of compound 48 80 and C'ASE and HDC activities as well as carnosine, histidine and histamine concentrations were monitored over a 72 h period post-injection. This treatment resulted in an 120% increase in muscle HDC activity and an 110% increase in muscle histamine concentration at 15 min post-injection, followed by an 80% increase in muscle C'ASE activity at 1 h and a 100% reduction in muscle carnosine concentration at 24 h post-injection when compared to control animals injected with 0.9% saline. Histidine concentration was not affected by treatment. The time frame of response, a rapid increase in muscle HDC activity and in muscle histamine concentration followed by an increase in muscle C'ASE activity and a later decrease in muscle carnosine concentration, suggests that carnosine is hydrolysed to liberate histidine and that carnosine, as a reservoir for histidine, is mobilized to maintain a constant muscle concentration of histidine for histamine synthesis.

Influence of locally altered in vivo shear stress on aortic histamine-forming capacity and aortic albumin uptake.

Effects of locally elevated shear stresses on thoracic histamine formation and transmural albumin uptake have been examined under in vivo conditions in anesthetized male, mongrel dogs. Results indicate that if endothelium remains intact, significant linear relationships exist between the shear intensity and aortic histamine-forming capacity and aortic content of fluorescein-labeled bovine serum albumin following 20 h of circulation time. These data suggest that in vivo the aortic (and endothelial) histidine decarboxylase system is sensitive to local alterations in applied shear stress, and that de novo aortic histamine synthesis in involved in mediating shear-induced increases in aortic transmural permeability.

Relationship between low intensity shear stress, aortic histamine formation, and aortic albumin uptake

The relationship between aortic histamine forming capacity (HFC) and aortic albumin uptake, as measured through fluorometric determination of the intraaortic content of bovine serum albumin conjugated to fluorescein isothiocyanate (FITCBSA) under steady-state conditions has been examined in relationship to the applied mean shear stress intensity created by pulsatile perfusion of rabbit aortas with platelet-free blood for a 1-hr period. HFC and FITCBSA determinations were made on aortic segments exposed to entrance and exit flow conditions as well as on those segments in which flow was stable; mean shear stresses in the latter ranged from 7 to 21 dynes/cm 2. Regression analyses between the HFC and intraaortic FITCBSA content yielded the equation y = 0.41x + 38.6, r = 0.81 ( P < 0.005), where y = HFC and x = FITCBSA. These results indicate that the local rate of aortic histamine formation may influence local wall permeability to blood-borne macromolecules such as albumin; they also suggest that de novo histamine synthesis, mediated via the aortic histidine decarboxylase system, may have the potential of coupling altered hemodynamic states with subsequent alterations in wall resistance to macromolecule penetration and, as such, may have important ramifications with respect to vascular wall permeability increases involved in the initiation of atherosclerosis.

Relationship between inhibition of aortic histamine formation, aortic albumin permeability and atherosclerosis

Effects of partial inhibition of aortic histamine formation on aortic albumin uptake and lipid deposition were examined in male, New Zealand white rabbits maintained on Purina Rabbit Chow containing 0.5% cholesterol for a 2-week period. Aortic histamine synthesis was inhibited by partial inhibition of aortic histidine decarboxylase (HD) through administration of α-hydrazinohistidine (α-HH, MK785, Regis Chemical Co., 25 mg/kg, i.p. at 12-h intervals). Additional rabbits were maintained on either the cholesterol diet or on Purina Rabbit Chow without cholesterol. Results indicate that administration of α-HH for the 2-week period produced a 31% reduction ( P < 0.05) in aortic HD activity in those rabbits maintained on the cholesterol diet, and that concurrently there was a 51% reduction in aorta albumin uptake ( P < 0.025) and a 63% reduction in the extent of oil red O staining. By regression analysis a significant correlation coefficient ( r = 0.71, P < 0.005) was obtained between the aortic albumin uptake and the aortic histamine forming capacity (HFC) in rabbits maintained on this cholesterol diet. These findings indicate that the aortic HD system may be an important enzymatic coupler involved in vascular permeability alterations occurring early in the atherogenic sequence.

Shear stress and aortic histamine synthesis.

Aortic histamine-forming capacity (HFC) has been examined in relationship to the applied mean shear stress intensity created by pulsatile perfusion of rabbit aortas with platelet-free blood for a 1-h period. Mean shear stress intensities ranged from 22 to 109 dyn/cm2. Results indicate that a high correlation exists between the shear stress and the HFC which is described by the regression equation y = 0.28 x -6.1, where y = HFC and x = mean shear stress intensity. Results suggest that the rate of histamine formation is sensitive to the applied shear stress, and that the histidine decarboxylase system of the aorta may have the potential of serving as one coupling agent between applied hemodynamic stress and resultant alterations in aortic wall resistance to macromolecules.

Variations in rabbit aortic endothelial and medial histamine synthesis in pre- and early experimental atherosclerosis.

SummaryThe histamine-forming capacity (HFC) of aortic endothelium and medial tissue has been examined in rabbits fed 0.5% cholesterol for 2- and 4-week periods, thereby producing both a preatherosclerotic and histologically identifiable early stage of atherosclerosis. With respect to the HFC of endothelium isolated from aortas of control animals, that of cells isolated from aortas following the 2-week feeding period is essentially double, while no difference exists between the HFC of aortic endothelium from control animals and that of the 4-week dietary group. The medial HFC is similar in all groups. These data thus suggest that one preatherosclerotic metabolic change is an increase in the capacity of endothelial cells to form histamine, and that such a process may occupy a role in increased aortic permeability, an essential component of the atherogenic process.

Gastric histamine metabolism in the aging rat

Rat glandular stomach histamine concentration increases from 15.5 μg/g at 25 days of age to 78 μg/g at 179 days of age, whereas histamine levels in the forestomach do not change with aging. This increase in histamine occurs primarily in the muscular layer of the glandular stomach but not the mucosal and serosal layers of this organ. There is little change in the histamine-forming capacity of the stomach in this age group, nor does Compound 48/80 lower histamine levels in vivo in glandular stomach ; it does lower levels in the forestomach and diaphragm. These data suggest that changes in rat stomach histamine storage capacity but not storage properties occur with aging.

Rabbit aortic histamine synthesis following short-term cholesterol feeding

The histidine decarboxylase (HD) activity of thoracic and abdominal aortic segments obtained from male, Dutch-belted rabbits fed a diet containing 0.5% cholesterol for periods of either 2 or 4 weeks was examined. Mean thoracic aortic HD activities, expressed as histamine-forming capacity (HFC), were 3911 ± 492, 6254 ± 656, and 6215± 878 dpm/100 mg benzenesulfonylhistamine (BSH) for the control group and from rabbits fed cholesterol for 2 and 4 weeks, respectively. Both treatment means were significantly higher than the control ( P < 0.05). Similar examination of abdominal aortic HD activities yielded mean HFC's of 4029 ± 399, 5694 ± 521, and 4762 ± 902 dpm/100 mg BSH for control animals and those of the 2- and 4-week treatment groups, respectively. The difference between mean HFC's of the control and 2-week treatment group was significant (P G 0.05). All increases occurred in the absence of either aortic structural alterations or any lipid deposition. These results give credence to the concept that the atherogenic process represents, at least in part, a delayed-prolonged inflammatory response phenomenon of the arterial wall.

Effect of sympathomimetic amines on the histamine forming capacity of human leucocytes.

1 The effects of alpha- and beta-adrenoceptor stimulants on the histamine-forming capacity (HFC) of human isolated leucocytes have been studied, in vitro.2 It was confirmed that antigen significantly stimulates the HFC of human leucocytes.3 beta-Adrenoceptor stimulants, such as isoprenaline and salbutamol (10(-6)-10(-3)M) significantly inhibited the HFC of human leucocytes in the presence and absence of antigen. At concentrations lower than 10(-6)M, this effect was not observed. In general the degree of inhibition of HFC by beta-adrenoceptor stimulants followed their potency as beta-adrenoceptor stimulants.4 alpha-Adrenoceptor stimulants significantly stimulated leucocyte HFC; noradrenaline within a limited concentration of 10(-6)M, while stimulation was seen consistently with phenylephrine at concentrations of 10(-7)-10(-4)M. Adrenaline, which stimulates both alpha- and beta-adrenoceptors, produced small inhibition, no effect, or a degree of stimulation.5 Phentolamine, an alpha-adrenoceptor blocking agent, produced an effect opposite to that of the alpha-adrenoceptor stimulants, i.e. a significant inhibition of the HFC of human isolated leucocytes.

Effects of shearing stress on aortic histamine synthesis

The potential of elevated shearing stresses imposed on the endothelial surface of rabbit thoracic aorta to increase aortic histamine synthesis through activation of aortic histidine decarboxylase (HD) has been examined. Using a Tyrodes-glycerine solution (37°C, pH 7.4, 3.5 centipoise) as the perfusion solution, aortas were subjected to shearing stresses of 8 (control), 27, and 800 dynes/cm 2, respectively. Additional nontreated and incubated controls were also used. The aortic HD activity, expressed as histamine forming capacity (HFC), for the three treatment groups were (in dpm/mg protein) 302 ± 10, 1537 ± 26, and 969 ± 16, respectively. Histological examination of similarly treated segments revealed no endothelium present in the 800 dynes/cm 2 stressed group. These data indicate that aortic histamine synthesis increased approximately 5-fold in response to a 3 1 2 - fold increase in shear exposure and that over 50% of the increase in histamine synthesis occurred in the endothelial monolayer. These data have been discussed both in relation to the role of the endothelium in regulation of, and the effects of histamine on, vascular wall permeability.

Histamine metabolism in human gastric mucosa.

1. The histamine-forming capacity, i.e. histidine decarboxylase activity, was studied in the acid-secreting mucosa of the human stomach employing a highly sensitive and specific isotope-dilution method. Activity was observed in each of six specimens. 2. The enzyme, histamine methyltransferase, which methylates ring nitrogen, was also present and the product, which is inactive as a gastric acid secretogogue, was observed. 3. The products of side-chain N-methylation, N-methylhistamine and N-dimethylhistamine, both of which are highly active in promoting acid secretion, could not be detected by biological and chromatographic techniques.

Effect of the venom from the scorpion Leiurus quinquestriatus (H & E) on histamine formation and inactivation in the rat

Injection of the venom from the scorpion Leiurus quinquestriatus into rats resulted in a significant decrease in the histamine-forming capacity of the glandular stomach. The endogenous histamine and gastric histamine were not significantly decreased, nor was the diamine oxidase activity of the rats' intestine decreased. The in vitro addition of the venom to an incubation mixture containing the stomachs of normal rats did not result in any significant change of the histamine-forming capacity.

Stimulation of histamine-forming capacity by antigen in sensitized human leucocytes.

(1) Three types of experiments showed that histamine is formed during the reaction of antigen &lt;i&gt;(D. pteronyssinus)&lt;/i&gt; with leucocytes of allergic human subjects: (a) total histamine of leucocytes (extracted + released) was increased; (b) histamine-forming capacity (HFC) of leucocytes was stimulated by antigen &lt;i&gt;in vitro&lt;/i&gt;; (c) HFC of leucocytes was stimulated by injecting antigen &lt;i&gt;in vivo&lt;/i&gt;. (2) Stimulation of HFC of leucocytes by antigen may provide a new and sensitive (though cumbersome) &lt;i&gt;in vitro&lt;/i&gt; test of allergy.

The mechanisms of tolerance towards histamine in the rat and mouse.

Rats and mice were rendered tolerant to histamine by prolonged treatment with the amine. Possible mechanisms of adaptation were examined in these species. Increased binding of histamine to nonmast cell sites in the skin and lung of the mouse and the lung and ileum of the rat was observed. The ability of the blood serum to bind histamine (histaminopexy) was increased in the histamine-treated mouse although serum from the rat possessed a lower binding capacity compared with controls. Prolonged administration of histamine to both species resulted in significant but relatively small increases in both in vivo and in vitro catabolism of histamine in several tissues. A reduction in the histamine-forming capacity of the kidney was observed in histamine-adapted rats. Adrenal changes were noted after histamine treatment and included increased weight in both species, lowered noradrenaline, and an increased level of adrenaline in the rat adrenals. It appears that no single mechanism examined explains the tolerance obtained but that the effect is a combination of factors.