Effect of Chain Length of Aliphatic Amines on Histamine Potentiation and Release

Mongar, J. L.

doi:10.1111/j.1476-5381.1957.tb00112.x

Cited by 20 publications

(13 citation statements)

References 11 publications

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“…The most frequently cited variations of this hypothesis (Taylor and Lieber,1979;Lyons et al,1983) assign the inhibition and potentiation to the fish spoilage-implicated biogenic amines, putrescine (butane-1,4diamine) and cadaverine (1,5-pentanediamine). Early evidence for the potentiation of histamine by putrescine and cadaverine was observed in experiments observing guinea pig ileum contraction and DAO inhibition (Mongar, 1957). Among the 38 fish-associated compounds tested by Taylor and Lieber (1979) for DAO inhibition, cadaverine was among the most potent.…”

Section: Inhibition-potentiationmentioning

confidence: 97%

Scombroid poisoning: A review

Hungerford

2010

Toxicon

417

294

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Scombroid poisoning, also called histamine fish poisoning, is an allergy-like form of food poisoning that continues to be a major problem in seafood safety. The exact role of histamine in scombroid poisoning is not straightforward. Deviations from the expected dose-response have led to the advancement of various possible mechanisms of toxicity, none of them proven. Histamine action levels are used in regulation until more is known about the mechanism of scombroid poisoning. Scombroid poisoning and histamine are correlated but complicated. Victims of scombroid poisoning respond well to antihistamines, and chemical analyses of fish implicated in scombroid poisoning generally reveal elevated levels of histamine. Scombroid poisoning is unique among the seafood toxins since it results from product mishandling rather than contamination from other trophic levels. Inadequate cooling following harvest promotes bacterial histamine production, and can result in outbreaks of scombroid poisoning. Fish with high levels of free histidine, the enzyme substrate converted to histamine by bacterial histidine decarboxylase, are those most often implicated in scombroid poisoning. Laboratory methods and screening methods for detecting histamine are available in abundance, but need to be compared and validated to harmonize testing. Successful field testing, including dockside or on-board testing needed to augment HACCP efforts will have to integrate rapid and simplified detection methods with simplified and rapid sampling and extraction. Otherwise, time-consuming sample preparation reduces the impact of gains in detection speed on the overall analysis time.

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Section: Inhibition-potentiationmentioning

confidence: 97%

Scombroid poisoning: A review

Hungerford

2010

Toxicon

417

294

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“…Though the potentiating mechanism would be equivalent for both histamine and tyramine, most of the published studies refer to histamine. In vitro diamines potentiate contractions of the guinea-pig ileum caused by histamine and inhibit its enzymatic destruction by DAO (Mongar, 1957). In rats, metabolism of histamine is inhibited by simultaneous oral administration of cadaverine, putrescine or a mixture of biogenic amines.…”

Section: Potentiation Of the Toxicity Of Other Biogenic Aminesmentioning

confidence: 99%

Scientific Opinion on risk based control of biogenic amine formation in fermented foods

Publication¹

2011

EFSA Journal

677

276

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A qualitative risk assessment of biogenic amines (BA) in fermented foods was conducted, using data from the scientific literature, as well as from European Union‐related surveys, reports and consumption data. Histamine and tyramine are considered as the most toxic and food safety relevant, and fermented foods are of particular BA concern due to associated intensive microbial activity and potential for BA formation. Based on mean content in foods and consumer exposure data, fermented food categories were ranked in respect to histamine and tyramine, but presently available information was insufficient to conduct quantitative risk assessment of BA, individually and in combination(s). Regarding BA risk mitigation options, particularly relevant are hygienic measures to minimize the occurrence of BA‐producing microorganisms in raw material, additional microbial controls and use of BA‐nonproducing starter cultures. Based on limited published information, no adverse health effects were observed after exposure to following BA levels in food (per person per meal): a) 50 mg histamine for healthy individuals, but below detectable limits for those with histamine intolerance; b) 600 mg tyramine for healthy individuals not taking monoamino oxidase inhibitor (MAOI) drugs, but 50 mg for those taking third generation MAOI drugs or 6 mg for those taking classical MAOI drugs; and c) for putrescine and cadaverine, the information was insufficient in that respect. Presently, only high‐performance liquid chromatography (HPLC)‐based methods enable simultaneous and high sensitivity quantification of all BA in foods, hence are best suited for monitoring and control purposes. Monitoring of BA concentrations in fermented foods during the production process and along the food chain would be beneficial for controls and further knowledge. Further research on BA in fermented foods is needed; particularly on toxicity and associated concentrations, production process‐based control measures, further process hygiene and/or food safety criteria development, and validation of analysis methods.

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“…Mongar [143] found that short-chain diamines are both substrates for and inhibitors of histaminase (=diamine oxidase) and that they can potentiate the effects of histamine. Lyons et al [144] reported that cadaverine potentiated histamine uptake in rat small intestine segments, an effect that they attributed to inhibition of histamine catabolism.…”

Section: Resultsmentioning

confidence: 99%

Polyamines as Snake Toxins and Their Probable Pharmacological Functions in Envenomation

Aird

Villar‐Briones

Roy

et al. 2016

Toxins

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While decades of research have focused on snake venom proteins, far less attention has been paid to small organic venom constituents. Using mostly pooled samples, we surveyed 31 venoms (six elapid, six viperid, and 19 crotalid) for spermine, spermidine, putrescine, and cadaverine. Most venoms contained all four polyamines, although some in essentially trace quantities. Spermine is a potentially significant component of many viperid and crotalid venoms (≤0.16% by mass, or 7.9 µmol/g); however, it is almost completely absent from elapid venoms assayed. All elapid venoms contained larger molar quantities of putrescine and cadaverine than spermine, but still at levels that are likely to be biologically insignificant. As with venom purines, polyamines impact numerous physiological targets in ways that are consistent with the objectives of prey envenomation, prey immobilization via hypotension and paralysis. Most venoms probably do not contain sufficient quantities of polyamines to induce systemic effects in prey; however, local effects seem probable. A review of the pharmacological literature suggests that spermine could contribute to prey hypotension and paralysis by interacting with N-methyl-d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, nicotinic and muscarinic acetylcholine receptors, γ-Aminobutyric acid (GABA) receptors, blood platelets, ryanodine receptors, and Ca2+-ATPase. It also blocks many types of cation-permeable channels by interacting with negatively charged amino acid residues in the channel mouths. The site of envenomation probably determines which physiological targets assume the greatest importance; however, venom-induced liberation of endogenous, intracellular stores of polyamines could potentially have systemic implications and may contribute significantly to envenomation sequelae.

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Effect of Chain Length of Aliphatic Amines on Histamine Potentiation and Release

Cited by 20 publications

References 11 publications

Scombroid poisoning: A review

Scombroid poisoning: A review

Scientific Opinion on risk based control of biogenic amine formation in fermented foods

Polyamines as Snake Toxins and Their Probable Pharmacological Functions in Envenomation

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