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Abstract. Recent trends in food quality and safety promote an increasing search for trace compounds that can affect human health. Biogenic amines belong to this group of substances. They can cause distinctive pharmacological, physiological and toxic effects in organisms. Their amounts are usually increasing as a consequence of the use of poor quality raw materials, during controlled or spontaneous microbial fermentation or in the course of food spoilage. The origin of biogenic amines makes them suitable as chemical indicators of the hygienic quality and freshness of some foods being associated to the degree of food fermentation or degradation. The development of appropriate manufacturing technologies to obtain products free or nearly free from biogenic amines is a challenge for the meat industry. This review briefly summarises current knowledge on the biological implications of biogenic amines on human health and collects data on the factors affecting their formation in meat and fermented meat products.
According to current teaching biogenic amines are released by exocytos- is, i. e. by evacuation of amine storing vesicles or granules into the extracellular space. The release of transmitter amines is quantal, i. e. occurs in packs of transmitter molecules. These packs are assumed to be identical with vesicle contents, in other words, the smallest releasable quantum equals the amine content of one vesicle. However, there are experimental observations which do not fit in with this version of an exocytotic release theory. Observed quantitative discrepancies could be explained if the release mechanism allowed a fractional release of transmitter amine from several vesicles instead of the total evacuation of a few. The lack of adequate knowledge about the mechanisms of storage of biogenic amines within the vesicles has up til now rendered it difficult to envisage the machinery behind a fractional release of the amine content of a vesicle. In extensive in-vitro studies we have found that the matrices of amine storing granules (i. e. from mast cells, chromaffin cells and nerve terminals) show the properties of weak cation exchanger materials, carboxyl groups serving as amine binding ionic sites. When exposed to cations like sodium and potassium ions, the amines are released from their storage sites according to kinetics characteristic of weak cation exchangers. In vivo, amine release from cat adrenals on splanchnic nerve stimulation also occurs according to ion echange kinetics. Histamine release from mast cells is considered to occur as the result of degranulation, i. e. the expulsion of histamine storing granules to the extracellular space, a typical example of exocytosis. The granules are assumed to loose their histamine by ion exchange, Na⁺ Hi⁺, on exposure to the sodium-rich extracellular medium. However, recent observations on histamine release from superfused mast cells suggest that the release of histamine, although caused by ion exchange, is due to intracellular ion exchange at granule sites between cytoplasmic potassium and activated mast cells as the consequence of intracellular potassium ion flux across the histamine carrying granules, degranulation and extracellular histamine release from expelled granules occurring only as the result of more extensive activation. The possibility of potassium ions being involved also in an ion exchange process behind the release of other biogenic amines e. g. at nerve terminals will be proposed. The amine release will still be quantal but the size of the released quanta will not depend on the total amine content of a vesicle but on the size of the fractions thereof being released, thereby explaining many of the quantitative discrepancies attached to the current exocytotic release theory. A fractional release theory may have interesting consequences for our thinking as to the physiology and pharmacology of processes involving storage and release of biogenic amines.
The nervous system of daughter sporocyst of D. pseudospathaceum is described on a basis of acetylcholinesterase activity, histofluorescence of biogenic amines and serotonin immunoreactivity. Description of the posterior part of the nervous system is added to the hitherto described brain ganglia and irregular network of nerve fibres surrounding anterior end of the sporocyst. The immunoreactivity of 5-HT was observed in laterally situated main nerve cords, which run along the whole length of the body and unite at its posterior end. Some ramifications of the main cords were also visible. A possible role of messenger molecules observed in daughter sporocyst nervous system is discussed.
The amounts of biogenic amines (putrescine, histamine, cadaverine, tyramine, spermidine, and spermine), lactic acid, pH, and number of Enterobacteriaceae, Escherichia coli, and coagulase producing Staphylococci were determined in healthy turkeys and in the fillets of turkey breasts with the signs of ascites and bursitis. The examination of the amines was performed by high performance liquid chromatography; the amount of lactic acid was determined by capillary isotachophoresis method; pH value and microbiological indicators - by standardised methods. All determinations were done after 24, 72, and 120 h after slaughter of the turkeys. The fillets of the breasts were stored in the refrigerator at 4°C. The significant differences in the total amounts of biogenic amines in carcasses of healthy turkeys and carcasses of turkeys with substantial lesions of bursitis and medium or substantial lesions of ascites were determined within 5 d after slaughter (P<0.00l). The amounts of biogenic amines in the breast fillets of turkeys with low lesions of ascites and bursitis were very similar to that of the control group during the whole period of maturation. The average amount of lactic acid throughout 5 d after slaughter increased only in the breast fillets of healthy turkey (maximum value was 1.032 mg/100 g) and insignificantly increased in the carcasses with low lesions of ascites and bursitis (maximum value was 0.983 mg/100 g). The results of investigation indicate the breast fillets of turkeys with medium and substantial lesions of ascites and substantial lesions of bursitis are not fit for human consumption. However, in the cases of low lesions of ascites and low and medium lesions of bursitis, the fillets are not fit for maturation, but could be thermally processed in the period of 24 h after slaughter.
Work by Ramsay in the 1950’s established the foundations for our current understanding of primary urine production by Malpighian tubules and we now have detailed knowledge of the epithelial transport processes underlying fluid secretion. Identified neuropeptides and biogenic amines have been shown to stimulate fluid secretion and, for some, detailed information is available on the second messenger pathways and transport processes they activate. There are significant gaps in our knowledge, however, particularly concerning the role of identified diuretics in vivo. The hormonal status of many has yet to be established and it is also unclear whether they are used to control different types of diuresis.
Pregnant Wistar rats received 50 ppm of zinc (ZnSO4 • 7H2O) in their drinking water for the entire duration of pregnancy. On the day of delivery zinc was removed from the drinking water. Another group, dams, received 50 ppm of zinc in drinking water during the suckling period (from delivery until the 21st day of postnatal life). Their offspring were weaned on the 21st day, at which time zinc was removed from the drinking water. The control group drank tap water only. In 8-12-week-old offspring of all three groups the DA, DOPAC, HVA, 3-MT, 5-HT, 5-HIAA, NA, and MOPEG synthesis rate in the brain was estimated by HPLC/ED technique. Independent behavioral exam were performed such as locomotor and exploratory activity, irritability, yawning and oral activity, stereotype behavior, catalepsy and others. For the above, cen­tral DA receptor agonists (quinpirole, SKF 38393, apomorphine, 7-OH-DPAT) or antagonists (haloperidol, SCH 23390) were used. It was found that exposure to zinc during early stages of ontogenic development produce changes in the central dopaminergic system activity of adult offspring. From the above we con­cluded that uncontrolled supplementation with zinc during pregnancy or lactation can induce disturbance of the central dopaminergic system in adult mammal.
Ethanol (EtOH) abuse in pregnancy is known to produce serious damage to internal organs of the fetus, a condition in humans that is classified as "fetal alcohol syndrome". Cadmium (Cd), a heavy metal pollutant of the environment, represents another toxin that produces retarded fetal growth and teratogenic effects. The developing brain is particularly sensitive to both toxins, being affected morphologically and neurochemically. Besides prenatal EtOH and Cd have been found to reduce endogenous dopamine (DA) levels and turnover in the brain and change reactivity of the central DA receptors to agonists. To test effect of separate and joint applications of the above xenobiotics on offspring during pregnancy, rats were given 10% (v/v) EtOH and/or Cd (5 or 50 ppm) in their drinking water. Numbers of pregnant rats, newborns in the litter, birth body mass, and the number of offspring surviving 3 weeks after birth were recorded. Then in 6-week-old offspring the anatomopathological study of internal organs, and the level of biogenic amines (NA, 5-HT, 5-HIAA) in the discrete parts of the brain were estimated spectrofluorometrically. Prenatal exposure to EtOH prevents some toxic effect of Cd in rat offspring (morphological, condition of offspring). On the other hand, EtOH intensified some effects of Cd on the biogenic amines level in the brain.
On the morning of the first day of pregnancy, Wistar rats were administered a single IP injection of either zinc sulfate (10.0 mg/kg) or saline. For the remainder of pregnancy, half the rats in each group then consumed filtered tap water while the other half consumed filtered tap water with 50 ppm of cadmium (CdCl₂ ). At eight weeks after birth, the behavioral profile of male offspring was assessed in the following way: Apomorphine (non-selective dopamine receptor agonist), (+)-7-hydroxy-2-(di-n-propylamino) tetralin (7-OH-DPAT) (D₃ agonist) and (+/-)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol (SKF 38393) (D₁ agonist) were used to evaluate stereotyped behavior, yawning activity and oral movements – indices for these respective agonists. In addition, two dopamine receptor antagonists, haloperidol (D₂ antagonist) and 7-chloro-8-hydroxy3-methyl-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzapine (SCH 23390) (D₁ antagonist) were used to evaluate cataleptogenic activity. Additional behavioral parameters studied were locomotor activity, irritability and reaction to a painful stimulus. Dopamine and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 3-methoxytyramine (3-MT) were quantified in the striatum, hippocampus and in the frontal cortex of the brain by means of HPLC/ED technique. In addition, cadmium levels were analyzed in the brain, liver, kidney and bone of newborn rats. Our results indicate that prenatal exposure of pregnant rats to cadmium produced alterations in the reactivity of central dopamine receptors and modulated the level of dopamine and its metabolites in the offsprings’ brains. A single injection of zinc, preceding cadmium consumption, attenuated some of the effects of cadmium on the offsprings’ dopaminergic system. Zinc also reduced cadmium deposition in the brain, kidney and bone, but enhanced its accumulation in liver. In summary, zinc may exert some neuroprotective effects against cadmium neurotoxicity.
Oznaczono zawartość histaminy i tyraminy w 32 próbkach kilku gatunków serów dojrzewających produkcji krajowej oraz 11 próbkach serów importowanych. Poziom histaminy wahał się od ilości śladowych do 157 mg/kg, tyraminy od 3,8 do 575 mg/kg.
It is common knowledge that fish are a nutritious component of a human diet, as they constitute a valuable and desired source of protein and polyunsaturated fatty acids. However, they are likely to pose a risk to consumer health. The presence of pathogenic bacteria or their toxins, parasites, biogenic amines and toxins or chemical residues may be a causal agent of foodborne illnesses in humans, sometimes even with fatal effect. Usually, infections are a result of insufficient thermal treatment or consumption of raw fish dishes. There are also risk factors that cannot be eliminated by such treatments as cooking, salting or freezing.
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