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At least 19 recordsLinked to original sources
PubMed1999

Quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid enhance the Fenton reaction in phosphate buffer.

Quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid enhanced the Fenton reaction in phosphate buffer, respectively. The enhancement by quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid of the Fenton reaction may be partly related to their respective actions in the biological systems such as a neurotoxic effect (quinolinic acid), a marked growth-inhibitory action on rice seeding (alpha-picolinic acid and fusaric acid), and an antiseptic (2,6-pyridinedicarboxylic acid). The ultraviolet-visible absorption spectrum of the mixture of alpha-picolinic acid with ferrous ion showed a characteristic visible absorbance band with a lambda(max) at 443 nm, suggesting that alpha-picolinic acid chelate of Fe2+ ion forms in the solution. Similar characteristic visible absorbance band was also observed for the mixture of Fe2+ ion with quinolinic acid (or fusaric acid, or 2,6-pyridinedicarboxylic acid). The chelation seems to be related to the enhancement by quinolinic acid, alpha-picolinic acid, fusaric acid, and 2,6-pyridinedicarboxylic acid of the Fenton reaction. alpha-Picolinic acid was reported to be a toxic substance isolated from the culture liquids of blast mould (Piricularia oryzae CAVARA). On the other hand, it has also been known that chlorogenic acid protects rice plants from the blast disease. The chlorogenic acid inhibited the formation of the hydroxyl radical in the reaction mixture of alpha-picolinic acid, FeSO4(NH4)2SO4, and H2O2. Thus the inhibition may be a possible mechanism of the protective action of the chlorogenic acid against the blast disease.

Buffers↗
PubMed1976

The hypotensive effect of fusaric acid: the results of long-term administration of fusaric acid in elderly hypertensive patients.

The hypotensive effect of fusaric acid calcium salt (Calcium salt of 5-butylpicolinic acid) was examined clinically in 10 elderly hypertensive patients by the long-term administration of this agent and the following results were obtained. 1) The means of the systolic and/or diastolic blood pressures of each patient were significantly lower during the first year of the trial period than those during the one year's control period in all patients. 2) The means of the systolic and/or diastolic blood pressures of each patient were significantly lower during the second year of the trial period than those during the one year's control period in whom administration of fusaric acid calcium salt was continued throughout two years. A significant reduction of the systolic blood pressure was observed in 3 out of 6 patients and that of the diastolic blood pressure was observed in 5 out of 6 patients. 3) Comparison was made between the means of the systolic and diastolic blood pressures during the one year's control period and those during the six month's placebo period after two year's administration of fusaric acid calcium salt. During the placebo period, both systolic and diastolic blood pressures showed a tendency of returning to the levels during the control period confirming the hypotensive effect of this agent. 4) Laboratory findings after one year's administration of fusaric acid calcium salt showed no adverse effect of this agent.

Aged↗
PubMed1984

Contractile responses of mammalian cerebral arteries to 15-hydroperoxyarachidonic acid vary in the presence of fusaric acid and verapamil.

The effects of fusaric acid and verapamil on 15-hydroperoxyarachidonic acid (15-HPAA)-induced cerebral arterial contraction were examined. Addition to the tissue bath of 15-HPAA in concentrations ranging from 1 X 10(-7) to 3 X 10(-5) M caused a dose-dependent contraction in canine basilar, middle cerebral, posterior cerebral and human basilar or middle cerebral arteries. Fusaric acid and verapamil antagonized the 15-HPAA-induced contraction of these cerebral arteries by different mechanisms, in a dose-dependent manner. In the presence of 1 X 10(-3) M fusaric acid, the dose-response curves of cerebral arteries for 15-HPAA were antagonized in a noncompetitive manner. However, the responses to 15-HPAA were restored completely after removal of fusaric acid from the bathing solution. Fusaric acid did not antagonize the CaCl2-induced contraction. The concentration of verapamil which antagonized the 15-HPAA-induced contraction was a good fit to the concentration of this antagonist which antagonized the CaCl2-induced contraction. These findings indicate that the antagonism seen with fusaric acid manifests as a block of the sites specific for 15-HPAA and that the antagonistic actions of verapamil on 15-HPAA may be produced by the inhibition of calcium influx.

Adult↗
PubMed1996

Production of fusaric acid by Fusarium species.

Fusaric acid is a mycotoxin with low to moderate toxicity, which is of concern since it might be synergistic with other cooccurring mycotoxins. Fusaric acid is widespread on corn and corn-based food and feeds and is frequently found in grain, where Fusarium spp. are also isolated. We surveyed 78 strains of Fusarium moniliforme, F. crookwellense, F. subglutinans, F. sambucinum, F. napiforme, F. heterosporum, F. oxysporum, F. solani, and F. proliferatum for their ability to produce fusaric acid. Strains in Fusarium section Liseola also were assigned to mating population of the Gibberella fujikuroi species complex. The fungi could be divided into three classes, low (< 100 micrograms/g), moderate (100 to 500 micrograms/g), and high (> 500 micrograms/g), based on the amounts of this mycotoxin produced in culture on autoclaved corn. Strains of mating populations C from rice consistently produced moderate to high concentrations of fusaric acid. Two isolates, one each from mating populations C and D, produced fusaric acid in excess of 1,000 micrograms/g of corn. No isolates of any of the Fusarium species examined were negative for the production of fusaric acid on autoclaved corn.

Fusaric Acid↗
PubMed1980

Interaction at the synaptic level of fusaric acid with neurotransmitters.

Fusaric acid (FA) is shown to induce inhibition of noradrenaline and dopamine uptake in synaptosomes from rat hypothalamus and corpus striatum. The basal overflow of noradrenaline and dopamine from "brain stem" and corpus striatum slices is stimulated by FA. While this influence of FA on noradrenaline release is further enhanced by other stimuli (raised K+ concentration or electrical stimulation), no comparable effect can be observed concerning dopamine release. The data show that FA which is known as a potent dopamine-beta-hydroxylase inhibitor of high specificity exerts also marked effect in the central nervous system by interference with other synaptosomal functions.

Animals↗
PubMed1985

In vivo release of adrenal catecholamines in rats by fusaric acid.

We studied the effect of fusaric acid, an inhibitor of dopamine beta-hydroxylase (D beta H), on plasma and peripheral tissue catecholamine (CA) content and on urinary excretion of CA in the rat. We found that fusaric acid treatment resulted in a rapid decline of adrenal epinephrine (E) and norepinephrine (NE) and an increase of adrenal dopamine (DA); the kidney and heart NE and DA contents were affected in a pattern similar to that of the adrenals. In contrast, the E concentrations in the kidneys and heart were markedly elevated after a single intraperitoneal dose of fusaric acid (100 mg/kg); the maximum response was observed at 60 min, when kidney E increased from 9.3 +/- 4.4 to 101 +/- 24 pmol/g tissue and heart E in both atrium and ventricle rose from 92 +/- 8 to 607 +/- 85 pmol/g tissue and from 70 +/- 4 to 632 +/- 50 pmol/g tissue, respectively. In addition, a large increase of CA (predominantly of E) was found in the plasma of treated rats, where E, NE and DA were 27, 6.6 and 2.7 times higher than control values, respectively. The excretions of urinary E and NE were also significantly elevated during treatment. Fusaric acid-treated bilaterally adrenalectomized rats did not exhibit any increase in plasma, heart and kidney E concentrations. The results suggest that fusaric acid stimulates adrenal CA release in vivo, resulting in large increases of the main adrenal CA, E in peripheral tissues, plasma and urine. The decline in the adrenal E content is thus not only due to its decreased synthesis but also increased release.

Adrenal Glands↗
PubMed1976

Urinary norepinephrine excretion in elderly hypertensive patients during administration of fusaric acid.

The urinary norepinephrine excretion during fusaric acid calcium salt administration was examined in 5 elderly hypertensive patients by double blind cross-over method. The average daily excretion of the last 5 days during fusaric acid calcium salt or placebo administration of 5 weeks' duration was compared in each patient. In 4 patients except for one, the average daily urinary excretion of norephinephrine during fusaric acid calcium salt administration showed an increase, being highly significant (p less than 0.01) statistically, when compared with that during placebo administration, the latter being essentially unchanged. In the one patient, however, the average daily urinary excretion of norepinephrine was significantly higher during placebo administration than that during fusaric acid calcium salt administration. The relationship between the changes in the average daily urinary excretion of norepinephrine and those in blood pressures seemed to be not consistent. The mechanism which brought about an increased norepinephrine excretion in the urine of the hypertensive patients is not obscure at present.

Blood Pressure↗
PubMed1976

The long-term hemodynamic effect of fusaric acid in elderly hypertensive patients.

The hemodynamic effect of fusaric acid calcium salt (calcium salt of 5-butylpicolinic acid), an inhibitor of dopamine beta-hydroxylase, was studied in long-term administration of this agent in 10 elderly hypertensive patients. The hemodynamic items were measured by dye-dilution method before and 3 months, 6 months and one year after administration of fusaric acid calcium salt. The main hemodynamic changes observed were as follows: 1) Heart rate did not show any consistent change. 2) Systolic, diastolic and mean blood pressure decreased. The mean values of these pressures after fusaric acid calcium salt administration were significantly lower than the mean values before administration of this agent. 3) Total peripheral vascular resistance index decreased. The mean values of this index at 3 months, 6 months and one year after fusic acid calcium salt administration were significantly lower than the mean value before administration of this agent. 4) Cardiac index showed various changes throughout administration of fusaric acid calcium salt. The changes in this index might be secondary following the changes in total peripheral vascular resistance index, an inverse correlation being existed between them. 5) Stroke volume index showed almost a similar pattern of change as observed in cardiac index. An inhibitory action of fusaric acid calcium salt on the inotropism of the heart could be hardly found. 6) Plasma volume showed no tangible changes after fusaric acid calcium salt administration throughout one year. It might be concluded that fusaric acid calcium salt elicited the hypotensive response primarily through the reduction of total peripheral vascular resistance index.

Aged↗
PubMed1976

[Effects of fusaric acid and its derivative on the cardiovascular system].

The cardiovascular effects of fusaric acid, a dopamine-beta-hydroxylase (DBH) inhibitor and a hypotensive agent, and 5-(4'-chlorobutyl) picolinic acid, one of the most potent DBH inhibitors in fusaric acid derivatives, were investigated in anesthetized dogs. Fusaric acid (10-30 mg/kg) given intravenously caused immediately and dose-dependently a fall in blood pressure, an increase in heart rate, a stimulation of respiration, a marked increase in the rate of superior mesenteric arterial flow, and a decrease in the rate of femoral arterial flow. Fusaric acid (0.3-3 mg) given close-arterially caused a dose-dependent decrease in the sinus rate and in the developed tension in isolated blood-perfused sinoatrial node and papillary muscle preparations, respectively. For the superior mesenteric, renal, and femoral circulations which were perfused with blood, a close-arterial injection of fusaric acid (10-30 mg) increased in the rates of flow in a dose-dependent manner. 5-(4'-Chlorobutyl) picolinic acid showed similar responses as fusaric acid quantitatively or qualitatively. These results indicate that hypotension induced rapidly after intravenous administration of fusaric acid or 5-(4'-chlorobutyl) picolinic acid is not due to the enzyme inhibition, but rather to the direct depression of cardiac function and decrease in peripheral vascular resistance.

Animals↗
PubMed1998

Effects of fusaric acid on rat liver mitochondria.

The effects of fusaric acid on hepatic energy metabolism were measured. Three experimental systems were employed: (a) Intact rat liver mitochondria; (b) freeze-thawing disrupted mitochondria; and (c) the isolated perfused rat liver. Fusaric acid affects mitochondrial energy metabolism by at least three modes of action: (1) Inhibition of succinate-dehydrogenase (in the 10(-3)-10(-2) M range); (2) inhibition of oxidative phosphorylation (in the 10(-5)-10(-4) M range); and (3) inhibition of alpha-ketoglutarate-dehydrogenase (in the 10(-5)-10(-4) M range). The inhibition of oxidative phosphorylation seems to be the result of a direct action on the ATP-synthase/ATPase without significant inhibition of the ATP/ADP exchange. In the isolated perfused rat liver, fusaric acid inhibits oxygen uptake and gluconeogenesis from pyruvate, the latter being strictly dependent on intramitochondrially generated ATP. The effects of fusaric acid on rat liver mitochondria are similar to those reported previously for maize root mitochondria. However, except for the action on succinate-dehydrogenase, rat liver mitochondria are approximately two orders of magnitude more sensitive than maize root mitochondria.

Adenosine Diphosphate↗
PubMed2000

Effects of the Fusarium spp. mycotoxins fusaric acid and deoxynivalenol on the growth of Ruminococcus albus and Methanobrevibacter ruminantium.

The Fusarium spp. mycotoxins fusaric acid and deoxynivalenol (DON) were tested for antimicrobial activity against Ruminococcus albus and Methanobrevibacter ruminantium. The growth of both organisms was inhibited by fusaric acid as low as 15 micrograms/mL (84 microM) but not by DON, at levels as high as 100 micrograms/mL (338 microM). No synergistic inhibitory effect was observed with DON plus fusaric acid. Neither organism was able to adapt to the fusaric acid and responses of each organism to the compound were different. The optical density (OD) maximum for R. albus, but not for M. ruminantium, was diminished after 28 days incubation at concentrations of fusaric acid below 240 micrograms/mL. Inhibition of R. albus started before significant growth had occurred, while M. ruminantium doubled twice before the onset of inhibition. Responses to picolinic acid, an analog of fusaric acid, were also dramatically different between the two microorganisms with M. ruminantium exhibiting a severe lag followed by a complete recovery of growth, while R. albus was only slightly inhibited with no lag. These results suggest that the mechanism of fusaric acid inhibition is specific to each microorganism. This is the first demonstration of the common mycotoxin fusaric acid inhibiting the growth of rumen bacteria.

Animals↗
PubMed1977

Suppression of elevated serum TSH levels in hypothyroidism by fusaric acid.

The effect of Fusaric acid (FA), a specific inhibitor of dopamine beta-hydroxylase, on humna TSH and thyroid hormone concentration (T4 and T3) was evaluated. Healthy subjects showed no significant changes in serum T3,T4 and TSH concentrations following the administration of FA calcium salt (FA-Ca) or placebo. Similarly, administration of FA-Ca for 4 weeks to hypertensive patients failed to produce significant changes in the serum T4 or T3 Resin Sponge Uptake values, and in the TSH and T3 responses to TRH. In contrast, FA-Ca produced a significant reduction on the high basal serum TSH level in patients with primary hypothyroidism. The mean nadir was 25% and ranged from 6 to 61%. As in the case of L-Dopa, the effect of FA-Ca on serum TSH is most clearly demonstrated in patients with primary hypothyroidism. Alterations in brain amines may directly or indirectly suppress pituitary TSH secretion. The possibility of changes in the peripheral distribution or turnover rate of TSH has not been excluded.

Adult↗
PubMedDate not supplied

Tachycardia in spontaneously hypertensive and normotensive rats after fusaric acid and bupicamide.

1. The effects of the dopamine-beta-hydroxylase inhibitors bupicamide, fusaric acid, FLA-63 and U-14,624 on blood pressure and heart rate of spontaneously hypertensive rats were examined. 2. Bupicamide and fusaric acid caused marked tachycardia whereas FLA-63 and U-14,624 caused modest bradycardia; all drugs decreased blood pressure. 3. In normotensive rats, fusaric acid caused the same degree of tachycardia as in spontaneously hypertensive rats, but blood pressure was only slightly reduced. 4. Tachycardia after fusaric acid was not due to increased sympathetic activity or decreased parasympathetic activity but required intact catecholamine stores. 5. It is concluded that fusaric acid causes tachycardia by releasing catecholamines indirectly and that a metabolite of fusaric acid is also involved.

Animals↗
PubMed2006

Growth-inhibiting effects of concentrations of fusaric acid on the growth of Bacillus mojavensis and other biocontrol Bacillus species.

AIMS: To determine the effects of concentrations of fusaric acid on the growth of several strains of the biocontrol bacterial endophyte Bacillus mojavensis and other species within the Bacillus subtilis group, as well as the genetic relationships within this small group of Gram-positive bacteria, and their antagonisms to Fusarium verticillioides, which produce fusaric acid. METHODS AND RESULTS: The growth of 50 Bacillus strains and species were tested at two concentrations of fusaric acid determined in maize infected by an isolate of F. verticillioides. Molecular characterizations of the strains and species of bacteria were determined with an automated ribotyper. The growth of bacteria measured under both concentrations with an automated turbidometer, Bioscreen, indicated that fusaric acid was toxic to most strains of the bacterial endophyte B. mojavensis. However, the effects of these two concentrations on other Bacillus species varied in that fusaric acid was either bacteriocidal or bacteriostatic to most species. CONCLUSIONS: These data indicate that the concentrations of fusaric acid are inhibitory to the growth of most Bacillus species, some of which are used as biocontrol agents. This suggests that the endophytic and saprophytic states of F. verticillioides and other Fusarium species cannot be controlled by fusaric-acid-sensitive Bacillus species. SIGNIFICANCE AND IMPACT OF STUDY: Mycotoxic Fusarium species, such as F. verticillioides, are competitive because all produce fusaric acid, which is inhibitory to biocontrol bacteria, and mutants tolerant to fusaric acid must be developed in order to be effective on biocontrol bacteria.

Bacillus↗
PubMed1995

Toxic interaction of fumonisin B1 and fusaric acid measured by injection into fertile chicken egg.

Toxic interactions of fusaric acid and fumonisin B1, two mycotoxins produced by Fusarium moniliforme, were studied in the chicken embryo. The yolk sacs of fertile White Leghorn eggs were injected before incubation with separate and combined solutions of either fusaric acid and or fumonisin B1. The toxins were administered in either a sterile 10 mM buffered phosphate solution, pH 6.90, which produced a final pH of 6.6 +/- 0.2, or sterile distilled water. Toxicity was based on absence of egg pip at the end of the 21-day incubation period. Toxins administered in the phosphate buffer solution were more toxic than those administered in distilled water. When both toxins were combined in equal concentrations and injected into eggs, increased toxicity resulted. Fusaric acid was shown to be a mild toxin to the eggs and when a relatively nontoxic concentration of it was combined with graded doses of fumonisin B1, a synergistic toxic response was obtained. Fusaric acid is only moderately toxic to the chicken egg, however its co-occurrence with other fusaria toxins found on corn and other cereals might present possible antagonisms or synergisms. The results of this egg model suggest that fusaric acid might play a role in enhanced and unpredicted toxicity in mammalian systems if it is consumed with other mycotoxins.

Animals↗