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K Yabe

Publications and source records attributed to K Yabe.

At least 19 recordsLinked to original sources

Does glycogen depletion play an important role in ischemic preconditioning?

The present study was undertaken to determine whether or not tissue glycogen depletion prior to ischemia, and subsequent attenuation of tissue lactate accumulation during ischemia, correlates with postischemic functional recovery of the preconditioned heart. Isolated rat hearts were subjected to 40-min ischemia and 30-min reperfusion. Preconditioning with 5-min ischemia and 5-min reperfusion reduced the preischemic glycogen and postischemic lactate levels of the heart to 60.5 +/- 5.6% and 66.9 +/- 7.7% respectively, of values in non-preconditioned hearts (n = 6), and improved the recovery of the rate-pressure product (RPP) of the ischemic/reperfused heart (87.0 +/- 5.8% versus 25.2 +/- 4.5% of the initial value for the non-preconditioned group, n = 8). Treatment with polymyxin B (50 microM) abolished the preconditioning-induced postischemic recovery of the RPP. Treatment of the non-preconditioned heart with phorbol 12-myristate 13-acetate (15 pmol/5 min) resulted in an improvement in the postischemic recovery of RPP. Neither of these treatments affected the preischemic glycogen and postischemic lactate levels. The results suggest that preischemic glycogen depletion and subsequent attenuation of ischemic lactate accumulation do not play a major role in the preconditioning-induced protection against postischemic contractile dysfunction in perfused rat hearts.

Animals

Activation of cardiac muscarinic receptor and ischemic preconditioning effects in in situ rat heart.

Activation of cardiac muscarinic receptors by vagal stimulation decreases cardiac work, which may have a protective effect against ischemic injury. To determine whether cardiac muscarinic receptors contribute to the mechanisms of preconditioning effects, we examined the effect of carbachol on ischemia/reperfusion damage and the effect of vagotomy on cardioprotection induced by ischemic preconditioning. Rats were subjected to 30 min of left coronary artery occlusion followed by 30-min reperfusion in situ. Pre-conditioning was induced by three cycles of 2-min coronary artery occlusion and, subsequently by 5 min of reperfusion. The incidence of ischemic arrhythmias, such as ventricular tachycardia (VT) and ventricular fibrillation (VF), and the development of myocardial infarction were markedly reduced by the preconditioning. Carbachol infusion (4 micrograms/kg per min) delayed the occurrence of VT and VF during ischemia and reduced the infarct size. Compared with non-ischemic left ventricle, the cyclic guanosine monophosphate (GMP) content in the ischemic region of the left ventricle was decreased by ischemia/reperfusion, whereas the cyclic adenosine monophosphate (AMP) content of this region was increased. These changes were reversed by preconditioning. Similar changes in cyclic GMP and AMP content in the ischemic region were seen in rats undergoing carbachol treatment. These results suggest the possible contribution of muscarinic receptor stimulation to preconditioning. Vagotomy prior to preconditioning diminished the antiarrhythmic effects, whereas it did not block the anti-infarct effect afforded by pre-conditioning. Vagotomy abolished the preconditioning effect on the tissue cyclic GMP, but it did not attenuate the decrease in tissue cyclic AMP. The results suggest that muscarinic stimulation exerts preconditioning-mimetic protective effects in ischemic/reperfused hearts, but that a contribution of reflective vagal activity to the mechanism for preconditioning is unlikely.

Animals

Preconditioning preserves mitochondrial function and glycolytic flux during an early period of reperfusion in perfused rat hearts.

OBJECTIVE: The purpose of the present study was to examine the effects of preconditioning on glycolysis and oxidative phosphorylation during reperfusion in perfused rat hearts. METHODS: Preconditioning was induced by 5 min of ischemia and 5 min of reperfusion before 40 min of sustained ischemia and subsequent 30 min of reperfusion. Tissue energy metabolite levels, mitochondrial oxygen consumption capacity and adenine nucleotide translocator content of the perfused hearts were assessed at 40 min of ischemia, 5 and 30 min of reperfusion. RESULTS: Preconditioning improved the postischemic recovery of rate x pressure product (92.5 +/- 8.7 vs. 24.9 +/- 1.2% for non-preconditioned group) and high-energy phosphate content (ATP and CrP; 39.5 +/- 2.0 and 96.2 +/- 4.9% of initial vs. 24.1 +/- 0.9 and 56.1 +/- 4.3% of initial for the non-preconditioned group). The mitochondrial oxygen consumption capacity and the adenine nucleotide translocator content of the non-preconditioned heart were decreased by sustained ischemia and remained decreased throughout reperfusion. Preconditioning prevented these decreases. The tissue lactate level of the non-preconditioned heart was high throughout reperfusion (16.5-fold vs. basal), whereas in the preconditioned heart it returned to the basal level within a few minutes of reperfusion. Furthermore, the ratios of [fructose 1,6-bisphosphate]/([glucose 6-phosphate] + [fructose 6-phosphate]) at 5-min reperfusion were higher (2.2-fold) than those of the non-preconditioned heart. CONCLUSIONS: The results suggest that preconditioning preserves the capacity for normal mitochondrial function and the facilitation of glycolysis during reperfusion, which may play an important role in the improvement of postischemic contractile function and high-energy phosphate content.

Adenosine Triphosphate

Beta-adrenoceptor stimulation-mediated preconditioning-like cardioprotection in perfused rat hearts.

To determine whether adrenergic stimulation induces preconditioning-like cardioprotection, rat hearts were perfused for 2 min with either norepinephrine, phenylephrine, or isoproterenol followed by 10-min drug-free perfusion. Then the hearts were subjected to 40-min ischemia and 30-min reperfusion. Little recovery of left ventricular developed pressure (LVDP) and loss of the myocardial creatine kinase (CK) during reperfusion were observed in the drug-untreated heart. Preperfusion with norepinephrine (0.25 microM) or isoproterenol (0.25 microM), but not phenylephrine (10 microM), resulted in a better recovery of LVDP in the postischemic reperfused heart and a reduction in CK release during reperfusion. A similar improvement of postischemic cardiac contractile dysfunction and CK loss was seen in the heart subjected to 5-min ischemia followed by 5-min reperfusion (ischemic preconditioning) before the prolonged period of ischemia/reperfusion. Pretreatment with timolol, a beta-adrenoceptor blocker, abolished the protective effect of norepinephrine, whereas pretreatment with bunazosin, an alpha 1-adrenoceptor blocker, did not affect the protective effect of isoproterenol. The results suggest that a brief period of stimulation of cardiac beta-adrenoceptor exerts the preconditioning-mimetic protective effect against postischemic contractile dysfunction in perfused rat hearts.

Adrenergic alpha-Agonists

Diagnosis of quinolone-induced arthropathy in juvenile dogs by use of magnetic resonance (MR) imaging.

The present study was carried out to confirm whether arthropathy in juvenile dogs induced by ofloxacin, a new quinolone antibacterial agent, may be diagnosed by magnetic resonance (MR) imaging. Three-month-old male beagle dogs were orally administered ofloxacin at 20 mg/kg once daily for 7 consecutive days. On day 8, MR images were obtained with a 4.7-tesla (T) super-conductive high magnetic field strength unit. An irregular cartilage surface and dissecans changes in the distal femoral condyle were observed. These MR findings were essentially consistent with pathologic observation showing multifocal blisters on the articular cartilage with an increased amount of turbid synovial fluid in the joint. The results demonstrate that occurrence of ofloxacin arthropathy in juvenile dogs can be clearly diagnosed by use of MR imaging.

Administration, Oral

Hypoxic preconditioning in isolated rat hearts: non-involvement of activation of adenosine A1 receptor, Gi protein, and ATP-sensitive K+ channel.

Activation of the adenosine A1(A1) receptor, Gi protein, and ATP-sensitive K+ (KATP)-channel system has been shown to play an important role in the cardioprotective effects of ischemic preconditioning in dogs. The present study was undertaken to elucidate the possible involvement of this system in hypoxic preconditioning, which ameliorates injury induced by prolonged ischemia and subsequent reperfusion in perfused rat hearts. Ten minutes of hypoxic preconditioning resulted in an appreciable improvement of post-ischemic cardiac contractile recovery. This was associated with a significant reduction in the release of creatine kinase (CK) from reperfused hearts. Hypoxic preconditioning shortened the time to ischemic contracture onset and prevented a further rise in left ventricular end-diastolic pressure (LVEDP) during reperfusion. Neither the selective A1 receptor antagonist, 8-cyclopentyltheophylline (CPT) nor the KATP channel blocker, glibenclamide, altered the beneficial effects of hypoxic preconditioning. In vivo pretreatment with an inhibitor of Gi protein, pertussis toxin (PTX), also did not diminish the preconditioning effect. The results suggest that, although hypoxic preperfusion ameliorates post-ischemic contractile dysfunction, neither the activation of the A1 receptor, nor the opening of the KATP-channel, nor transduction through Gi protein are involved in the post-ischemic functional recovery of hypoxic preconditioning in the perfused rat heart.

Adenosine Triphosphate

Effects of premotion silent period on single motor unit firing at initiation of a rapid contraction.

We compared the single motor unit (SMU) activity between movements with a premotion silent period (PMSP) and without PMSP in EMG. Fourteen SMUs in the gastrocnemius muscle and 6 SMUs in the soleus muscle were recorded from 5 volunteers during isometric plantar flexion. Tonically firing SMUs failed to fire just before the onset of a rapid contraction with PMSP more frequently than without PMSP. SMUs tended to fire within 10 msec (the gastrocnemius SMUs) or 20 msec (the soleus SMUs) from the onset of the phasic EMG discharge when PMSP occurred. In a rapid contraction without PMSP, the initial firing of SMUs occurred with longer latency than that in a rapid contraction with PMSP. The latency of the initial SMU firing in a rapid contraction related to the preceding time of the last SMU firing during a sustained contraction to the onset of the phasic EMG discharge. When the preceding firing was long enough, the latency distributed around 10 msec. On the other hand, for shorter preceding times, the latency lengthened with shortening of the preceding time. It is suggested that the PMSP makes the preceding time long and increases the susceptibility of motor units to the descending command at the initiation of a rapid contraction.

Adult

Reperfusion at reduced flow rates enhances postischemic contractile recovery of perfused heart.

The effects of reperfusion at reduced flow rates on postischemic cardiac contractile function were examined in perfused rat hearts. Isolated hearts were subjected to 35-min ischemia followed by reperfusion at the preischemic flow rate (9.0 ml.g-1.min-1; ordinary flow rate) or at reduced flow rates (0.9-8.1 ml.g-1.min-1). Reperfusion at ordinary flow rate did not generate any left ventricular developed pressure (LVDP), whereas reperfusion at reduced flow rates (0.9-7.2 ml.g-1.min-1) elicited 13-57% of initial contractile force at reperfusion's end; optimal recovery occurred at 3.6 ml.g-1.min-1 (reduced flow rate). Reduced flow rate reperfusion attenuated ischemia-reperfusion-induced increase in left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP), alteration in tissue Na+, K+, Ca2+, and Mg2+, release of creatine kinase and ATP metabolites, and development of triphenyltetrazolium chloride-unstained areas. Enhanced postischemic LVDP recovery was inversely related to higher coronary PP at the initial stage (4 min) of reperfusion (r = -0.763). The benefit of reduced flow rate reperfusion could not be attributed to rate of calcium delivery to the heart, formation of oxygen free radicals in myocardium, endothelium-dependent coronary artery dilation, or LVDEP reduction. Enhancement of postischemic LVDP recovery was associated with attenuation of ischemia-reperfusion-induced increases in myocardial sodium and calcium; failure of postischemic LVDP recovery was accompanied by an increase. Reduction in sodium and calcium overload may underlie the beneficial effects of reduced flow rate reperfusion in ischemic-reperfused heart.

Adenosine Triphosphate

Relationship of task strain and physical strength to end-of-work fatigue among nurses at social welfare facilities.

To study the relationship of task strain and physical fitness to fatigue among nurses employed at social welfare facilities, we investigated the degree of habitual end-of-work fatigue among 99 nurses (ages 20-49 years) in its relationship to both the degree of strain in various tasks and various indices of physical fitness. Results were as follows: (1) Fatigue complaint rates were nearly the same (35-38%) regardless of age. (2) Mean arm power and maximal oxygen uptake (VO2max) were significantly lower in a high degree of fatigue group than a low degree of fatigue group. (3) Four of 21 tasks elicited strain complaint rates greater than 50%: "nursing of seriously ill patients", "nursing of medical device-assisted patients", "bathing care", and "excretory/diaper changing care". (4) Significant positive correlations were noted between the degree of fatigue and the degree of strain complaint with regard to "nursing of medical device-assisted patients", "bathing care", and "excretory/diaper changing care". (5) Strain complaint rates were significantly higher in a low arm power group than a high arm power group with regard to "nursing of seriously ill patients", "nursing of medical device-assisted patients", and "excretory/diaper changing care". (6) Strain complaint rates were significantly higher in a low VO2max group than a high VO2max group with regard to "nursing of medical device-assisted patients", "bathing care", and "excretory/diaper changing care". These results suggest the need for measures to alleviate task strain and to increase arm strength and overall stamina so that nursing work does not result in excessive fatigue.

Adult

Quantitative analysis of immunohistochemical distributions of cholinergic and catecholaminergic systems in the human brain.

The distributions of the cholinergic system and catecholaminergic system in the normal human brain were analysed quantitatively by a microphotometry system. Consecutive coronal sections were obtained from the anterior area of the left hemisphere and were stained alternately with fluorescent immunohistochemical staining for choline acetyltransferase or tyrosine hydroxylase. Each stained section was divided into approximately 120,000 areas and the fluorescence intensity in each area was measured by a fluorescence microphotometry system which is a measuring microscope for distribution of fluorescence intensity in the tissue slice. Nonspecific autofluorescence was distributed in myelinated nerve fiber throughout the entire area, which was subtracted from the fluorescence intensity value in each measuring area. The obtained immunohistochemical fluorescence intensities of choline acetyltransferase and tyrosine hydroxylase were classified into eight ranks and were indicated by color graphics. Also, the intensity values of actual immunohistochemical fluorescence in the various brain regions were presented. The choline acetyltransferase and tyrosine hydroxylase concentrations varied greatly depending on the brain region. Relatively high levels of choline acetyltransferase and tyrosine hydroxylase were distributed in the putamen, caudate nucleus, claustrum, insula and some cortical regions. The immunohistochemical level of tyrosine hydroxylase was lower than that of choline acetyltransferase in a few brain regions such as the globus pallidus and amygdala. High levels of choline acetyltransferase and tyrosine hydroxylase were localized in the one area of the basal ganglia which developed from the telencephalic area, whereas middle levels of these were distributed in another, part of which developed from the diencephalic area.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine

Stereochemistry during aflatoxin biosynthesis: conversion of norsolorinic acid to averufin.

A reaction sequence, norsolorinic acid (NA)-->averantin (AVN)-->5'-hydroxyaverantin (HAVN)-->averufin (AVR), is the early part of a biosynthetic pathway for aflatoxins. In this study, we determined the stereochemical relationship among these metabolites by using chiral high-performance liquid chromatography. In cell-free experiments using the cytosol fraction of Aspergillus parasiticus NIAH-26, (1'S)-AVN was exclusively produced from NA in the presence of NADPH. Also, only (1'S)-AVN, and not (1'R)-AVN, served as a substrate for the reverse reaction from AVN to NA. When the microsome fraction of NIAH-26 was incubated with (1'S)-AVN in the presence of NADPH, two HAVN diastereomers and one AVR enantiomer were formed, whereas these substances were never produced from (1'R)-AVN. Moreover, (1'S,5'R)-AVR was exclusively formed from both HAVN diastereomers by the cytosol fraction in the presence of NAD. The feeding experiments using this mutant showed that aflatoxins were produced from (1'S,5'R)-AVR but not from (1'R,5'S)-AVR. These results indicate that the enzymes involved in this pathway show strict stereospecificity to their substrates and that the configuration of (1'S,5'R)-AVR leading to the formation of aflatoxins is due to the stereospecificity of NA dehydrogenase which catalyzes the reaction between (1'S)-AVN and NA.

Aflatoxins

Stereochemistry during aflatoxin biosynthesis: cyclase reaction in the conversion of versiconal to versicolorin B and racemization of versiconal hemiacetal acetate.

(1'R,2'S)-(-)-aflatoxins are produced from racemic versiconal hemiacetal acetate (VHA) through complicated pathways, including a metabolic grid involving VHA, versiconol acetate (VOAc), versiconol, and versiconal (VHOH), and a reaction sequence from VHOH to versicolorin A (VA) through (-)-versicolorin B (VB) [or (+/-)-versicolorin C] (K. Yabe, Y. Ando, and Y. Hamasaki, J. Gen. Microbiol. 137:2469-2475, 1991; K. Yabe, Y. Ando, and T. Hamasaki, Agric. Biol. Chem. 55:1907-1911, 1991). In this study, we examined stereochemical changes of substances formed during the conversion of VHA to VA by using chiral high-performance liquid chromatography. In cell-free experiments using the cytosol of Aspergillus parasiticus NIAH-26, both (2'S)- and (2'R)-VOAc enantiomers were formed at about a 1:2 ratio from racemic VHA in the presence of NADPH and dichlorvos (dimethyl 2,2-dichlorovinylphosphate). Also, the esterase activity catalyzing the conversion of VHA to VHOH or of VOAc to versiconol did not show the stereospecificity for the 2' carbon atom of VHA or VOAc. However, when racemic VHA or racemic VHOH was incubated with the cytosol, (1'R,2'S)-(-)-VB was formed exclusively. Furthermore, only (1'R,2'S)-(-)-VB, and not (1'S,2'R)-(+) antipode, served as a substrate for desaturase activity in the microsome fraction catalyzing the conversion of VB to VA. These results demonstrate that the stereoconfiguration of bis-furan moiety in aflatoxin molecules is determined by the cyclase enzyme catalyzing the reaction from VHOH to VB, and the (1'R,2'S)-(-) configuration was further confirmed by the subsequent desaturase reaction. Remarkably, we found nonenzymatic racemization in both the (2'R)- and (2'S)-VHA enantiomers, and it was dependent upon the temperature and alkaline conditions.

Aflatoxins

Quantitative immunohistochemical distributions of tyrosine hydroxylase and calmodulin in the brains of spontaneously hypertensive rats.

Immunohistochemical distributions of tyrosine hydroxylase and calmodulin in the rat forebrain were analyzed quantitatively as a possible model for the hypertension mechanism. The brain slices of spontaneously hypertensive rats (SHR) at 12 weeks of age were stained immunohistochemically for tyrosine hydroxylase and for calmodulin, and the distributions and amounts of these proteins were measured at 40-microns intervals by a fluorescence microphotometry system in comparison with those in normotensive control, Wistar Kyoto rats (WKY, the parent strain of SHR). Tyrosine hydroxylase levels in the neostriatum, nucleus accumbens, nucleus septi lateralis and tractus diagonalis, and calmodulin levels in the medial part of the neostriatum of SHR were lower than those in WKY. We reported previously that the decrease of the serum calcium level in SHR causes a decrease of the dopamine levels in the neostriatum and nucleus accumbens regions through a calmodulin-dependent system, and subsequent low levels of dopamine in the brain which may produce an increase in blood pressure. Combining this finding and our previous reports, we also suggest that the lower dopamine levels seen in the neostriatum and nucleus accumbens regions of SHR may result from the decrease in tyrosine hydroxylase and/or calmodulin levels in these regions in addition to the abnormality of calcium metabolism, and low levels of dopamine may produce an increase in blood pressure through functions of cerebral dopaminergic neurons and peripheral sympathetic nerves.

Animals

[The effect of a p-phenylenediamine containing hair dye on the Ca2+ mobilization in the chemically skinned skeletal muscle of the rat].

In order to clarify the mechanism of a p-phenylenediamine (PPD)-related occurrence of rhabdomyolysis, the pharmacological effects of PPD, a main component of hair dyes, on the function of the contractile proteins and the sarcoplasmic reticulum (SR) have been investigated in single skeletal muscle fibers of the rat by using the skinned fiber method. The results of our findings are enumerated below 1) A positive contraction of the skinned fibers by the PPD, and a complete suppression of the contraction by Mg2+, and a negative contraction by caffeine while under conditions with 50 mM of PPD were noted, suggesting that the contraction of the muscle by PPD is caused by the release of Ca2+ from the SR. 2) PPD inhibited the Ca2+ uptake by the SR in a concentration-dependent manner. 3) PPD greatly accelerated Ca2+ leakage from the SR, and the number of Ca2+ remnants 3 minutes after the administration of 50 mM of PPD amounted to only 3%. 4) The calcium-induced calcium release (CICR) was accelerated in areas with a low Ca2+ concentration, and the amount of Ca2+ released at a pCa of 7.5 showed an increase of up to 63% on PPD administration of 50 mM. 5) PPD did not influence the Ca2+ sensitivity of the contractile system. It thus has been speculated that PPD can bring about rhabdomyolysis by promoting the CICR and leakage of Ca2+ from the SR, this being followed by an increase in the Ca2+ concentration and by consequent changes that develop in the muscle, such as continuous contraction, an irreversible change in the muscle's structure and/or a hypermetabolic change.

Animals

Quantitative immunohistochemical distribution of choline acetyltransferase in the rostral forebrain of the rat.

The immunohistochemical distribution of choline acetyltransferase (CAT) in the rat rostral forebrain was analyzed quantitatively and minutely by means of a microphotometry system. The CAT concentrations varied greatly depending on the brain region. Within the neostriatum, CAT tended to be distributed with a lateral (high) to medial (low) gradient of approximately 1.2:1 and a caudal (high) to rostral (low) gradient of approximately 1.4:1, with the highest level in the medius lateralis. In the cortex cerebri, the CAT concentration in the area cinguli was high, while those in the area frontalis, area parietalis and area pyriformis were relatively low. High levels of CAT were also localized in other regions: e.g., hippocampus pars posterior, nucleus preopticus, nucleus anterior hypothalami, nucleus interstitialis striae terminalis, nucleus suprachiasmaticus and nucleus accumbens septi. The quantitative data obtained from the present microphotometric examination can be useful for analysis of a dynamic aspect of neurochemical substances under physiological as well as pathological conditions of the brain.

Animals

Multiple analysis of tyrosine hydroxylase and calmodulin distributions in the forebrain of the rat using a microphotometry system.

Immunohistochemical distributions of tyrosine hydroxylase and calmodulin in the rat forebrain were analyzed quantitatively to confirm our previous results that the activities of central catecholamine-synthesizing enzymes are regulated by a calcium-calmodulin-dependent system. The adjacent slices of adult rat brain were stained immunohistochemically for tyrosine hydroxylase and for calmodulin, and the distributions and amounts of these proteins were measured by a fluorescence microphotometry system that was developed in our laboratory. Immunohistochemical fluorescence intensity was measured stepwise at 40 microns intervals through a 6 microns phi (on the slice) pin hole. Each stained brain slice was divided into approximately 100,000 areas, and measured for fluorescence intensity and displayed two- and three-dimensionally. Immunoreactive staining of tyrosine hydroxylase and calmodulin was observed in almost all areas of the brain, but its intensity varied. The relatively high levels of calmodulin could be observed in brain regions with high levels of tyrosine hydroxylase distribution, though high levels of tyrosine hydroxylase could not always be observed in brain regions where high levels of calmodulin were distributed. In the present study, high levels of tyrosine hydroxylase and calmodulin were distributed in the nucleus accumbens septi and the lateral part of the neostriatum regions in which the amount of dopamine was increased by the intraventricular administration of calcium. These findings suggest that the synthesis of central catecholamines is regulated by a calcium-calmodulin-dependent system.

Animals

A metabolic grid among versiconal hemiacetal acetate, versiconol acetate, versiconol and versiconal during aflatoxin biosynthesis.

Dichlorvos treatment of aflatoxigenic Aspergillus parasiticus SYS-4 (NRRL 2999) or a verscolorin A-accumulating mutant, NIAH-9, resulted in accumulation of versiconol acetate (VOAc) and versiconal hemiacetal acetate (VHA), whereas the production of aflatoxins, versicolorin A (VA), and versiconol (VOH) decreased. In feeding experiments using another non-aflatoxigenic mutant, NIAH-26, aflatoxins were newly produced from each of VHA, VOAc, VOH, versicolorin B (VB) and versicolorin C (VC). In these experiments, aflatoxin production from VHA or VOAc was inhibited by dichlorvos, whereas that from each of VOH, VB and VC was insensitive to dichlorvos. In cell-free experiments using the cytosol fraction of NIAH-26, VHA was converted to VC (or VB) and a substance tentatively identified as versiconal (VHOH). By further addition of NADH or NADPH to the same reaction mixture, VOAc and VOH were also formed together with VC (VB) and VHOH. VOH was produced from VOAc irrespective of nicotinamide adenine nucleotide. Also, the incubation of VOH in the presence of NAD or NADP led to the formation of VC (VB). The production of VC (VB) and VHOH from VHA, and that of VOH from VOAc was inhibited by dichlorvos, whereas the production of VOAc from VHA, and that of VC (VB) from VOH, was insensitive to dichlorvos. These results indicate that a metabolic grid catalysed by dehydrogenase and esterase among VHA, VOAc, VOH and VHOH, and a reaction from VHOH to VC (VB) are involved in aflatoxin biosynthesis. These enzyme activities were also detected when yeast extract peptone medium was used, or when A. oryzae SYS-2 was examined.

Aflatoxins