Nucleotide Catabolites Research Articles

DPP9 as a Potential Novel Mediator in Gastrointestinal Virus Infection.

Dipeptidyl peptidase 9 (DPP9) is a member of the dipeptidyl peptidase IV family. Inhibition of DPP9 has recently been shown to activate the nucleotide-binding domain leucine-rich repeat 1 (NLRP1) inflammasome. NLRP1 is known to bind nucleic acids with high affinity and directly interact with double stranded RNA, which plays a key role in viral replication. DPP9 has also recently emerged as a key gene related to lung-inflammation in critical SARS-CoV-2 infection. Importantly, DPP9 activity is strongly dependent on the oxidative status. Here, we explored the potential role of DPP9 in the gastrointestinal tract. We performed transcriptomics analyses of colon (microarray, n = 37) and jejunal (RNA sequencing, n = 31) biopsies from two independent cohorts as well as plasma metabolomics analyses in two independent cohorts (n = 37 and n = 795). The expression of DPP9 in the jejunum, colon, and blood was significantly associated with circulating biomarkers of oxidative stress (uric acid, bilirubin). It was also associated positively with the expression of transcription factors (NRF-2) and genes (SOD, CAT, GPX) encoding for antioxidant enzymes, but negatively with that of genes (XDH, NOX) and transcription factors (NF-KB) involved in ROS-generating enzymes. Gene co-expression patterns associated with DPP9 identified several genes participating in antiviral pathways in both tissues. Notably, DPP9 expression in the colon and plasma was strongly positively associated with several circulating nucleotide catabolites (hypoxanthine, uric acid, 3-ureidopropionic acid) with important roles in the generation of ROS and viral infection, as well as other metabolites related to oxidative stress (Resolvin D1, glutamate-containing dipeptides). Gene-drug enrichment analyses identified artenimol, puromycin, anisomycin, 3-phenyllactic acid, and linezolid as the most promising drugs targeting these DPP9-associated genes. We have identified a novel potential pathogenic mechanism of viral infection in the digestive tract and promising existing drugs that can be repositioned against viral infection.

Rosiglitazone Ameliorates Cardiac and Skeletal Muscle Dysfunction by Correction of Energetics in Huntington's Disease.

Huntington’s disease (HD) is a rare neurodegenerative disease that is accompanied by skeletal muscle atrophy and cardiomyopathy. Tissues affected by HD (central nervous system [CNS], skeletal muscle, and heart) are known to suffer from deteriorated cellular energy metabolism that manifests already at presymptomatic stages. This work aimed to test the effects of peroxisome proliferator-activated receptor (PPAR)-γ agonist—rosiglitazone on grip strength and heart function in an experimental HD model—on R6/1 mice and to address the mechanisms. We noted that rosiglitazone treatment lead to improvement of R6/1 mice grip strength and cardiac mechanical function. It was accompanied by an enhancement of the total adenine nucleotides pool, increased glucose oxidation, changes in mitochondrial number (indicated as increased citric synthase activity), and reduction in mitochondrial complex I activity. These metabolic changes were supported by increased total antioxidant status in HD mice injected with rosiglitazone. Correction of energy deficits with rosiglitazone was further indicated by decreased accumulation of nucleotide catabolites in HD mice serum. Thus, rosiglitazone treatment may not only delay neurodegeneration but also may ameliorate cardio- and myopathy linked to HD by improvement of cellular energetics.

The comparison of nucleotide metabolites and amino acids patterns in patients with eating disorders, with and without symptoms of depression

Purines, pyrimidines, and amino acid level have gained attention recently as potential determinants of mental disorders. However, eating disorders patients (ED) have not been yet appropriately studied, especially subjects with coexisting mood disorders. This paper examines the serum level of nucleotide catabolites and plasma amino acids in eating disorders with hyperphagia, with and without Major Depressive Disorder (MDD). Samples were taken from adult persons suffering from eating disorders (two forms: simple obesity and binge eating disorder) with MDD (n = 20) and without (n = 17). Serum nucleotides and plasma amino acids concentrations were analyzed with high-performance liquid chromatography-mass spectrometry. The nucleotides metabolite in MDD patients had a significantly (p < 0.05) lower uridine. Among MDD patients with ED significantly (p < 0.05) higher levels of asparagine, glutamine, proline, and arginine were found as compared to the control group. This study demonstrated differences in nucleotide metabolite and amino acid pattern in depression patients with eating disorders. This may be relevant to the mechanisms and may help identify biomarkers.

Huntingtin protein maintains balanced energetics in mouse cardiomyocytes

Huntingtin (HTT) is a multifunctional protein crucial for proper embryogenesis and nervous system development. Mutation of a single allele in gene coded this protein results in the Huntington׳s disease (HD). There is growing evidence of cardiovascular system pathologies coexisting with the neurological symptoms in HD patients. Thus, this study aims to establish the role of huntingtin protein in cardiomyocytes cellular energy and nucleotides metabolism. We used HTT KO mice embryonic stem cells (ESC) obtained with CRISPR method, wild type mice ESC treated by CRISPR with Scramble control sequence (SCR) as well as wild type (WT) mice ESC and differentiate it into cardiomyocytes. Analysis of intracellular concentration of ATP, ADP, and NAD+, as well as nucleotide catabolites were performed with HPLC. We noted that HTT null cardiomyocytes showed diminished intracellular ATP (4.9 ± 0.5; 6.7 ± 0.4 nmol/mg protein HTT KO vs. SCR) and NAD+ (0.9 ± 0.1; 1.6 ± 0.1 nmol/mg HTT KO vs. SCR). We noted also reduced cellular medium concentration of total purines pool (17.1 ± 1.7; 24.7 ± 2.7 nmol/ml HTT KO vs. SCR) as well as IMP concentration (7.7 ± 0.6; 10.2 ± 0.4 nmol/ml HTT KO vs. SCR). This study indicates that HTT plays an important role in cellular energy balance as well as in nucleotide metabolism in cardiomyocytes. Furthermore, our findings underline that the deterioration in energy metabolism observed in HD may be caused not only by cellular mutant HTT accumulation but also by the loss of HTT function.

Autophagy Plays Prominent Roles in Amino Acid, Nucleotide, and Carbohydrate Metabolism during Fixed-Carbon Starvation in Maize.

Autophagic recycling of proteins, lipids, nucleic acids, carbohydrates, and organelles is essential for cellular homeostasis and optimal health, especially under nutrient-limiting conditions. To better understand how this turnover affects plant growth, development, and survival upon nutrient stress, we applied an integrated multiomics approach to study maize (Zea mays) autophagy mutants subjected to fixed-carbon starvation induced by darkness. Broad metabolic alterations were evident in leaves missing the core autophagy component ATG12 under normal growth conditions (e.g., lipids and secondary metabolism), while changes in amino acid-, carbohydrate-, and nucleotide-related metabolites selectively emerged during fixed-carbon starvation. Through combined proteomic and transcriptomic analyses, we identified numerous autophagy-responsive proteins, which revealed processes underpinning the various metabolic changes seen during carbon stress as well as potential autophagic cargo. Strikingly, a strong upregulation of various catabolic processes was observed in the absence of autophagy, including increases in simple carbohydrate levels with a commensurate drop in starch levels, elevated free amino acid levels with a corresponding reduction in intact protein levels, and a strong increase in the abundance of several nitrogen-rich nucleotide catabolites. Altogether, this analysis showed that fixed-carbon starvation in the absence of autophagy adjusts the choice of respiratory substrates, promotes the transition of peroxisomes to glyoxysomes, and enhances the retention of assimilated nitrogen.

A model for the biochemical degradation of inosine monophosphate in hake (Merluccius merluccius)

ATP-derived products are typically used as early indicators of fish quality loss during storage. In this work, we explore different biochemical routes that are potentially relevant in contributing to nucleotide degradation in hake (Merluccius merluccius). A major motivation of this study is to get more insight on the biochemical degradation mechanisms of nucleotide catabolites in hake muscle at fish storage and transport conditions. This requires the identification of its relevant pathways.To that purpose, different degradation routes proposed in the literature are considered and a mathematical model for the degradation process is derived. First order kinetics are assumed for all the reactions and temperature dependence is taken into account through the Arrhenius equation. Unknown model parameters, namely activation energies and pre-exponential Arrhenius coefficients, are estimated via fitting to experimental data. From the estimation results, relevant routes are identified. The kinetic study is performed on sterile fish juice to avoid coupling with microbial degradation mechanisms or possible interferences of the food matrix that might hide biochemical interactions.The proposed scheme adequately describes biochemical changes in nucleotide catabolites under variable temperature profiles. It also reveals a pathway which at least seems relevant for nucleotide degradation in hake.

An impaired metabolism of nucleotides underpins a novel mechanism of cardiac remodeling leading to Huntington's disease related cardiomyopathy

Huntington's disease (HD) is mainly thought of as a neurological disease, but multiple epidemiological studies have demonstrated a number of cardiovascular events leading to heart failure in HD patients. Our recent studies showed an increased risk of heart contractile dysfunction and dilated cardiomyopathy in HD pre-clinical models. This could potentially involve metabolic remodeling, that is a typical feature of the failing heart, with reduced activities of high energy phosphate generating pathways. In this study, we sought to identify metabolic abnormalities leading to HD-related cardiomyopathy in pre-clinical and clinical settings. We found that HD mouse models developed a profound deterioration in cardiac energy equilibrium, despite AMP-activated protein kinase hyperphosphorylation. This was accompanied by a reduced glucose usage and a significant deregulation of genes involved in de novo purine biosynthesis, in conversion of adenine nucleotides, and in adenosine metabolism. Consequently, we observed increased levels of nucleotide catabolites such as inosine, hypoxanthine, xanthine and uric acid, in murine and human HD serum. These effects may be caused locally by mutant HTT, via gain or loss of function effects, or distally by a lack of trophic signals from central nerve stimulation. Either may lead to energy equilibrium imbalances in cardiac cells, with activation of nucleotide catabolism plus an inhibition of re-synthesis. Our study suggests that future therapies should target cardiac mitochondrial dysfunction to ameliorate energetic dysfunction. Importantly, we describe the first set of biomarkers related to heart and skeletal muscle dysfunction in both pre-clinical and clinical HD settings.

Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts

IntroductionPostischemic injury to the coronary vascular endothelium, in particular to the endothelial glycocalyx, may provoke fluid extravasation. Shedding of the glycocalyx is triggered by redox stress encountered during reperfusion and should be alleviated by the radical scavenger nitric oxide (NO). The objective of this study was to investigate the effect of exogenous administration of NO during reperfusion on both coronary endothelial glycocalyx and vascular integrity.MethodsIsolated guinea pig hearts were subjected to 15 minutes of warm global ischemia followed by 20 minutes of reperfusion in the absence (Control group) and presence (NO group) of 4 μM NO. In further experiments, the endothelial glycocalyx was enzymatically degraded by means of heparinase followed by reperfusion without (HEP group) and with NO (HEP+NO group).ResultsIschemia and reperfusion severely damaged the endothelial glycocalyx. Shedding of heparan sulfate and damage assessed by electron microscopy were less in the presence of NO. Compared with baseline, coronary fluid extravasation increased after ischemia in the Control, HEP, and HEP+NO groups but remained almost unchanged in the NO group. Tissue edema was significantly attenuated in this group. Coronary vascular resistance rose by 25% to 30% during reperfusion, but not when NO was applied, irrespective of the state of the glycocalyx. Acute postischemic myocardial release of lactate was comparable in the four groups, whereas release of adenine nucleotide catabolites was reduced 42% by NO. The coronary venous level of uric acid, a potent antioxidant and scavenger of peroxynitrite, paradoxically decreased during postischemic infusion of NO.ConclusionThe cardioprotective effect of NO in postischemic reperfusion includes prevention of coronary vascular leak and interstitial edema and a tendency to forestall both no-reflow and degradation of the endothelial glycocalyx.

Intracellular high energy metabolite depletion and cell membrane injury with antioxidant enzymes during oxidant exposure in vitro

We compared oxidant-induced intracellular adenine nucleotide catabolism and cell membrane injury in 4 different human cell types. Responses to oxidant exposure were correlated with endogenous antioxidant enzyme activities in these cells. Blood monocytes, amniotic fibroblasts, umbilical vein endothelial cells in primary culture, and transformed bronchial epithelial cells (BEAS 2B) were exposed to 0.1–5 mM hydrogen peroxide (H 2O 2) for 4 h. Some experiments were conducted in cells pretreated with 3-amino 1:2,4-triazole (ATZ) to inactivate catalase or with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) to inactivate glutathione (GSH) reductase. Depletion of adenine nucleotides and accumulation of their catabolic products (hypoxanthine, xanthine and uric acid) occurred to varying extent, monocytes being the most resistant. There was a mutual relationship between catalase and GSH reductase activities and maintenance of cellular adenine nucleotide levels during H 2O 2 exposure. GSH reductase inhibition rendered BEAS 2B cells susceptible to lytic injury by H 2O 2, assessed by release of lactate dehydrogenase and intact nucleotides into the medium, there was no correlation between these markers of such injury and endogenous antioxidant enzymes. We conclude that adenine nucleotide depletion and nucleotide catabolite accumulation relate closely with the antioxidant enzyme activities, whereas the lack of a similar correlation between the enzyme levels and markers of lytic cell injury suggest that intracellular antioxidant enzymes do not protect cells from membrane damage due to extracellular oxidants.

Neutrophil and asbestos fiber-induced cytotoxicity in cultured human mesothelial and bronchial epithelial cells

This study investigates reactive oxygen species generation and oxidant-related cytotoxicity induced by amosite asbestos fibers and polymorphonuclear leucocytes (PMNs) in human mesothelial cells and human bronchial epithelial cells in vitro. Transformed human pleural mesothelial cells (MET 5A) and bronchial epithelial cells (BEAS 2B) were treated with amosite (2μg/cm 2) for 48 h. After 24 h of incubation, the cells were exposed for 1 h to nonactivated or amosite (50 μg) activated PMNs, washed, and incubated for another 23 h. Reactive oxygen species generation by the PMNs and the target cells was measured by chemiluminescence. Cell injury was assessed by cellular adenine nucleotide depletion, extracellular release of nucleotides, and lactate dehydrogenase (LDH). Amosite-activated (but also to a lesser degree nonactivated) PMNs released substantial amounts of reactive oxygen metabolites, whereas the chemiluminescence of amosite-exposed mesothelial cells and epithelial cells did not differ from the background. Amosite treatment (48 h) of the target cells did not change intracellular adenine nucleotides (ATP, ADP, AMP) or nucleotide catabolite products (xanthine, hypoxanthine, and uric acid). When the target cells were exposed to nonactivated PMNs, significant adenine nucleotide depletion and nucleotide catabolite accumulation was observed in mesothelial cells only. In separate experiments, when the target cells were exposed to amosite-activated PMNs, the target cell injury was further potentiated compared with the amosite treatment alone or exposure to nonactivated PMNs. In conclusion, this study suggests the importance of inflammatory cell-derived free radicals in the development of amosite-induced mesothelial cell injury.

Pattern of AMP degradation in ischemic rabbit lung tissue.

Because adenine nucleotide catabolites may be important during postischemic lung reperfusion, we examined the pathway of adenosine monophosphate (AMP) degradation in ischemic lung tissue. Once the pattern of degradation is known, pharmacological interventions can be considered, offering new methods of reducing lung reperfusion injury. For this purpose we used the isolated rabbit lung. Rabbit lungs were flushed in situ with a modified Krebs Henseleit solution (60 ml/kg). The lungs were removed and stored deflated, immersed in saline solution at 37 degrees C. At regular times, biopsies were taken, and adenine nucleotides, nucleosides, and bases were measured in these biopsies using high performance liquid chromatography (HPLC). During lung ischemia, a very significant increase of inosine monophosphate (IMP) was found. Adenosine levels on the other hand did not increase. Hypoxanthine was the major end catabolite of ischemic lung tissue (constituting 92% of the nucleoside and purine base fraction at 4 hours ischemia). To further determine the pathway of AMP degradation, 400 mM of the adenosine deaminase inhibitor erythro-9-[2-hydroxy-3-nonyl]adenine (EHNA) was added to the lung flush solution. During ischemia, adenosine triphosphate (ATP) breakdown was unaltered but adenosine became the major catabolite (2.8 times the concentration of hypoxanthine at 4 hours ischemia). These data suggest that: 1) in rabbit lung tissue, dephosphorylation of AMP to adenosine is more important than deamination to IMP; 2) hypoxanthine is the major end catabolite of ischemic lung tissue. By inhibiting the enzyme deaminase, reduced hypoxanthine levels and increased adenosine levels were obtained. Pharmacological interventions are now available to interfere with the formation of adenine nucleosides and bases in ischemic lung tissue. The importance of adenine nucleotide catabolites to postischemic lung reperfusion injury is discussed.

Dynamics of energy metabolism in the transplanted human heart during reperfusion

Reperfusion after ischemia of the heart generates further damage to the myocardium through a variety of mechanisms including free radical generation, calcium overload, and abnormalities of energetics. In this study, the uptake and release of metabolites involved in energy metabolism were investigated during 45 minutes of reperfusion of donor human heart after transplantation to evaluate the nature of the metabolic abnormalities and the time course of recovery. Analysis of coronary sinus and arterial blood samples in 11 transplant recipients showed the following: (1) In the first minute of reperfusion, lactate release was observed accompanied by an uptake of pyruvate, resulting in a markedly elevated lactate/pyruvate ratio. The pH value of coronary sinus blood was lower than that of arterial blood by 0.1 unit, inorganic phosphate was released, and a massive efflux of nucleotide catabolites was observed. Hemoglobin oxygen saturation of coronary sinus blood was almost equal to that of arterial blood, showing minimal myocardial oxygen extraction. Coronary flow was approximately 300 ml/min at reperfusion with minor changes in the first minute. (2) From the second minute onward, pyruvate was released for over 45 minutes, contrasting with the first minute of reperfusion. Lactate was significantly released for up to 10 minutes of reperfusion, but myocardial uptake of lactate was not restored by the end of the observation period. However, the lactate/pyruvate ratio in coronary sinus blood recovered at the onset of this phase. Both pH changes in coronary sinus blood and phosphate release were restored within 5 minutes, but release of nucleotide catabolites was still significant after 30 minutes of reperfusion. The oxygen saturation of hemoglobin in coronary sinus blood decreased gradually in a biphasic mode over the 45 minutes, indicating gradual restoration of myocardial oxygen uptake. Coronary flow measured for up to 10 minutes of reperfusion decreased to a minimal value of 200 ml/min in the third minute, followed by restoration of initial flow. These data highlight the profound alterations in energy metabolism that occur during reperfusion of the transplanted heart. These changes, which may result from the preceding ischemia and impaired oxidative metabolism at the onset of reperfusion, were partially reversed in the first minutes. However, impaired pyruvate and lactate use and underperfusion reflected by the release of purine catabolites persisted for a period of more than 30 minutes of reperfusion.

Liquid chromatographic evaluation of purine production in the donor human heart during transplantation.

A reversed phase high performance liquid chromatographic technique is presented allowing purine catabolite determination in a whole blood extract without a prior purification step. The method was applied to determine the timing and the profile of myocardial nucleotide catabolite release during reperfusion of the transplanted human heart. Samples of arterial and coronary sinus blood collected at various times within 1 h after aortic declamping during heart or heart-lung transplantations were used for nucleotide catabolite determination. Massive release of inosine and hypoxanthine from the heart was demonstrated. Production of adenosine was also shown but there was no liberation of xanthine or uric acid. Nucleotide catabolite release was greatest in the first 5 min (coronary sinus-arterial difference = 15-20 microM), but was still significant after 30 min of reperfusion. The determination of inosine and hypoxanthine--major catabolites released--was found to be reproducible in coronary sinus blood (coefficient of variation < 10%). However, immediate protein precipitation afer blood sample collection was necessary, as rapid metabolism of both exogenous and endogenous adenosine and inosine was demonstrated.

Adenine nucleotide catabolism in human myocardium during heart and heart-lung transplantation.

The influence of ischemia and reperfusion on nucleotide concentration in human myocardium was investigated during heart and heart-lung transplantation. Myocardial preservation during heart transplantation was achieved by infusion of cold St. Thomas' Hospital cardioplegic solution followed by storage in Ringer's solution at 4 degrees C during transport. In contrast, the hearts of heart and lung donors were preserved by core cooling using cardiopulmonary bypass and infusion of cold blood cardioplegia containing 26 mM potassium. The heart-lung block was transported in cold donor blood. Nucleotides and their catabolite concentrations were measured in donor tissue specimens taken before organ collection, before commencement of implantation and 30 min after aortic clamp removal. During reperfusion, samples of coronary sinus and arterial blood were collected and analysed for nucleotide catabolite concentration. Myocardial ATP and total nucleotide pool remained almost unchanged during the ischemic transport of the donor organs with only very small increases in myocardial inosine and hypoxanthine concentrations. However, a significant decrease of total adenine nucleotide pool by 10%-20% was demonstrated between the start of implantation and 30 min post-reperfusion. A release of inosine + hypoxanthine was greatest in the 1st minute (15-25 microM), but was still substantial after 10 min of reperfusion (5-15 microM). Metabolic changes tended to be more pronounced during heart-lung transplantation than during heart transplantation.

Effect of exogenous adenosine deaminase on arrhythmias and the release of adenine nucleotide catabolites in isolated rat hearts with coronary occlusion and reperfusion

In isolated perfused rat hearts with occlusion of the left coronary artery the release of adenosine and its degradation products inosine, hypoxanthine, xanthine and uric acid was investigated with and without exogenous addition of adenosine deaminase. In the control experiments large amounts of the adenine nucleotide catabolites appeared in the perfusate during coronary reperfusion. The greater part was represented by adenosine and inosine. During the coronary occlusion itself only a minor increase in the release of adenine nucleotide catabolites was observed, compared with the basal release before the coronary occlusion. Depending on the duration of the coronary occlusion more or less severe tachyarrhythmias occurred during the reperfusion of the previously ischaemic myocardium. Reperfusion-induced ventricular fibrillation was associated with a significant increase in the release of adenine nucleotide catabolites, compared with non-fibrillating hearts. In the presence of exogenously-added adenosine deaminase the release of adenine nucleotide catabolites from reperfused hearts was further increased. Adenosine itself, however, almost completely disappeared from the perfusate. In adenosine-deaminase treated hearts the incidence of reperfusion-induced fibrillation increased, thereby contributing to the enhanced release of adenine nucleotide catabolites. However, the release was also increased by the enzyme when only the fibrillating hearts were considered, suggesting that rapid elimination of adenosine from the interstitial space also directly increases the release of adenine nucleotide catabolites from the heart.

Nucleotide catabolite release and myocardial contractility after short and prolonged ischemia

Nucleotide catabolite release and myocardial contractility after short and prolonged ischemia

The influence of calcium antagonists on the adenine nucleotide metabolism in the guinea-pig working heart during ischaemia and reperfusion

With the aim of gaining more insight into the metabolism of adenine nucleotides in working normoxic guinea-pigs and in hearts subjected to 45 min of global ischaemia and subsequent reperfusion for 25 min, we evaluated the effect of nifedipine, verapamil, diltiazem, bepridil, CERM 11956, lidoflazine, mioflazine and dipyridamole on the adenine nucleotide catabolite levels in these hearts. The drugs were applied at the concentrations that reduced the aortic dP/dt of normoxic working hearts by 10% (EC10) and 30% (EC30). In globally ischaemic hearts there was a large accumulation of adenine nucleotide catabolites. Inosine proved to be the major catabolite. The drugs, with the exception of bepridil, CERM 11956 and dipyridamole (3 mumol/l), decreased the accumulation of catabolites. In hearts treated with mioflazine and dipyridamole the amount of adenosine increased. A deficit in the balance between adenine nucleotides and catabolites indicated that in globally ischaemic hearts there was a large accumulation of inosine monophosphate. Indeed, a substantial amount of inosine monophosphate was determined in untreated hearts, and hearts treated with nifedipine (EC30) and mioflazine (EC10). During the first 5 min of reperfusion a large quantity of catabolites, mainly inosine, was washed out. During 20 min of subsequent reperfusion in untreated hearts and in nifedipine and mioflazine-treated hearts the efflux of catabolites returned to normoxic values. Similar to the effect in ischaemic hearts, in early perfusate from lidoflazine, mioflazine and dipyridamole-treated hearts the adenosine/inosine ratio was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of gamma irradiation on the keeping quality and nutrients of tilapia (Oreochromis mossambicus) and silver carp (Hypophthalmichthys molitrix) stored at 1.C

Fillets (skin on) obtained from freshly killed tilapia (Oreochromis mossambicus Peters) and silver carp (Hypophthalmichythys molitrix Curier & Valenciennes) were gamma irradiated at 1.0 kGy at 2–4.C. The chemical con position and thiamin and riboflavin contents of irradiated fish fillets were analysed and compared with those of the non-irradiated fish. Loss of thiamin content of silver carp fillets was significant whereas the thiamin content of tilapia and other constituents of tilapia and silver carp were unaffected. Irradiation at 1.0 kGy markedly reduced the bacterial level of tilapia and silver carp. No significant increase in total counts in both irradiated and non-irradiated samples was found during 5 days' storage at 1.C. The pattern of nucleotide changes in tilapia and silver carp was different. Irradiation had little effect on the concentrations of nucleotide catabolites in both species. Sensory evaluation of flesh colour and flavour was conducted after 5 days' refrigerated storage. Except that the colour of irradiated carp was more reddish, there were no significant differences in other qualities.

Shelf‐life of Sterile Snapper (Chrysophrys auratus)

ABSTRACTThe deterioration of snapper (Chrysophrys aurutus) held at 0°C in the presence or absence of bacteria was studied using frozen fillets held at ‐30°C as a reference. Chilled snapper with or without bacteria lost the characteristics of fresh snapper by 9 days and developed unpleasant odors and flavors by 15 days storage. Over this period the sterile portions were never of a better quality than those undergoing normal microbial spoilage. Regression equations for predicting fish quality from the levels of nucleotide catabolites were considered.

Uric acid, the major adenine nucleotide catabolite released from isolated perfused guinea pig hearts, is formed in the coronary endothelium

Uric acid, the major adenine nucleotide catabolite released from isolated perfused guinea pig hearts, is formed in the coronary endothelium