Uridine is one of the essential nutrients in organisms. To maintain normal cell growth and intracellular metabolism, the uridine must be maintained at certain concentration. Recent studies have shown that uridine can reduce inflammatory response in organisms, participate in glycolysis, and regulate intracellular protein modification, such as glycosylation and acetylation. Furthermore, it can protect cells from hypoxic injury by reducing intracellular oxidative stress, promoting high-energy compounds synthesis. Previous studies have shown that the protective effects of uridine are closely related to its effect on mitochondria. This review summarizes the effect of uridine on mitochondrial function.
Uridine/metabolism* ; Mitochondria/metabolism*

Ginsenoside F1 is a rare ginsenoside in medicinal plants such as Panax ginseng,P. notogingseng and P. quinquefolius. It has strong pharmacological activities of anti-tumor,anti-oxidation and anti-aging. In order to directly produce ginsenoside F1 by using inexpensive raw materials such as glucose,we integrated the codon-optimized P.ginseng dammarenediol-Ⅱ synthase(Syn Pg DDS),P.ginseng protopanaxadiol synthase(Syn Pg PPDS),P. ginseng protopanaxatriol synthase(Syn Pg PPTS) genes and Arabidopsis thaliana cytochrome P450 reductase(At CPR1) gene into triterpene chassis strain BY-T3. The transformant BY-PPT can produce protopanaxatriol. Then we integrated the Sacchromyces cerevisiae phosphoglucomutase 1(PGM1),phosphoglucomutase 2(PGM2) and UDP-glucose pyrophosphorylase 1(UGP1) genes into chassis strain BY-PPT. The UDP-glucose supply module increased UDP-glucose production by 8. 65 times and eventually reached to 44. 30 mg·L-1 while confirmed in the transformant BY-PPT-GM. Next,we integrated the UDPglucosyltransferase Pg3-29 gene which can catalyze protopanaxatriol to produce ginsenoside F1 into chassis strain BY-PPT-GM. The transformant BY-F1 produced a small amount of ginsenoside F1 which was measured as 0. 5 mg·L-1. After the fermentation process was optimized,the titer of ginsenoside F1 could be increased by 900 times to 450. 5 mg·L-1. The high-efficiency UDP-glucose supply module in this study can provide reference for the construction of cell factories for production of saponin,and provide an important basis for further obtaining high-yield ginsenoside yeast cells.
Ginsenosides/metabolism* ; Glucose ; Panax ; Saccharomyces cerevisiae/metabolism* ; Uridine Diphosphate Glucose

Oxidative Phosphorylation ; Acetylglucosamine ; Uridine Diphosphate N-Acetylglucosamine/metabolism*

Activities of hepatic cytosol enzymes involved in UDP-g1ucuronic acid synthesis as well as in glutathione reduction and conjugation systems were determined following administrations of butylated hydroxyanisole (approximately 5 mmol/kg body weight/day) and of equimolar intake doses of its structural anglogs. These compounds included the multi-functional group side chain compounds (t-butyl hydroquinone, 4-hydroxy- anisole, hydroquinone, benzoquinone) and the mono-functional side chain compounds (t-butyl benzene, anisole, phenol). They were administered to mice for 10 days either by mixing them in the diet or by oral intubations. Results showed that glutathione Stransferase activities were markedly increased by all tested compounds except for the t-butyl benzene. Activities of glutathione reductase and glucose 6-phosphate dehydrogenase were increased together on1y by BHA and t-butyl hydroguinone. UDP-glucose dehydrogenase and NADH:quinone reductase activities were significantly elevated by the multi-functional side chain compounds, but not by the mono-functional analogs. The relations between chemical structures of tested BHA analogs and elevations of the measured hepatic cytosol conjugation (detoxification) system enzyme activities for the metabolism and excretion of BHA analogs are discussed.
Animal ; Anisoles/metabolism* ; Butylated Hydroxyanisole/analogs & derivatives ; Butylated Hydroxyanisole/metabolism* ; Cytosol/enzymology* ; Glutathione/metabolism* ; Mice ; Uridine Diphosphate Glucuronic Acid/biosynthesis* ; Uridine Diphosphate Sugars/biosynthesis*

In plants, UDP-L-rhamnose is one of the major components of cell wall skeleton. Rhamnose synthase plays a key role in rhamnose synthesis which converts UDP-D-glucose into UDP-L-rhamnose in plants. In this study, we isolated the 1058 bp promoter region of the rhamnose synthase gene AtRHM1 from Arabidopsis genome by PCR, and created a series of deletions of AtRHM1 promoter ranging from -931 bp to +127 bp. The full length of the promoter and its deletion derivatives fused with GUS reporter gene were introduced into wild-type Arabidopsis by Agrobacterium-mediated transformation respectively. The GUS staining and GUS enzymatic activity assay showed that the expression of AtRHM1 is induced at transcriptional level by glucose and the regulatory elements involved in the glucose response are located in the region of -931 bp - -752 bp which contains three G-box motifs.
Arabidopsis ; genetics ; Arabidopsis Proteins ; genetics ; Glucosyltransferases ; genetics ; Plants, Genetically Modified ; genetics ; Promoter Regions, Genetic ; Uridine Diphosphate Glucose ; genetics ; metabolism ; Uridine Diphosphate Sugars ; genetics ; metabolism

Uridine-cytidine kinase, an important catalyst in the compensation pathway of nucleotide metabolism, can catalyze the phosphorylation reaction of cytidine to 5'-cytidine monophosphate (CMP), but the reaction needs NTP as the phosphate donor. To increase the production efficiency of CMP, uridine-cytidine kinase gene from Thermus thermophilus HB8 and polyphosphate kinase gene from Rhodobacter sphaeroides were cloned and expressed in Escherichia coli BL21(DE3). Uridine-cytidine kinase was used for the generation of CMP from cytidine and ATP, and polyphosphate kinase was used for the regeneration of ATP. Then, the D403 metal chelate resin was used to adsorb Ni²⁺ to form an immobilized carrier, and the immobilized carrier was specifically combined with the recombinant enzymes to form the immobilized enzymes. Finally, single-factor optimization experiment was carried out to determine the reaction conditions of the immobilized enzyme. At 30 °C and pH 8.0, 60 mmol/L cytidine and 0.5 mmol/L ATP were used as substrates to achieve 5 batches of high-efficiency continuous catalytic reaction, and the average molar yield of CMP reached 91.2%. The above method has the advantages of low reaction cost, high product yield and high enzyme utilization rate, and has good applied value for industrial production.
Cytidine Monophosphate ; metabolism ; Escherichia coli ; genetics ; Industrial Microbiology ; methods ; Phosphotransferases (Phosphate Group Acceptor) ; metabolism ; Uridine Kinase

The energy metabolism of the brain has been measured in cat model using high performance liquid chromatography(HPLC). The experimental groups were divided into three according to the duration of ischemia. In 1- and 3-hour ischemia groups, recirculation had increased the ATP, UTP and GTP significantly to 39-49%, 53-57% and 39-62% of the sham control value respectively. Also in these groups, recirculation had increased adenylate energy charge(E.C.) to 75-82% of sham control value. Whereas there were slight increase in adenylate E.C. after recirculation in 5-hr ischemia group, with the remainders not increasing significantly. The Na+, K+-ATPase activities were not significant statistically among the groups. These results suggest that in order to prevent from the irreversible ischemic brain damage, restoration of blood flow must be accomplished within 3 hours from the onset of the acute focal ischemia in cat.
Adenosine Triphosphate ; Animals ; Brain ; Cats ; Chromatography, High Pressure Liquid ; Energy Metabolism* ; Guanosine Triphosphate ; Ischemia ; Uridine Triphosphate

Galactosemia, a term that denotes the presence of galactose in the blood, is the name of rare inborn error of galactose metabolism due to a deficiency of the enzyme galactokinase (GALK), galactose-1-phosphate uridyltransferase (GALT) and uridine diphosphate-galactose 4-epimerase (GALE). GALT deficiency is the most common and shows the most severe clinical manifestation, including hepatomegaly, cataracts, and mental retardation. The main symptom of GALT deficiency is juvenile cataracts. GALE deficiency has two different forms; benign and severe forms. The benign form has no clinical significance, however, the severe form shows the same clinical manifestations as those of GALT deficiency.
Cataract ; Galactokinase ; Galactose ; Galactosemias* ; Hepatomegaly ; Intellectual Disability ; Metabolism ; Uridine ; UTP-Hexose-1-Phosphate Uridylyltransferase

The study was designed to examine the effects of pretreatment with mannitol, methyl prednisolone and nimodipine on the acute focal cerebral ischemia in the cats of occlusion of the proximal part of the middle cerebral artery via the postorbital approach. The energy metabolisms of the brain was measured utilizing the high liquid performance chromatography in the brain tissues of cats. The experimental animals were seperated into 3 groups. group I: the sham control group. group II: the recirculation group. group III: the treatment group. There were significant increase in the ATP, GTP, UTP and E.C. levels in focal ischemic cerebral tissues of the treatment group when compared with the recirculation group. It is suggested that pretreatment with the combination of these drugs may prevent the ischemic damage from the acute focal cerebral ischemia by the maintenance of high energy metabolites. However further studies should determine the synergistic pharmacologic mechanisms in this therapeutic strategy.
Adenosine Triphosphate ; Animals ; Brain ; Brain Ischemia* ; Cats ; Chromatography ; Energy Metabolism ; Guanosine Triphosphate ; Mannitol ; Middle Cerebral Artery ; Nimodipine ; Prednisolone ; Uridine Triphosphate

Uridine 5'-triphosphate (UTP) is stored in the granules of cells such as platelets and is released into the extracellular space upon cell stimulation. Extracellular UTP is known to influence many biological processes. We investigated the hemodynamic effects of UTP on the perfused rat liver and characterized its receptors. Liver perfusions were performed in a recirculation system under constant pressure (28 cmH2O). The perfusion flow and oxygen consumption rate were measured at 30 second intervals. UTP decreased the perfusion flow and the oxygen consumption rate, dose-dependently. UTP-induced changes were transient and disappeared in about 10 minutes. Suramin (P2-purinergic antagonist, 100 uM) and indomethacin (cyclooxygenase inhibitor, 20 uM) blocked UTP-induced hemodynamic changes significantly. The effects of UTP were also inhibited when Kupffer cells were damaged with treatment of gadolinium chloride (10 mg/kg iv). L-NAME (1 mM), a potent inhibitor of nitric oxide synthase, markedly enhanced and prolonged the contractile response of UTP in the hepatic vessel. These results suggest that UTP acts mainly on suramin-sensitive UTP receptors on the Kupffer cell through prostanoid synthesis. The nitric oxide systems in the endothelium seem to counteract the vasoconstrictile action of UTP in the hepatic circulation.
Animal ; Extracellular Space/*metabolism ; Hemodynamics ; Liver/*metabolism ; *Liver Circulation ; Perfusion ; Rats ; Rats, Sprague-Dawley ; Support, Non-U.S. Gov't ; Uridine Triphosphate/*metabolism