Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OROTIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1975

Citric, orotic, and other organic acids in rats injected with active or inactive urease.

Male rats were fed laboratory chow or a purified L-amino acid diet containing 11.2 or 5.6 g arginine/kg. Hyperammonemia was produced by injection of crystalline jackbean urease. Control animals were injected with saline or inactivated urease. Rats injected with 55 U urease activity/kg body wt (an LD50 dose) exhibited acute signs of hyperammonemia and elevated orotate and citrate in their urine. Plasma glucose, lactate, citrate, and alpha-ketoglutarate concentrations were also markedly elevated. Three injections of active urease (10 U/kg body wt) given at intervals of about 10 h produced hyperammonemia, which persisted for 25 h after the first injection. Blood glucose and ammonia concentrations were increased 2.6- and 22-fold, respectively, when compared with controls. Total urinary citrate excretion for 25 h was 371 mueq for active urease-injected rats compared with 62 mueq for rats injected with inactivated urease. Rats fed a purified amino acid diet containing 5.6 g arginine/kg excreted greater quantities of urea, citrate, and orotic acid than rats fed 11.2 g arginine/kg of diet. Injection of active urease increased citrate excretion by rats fed either concentration of dietary arginine. Changes produced with active urease were not observed if inactivated urease was injected.

Acetates↗
PubMed2002

Steatosis is not sufficient to cause an impaired regenerative response after partial hepatectomy in rats.

BACKGROUND/AIMS: Fatty liver is known to be associated with increased mortality and morbidity after liver resection. The ability of fatty liver to regenerate after two-thirds partial hepatectomy was studied in three different models of steatosis in rats: obese Zucker rats, orotic acid-fed Wistar rats and Wistar rats fed a methionine-low, choline-deficient diet. METHODS: Liver regeneration was assessed 24 h after partial hepatectomy by bromodeoxyuridine incorporation (immunohistochemistry), proliferating cell nuclear antigen, cyclin E and cyclin-dependent kinase 2 protein expression (Western blot analysis) and cyclin-dependent kinase 2 activity (kinase assays using histone H1 as a substrate). RESULTS: No significant difference of proliferative response was found between orotic acid or methionine-low, choline-deficient diet-fed and control Wistar rats 24 h after partial hepatectomy. In contrast, hepatocyte proliferation in obese Zucker rats after partial hepatectomy was significantly reduced when compared with their lean controls. CONCLUSIONS: Steatosis per se does not impair liver regeneration. The reduced liver regeneration observed in obese Zucker rats may not be due to fatty infiltration itself but to other factors such as leptin receptor dysfunction.

Animal Feed↗
PubMed2004

Response of the senescent heart to stress: clinical therapeutic strategies and quest for mitochondrial predictors of biological age.

The aging heart has an impaired response to many kinds of stress. In clinical practice, there is a need for senescence-specific therapies to protect against stress and for biochemical markers of senescence to identify those patients most in need of therapy. In isolated rat hearts, in human tissues, and in a clinical trial, we have shown previously that coenzyme Q(10) has the ability to protect the heart against stress especially in senescence. We recently have devised a regimen of therapy to protect the senescent heart against stress, combining metabolic therapy (coenzyme Q(10), alpha lipoic acid, magnesium orotate, and omega 3 polyunsaturated fatty acids) with physical exercise and mental stress reduction. The preliminary results of this program are promising. In an endeavor to predict the likely response of individual senescent hearts to stress, we correlated the tissue load of mitochondrial DNA deletions and total cellular mitochondrial DNA copy number in human cardiac tissue with recovery of the same tissue from ischemia/reperfusion stress. We found that these mitochondrial markers actually were less predictive of impaired response to stress than age alone. We conclude that the aging heart has a diminished capacity to recover from stress that is not readily predictable by cardiac content of intact mitochondrial DNA and that this recovery can be improved by metabolic therapy combined with physical exercise and mental stress reduction.

Aging↗
PubMed1987

An arginine-deficient diet in humans does not evoke hyperammonemia or orotic aciduria.

The essentiality of dietary arginine was examined in adult humans with three biochemical indices: plasma levels of ammonium and amino acids and urinary orotic acid excretion. Three male and two female subjects participated in the 10-d study. Subjects consumed an L-amino acid diet containing 0.74 g protein equivalent/kg body weight on d 1-5; these amino acid concentrations were doubled on d 6-10. The diet was devoid of arginine on d 3-8. Daily urine was collected and blood samples were drawn on 6 of the 10 d at 0, 0.5, 1, 2, 3 and 4 h after the breakfast meal. When arginine was removed from the diet, urinary orotic acid did not increase, in contrast to what has been reported in most other animal species tested. Plasma ammonium concentrations remained within normal limits throughout the study. A small postprandial decrease in plasma arginine concentration was observed when the arginine-deficient diet was consumed; this decline disappeared when the diet was resupplied with arginine. The results of this study suggest that over the short term the adult human's capacity for de novo arginine synthesis when fed a dietary deficiency of arginine is sufficient for the maintenance of normal cellular metabolism.

Adult↗
PubMed1996

Antagonistic effect of nucleic acid precursors on the anticoccidial activity of 6-azauracil.

The antagonistic phenomena to anticoccidial activities of 6-azauracil (AzU) induced by certain nucleic acid precursors were examined in battery experiments. Each nucleic acid precursor, orotate, orotidine, uracil, uridine, adenine and adenosine was mixed in feed in combination with effective levels of AzU. The test feed was provided through the test term to White Leghorn cockerels which were infected with Eimeria tenella, E. necatrix or E. acervulina. In vitro tests were also conducted for antagonistic phenomena similarly to in vivo test using E. tenella cultured in chick kidney (CK) cells. Orotate and uridine reduced dose-dependently the anticoccidial activity of AzU in E. tenella infection in chickens. Uracil and orotidine revealed similar effect. Adenine and adenosine did not show any antagonistic effect to AzU. In E. necatrix infection, orotate and uridine had a similar tendency to that of E. tenella, whereas uracil and orotidine was less pronounced. The activity of AzU against E. acervulina was also blocked by the treatment with uridine and orotate. AzU inhibited the schizont's development of E. tenella in the CK cells, and this effect was reduced by uridine, but not by orotate and orotidine. The antagonistic effect of the pyrimidine nucleic acid precursors on AzU activity suggested that the anticoccidial effect of AzU to E. tenella, E. necatrix and E. acervulina is derived from inhibition of the metabolism of pyrimidine nucleotide synthesis in these parasites.

Adenine↗
PubMed1975

Urea, citrate and orotate excretion in growing rats fed amino acid-deficient diets.

Male, weanling rats were fed a control purified amino acid diet or the same diet with lysine, phenylalanine, tryptophan, valine, or arginine omitted singly, or both arginine and lysine omitted. Blood urea reached three to four times that of control levels with all deficient diets. Urea excretion increased almost linearly with time during the first 3 days of amino acid deficiency. Rates of urea excretion on day 3 in decreasing order for various deficiencies were as follows: lysine and arginine combined are more than lysine is more than tryptophan equals valine is more that phenylalanine equals arginine. Urinary citrate was 26 and 21.8 times that of control values without arginine and 11.4 and 6.2 times that of control values without lysine on days 2 and 3, respectively. By day 8 citrate excretion had returned to control levels without lysine but not without arginine. Citrate excretion was unchanged with other deficiencies. Orotic acid excretion increased markedly only without arginine and slightly without tryptopahn. A deficiency of arginine and lysine increased urea and citrate excretions to a greater extent than either deficiency alone. Two injections of arginine or homoarginine (0.50 mmole/injection) given at 12-hour intervals to rats fed no lysine and arginine for 3 days decreased citrate excretion immediatedly and on the following day. Urea excretion decreased with injected homoarginine, but not with arginine. Orotic acid excretion increased more than four times on the day of homoarginine injection compared with that of the preceding day. Arginine injection returned orotic acid excretion to nearly control levels within 24 hours. Urea degradation in the gastrointestinal tract was increased in animals fed amino acid-deficient diets.

Amino Acids, Essential↗
PubMed2005

Ornithine aminotransferase deficiency: diagnostic difficulties in neonatal presentation.

We describe two unrelated cases of ornithine aminotransferase (OAT) deficiency with rare neonatal presentation of hyperammonaemia. The diagnosis in the neonatal presentation of OAT deficiency is hampered as hyperornithinaemia is absent. Enzyme and mutation studies confirmed the diagnosis. OAT deficiency should be included in differential diagnosis of neonatal hyperammonaemia.

Amino Acid Metabolism, Inborn Errors↗