Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were conducted to evaluate the involvement of food intake in the lysine-arginine antagonism. Diets were formulated to compensate for the metabolic consequences of excess dietary lysine; induction of renal arginase activity, depression of heptic glycine transamidinase, and urinary losses of arginine. This was accomplished by inclusion of creatine in the basal diet, use of a moderate excess of lysine that did not increase urinary arginine excretion, and addition of the arginase depressors, alpha-aminoisobutyric acid (AIB) and L-threonine, to diets containing excess lysine. When chicks were fed diets containing excess lysine ad libitum, growth and efficiency of arginine retention were reduced. Supplementation of the diets with AIB and threonine markedly reduced the growth depression and restored efficiency of arginine utilization. When chicks were force-fed the diet containing excess lysine, growth was depressed, and body composition was altered. Inclusion of AIB and threonine in the diet containing excess lysine resulted in growth and body composition equivalent to levels of force-fed controls. In a second experiment the basal diet and basal supplemented with AIB and threonine were pair-fed to lysine-supplemented diets containing AIB and threonine. Body weight gains and body composition of all groups were similar. In other experiments, food intake increased within 24 hours (P less than 0.05) and probably within 12 hours (P less than 0.10) after removal of excess lysine from the diet. It is concluded that a portion of the lysine-arginine antagonism is due to a primary effect of lysine on regulation of food intake.
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PMID:Involvement of food intake in the lysine-arginine antagonism in chicks. 115 27

Protein from many sources show negative correlation between their biological values and the levels of urea in the blood or urine of rats or pigs. On the basis of the difference in protein quality between raw and heated soybeans, it would be predicted that there should be a higher level of urea in the blood and urine of rats fed raw soybean meal. In the present study, however, little or no difference in the levels of urea in the blood and urine of animals fed raw or autoclaved soybean meal could be demonstrated. It is postulated that the increased catabolism of the poor quality protein of raw soybeans may be masked by a concomitant depression of liver arginase activity and/or a decrease in the total quantity of amino acids available for catabolism because of lower digestibility of the raw soybean protein.
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PMID:Levels of urea in the blood and urine of rats fed raw and heated soybean meal. 124 8

Coccinia indica (Family: Cucurbitaceae, locally known as telakucha) leaves were extracted with 95% ethanol. Following evaporation of the solvents, the residue was suspended in distilled water. When this suspension was fed orally to male normal-fed and 48-hr starved rats, the blood glucose was lowered 21% (P less than 0.01) in normal-fed and 24% (P less than 0.001) in 48-hr starved animals respectively. Starvation had induced a 3-fold increase in the activity of glucose-6-phosphatase and this activity was depressed 19% (P less than 0.05) by extract feeding while basal activity of the enzyme in normal-fed rats remained unaffected. Consistent with the depression of glucose-6-phosphatase, urea cycle enzyme arginase was also depressed 21% (P less than 0.001) and 12% (P less than 0.01) in the liver of 48 hr-starved and normal-fed animals respectively. Unlike glucose-6-phosphatase, starvation induced levels of gluconeogenic enzymes alanine aminotransferase and aspartate aminotransferase were not affected by Coccinia extract. These results suggest that the hypoglycemic effect of C. indica is partly due to the repression of the key gluconeogenic enzyme glucose-6-phosphatase.
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PMID:Hypoglycemic effects of Coccinia indica: inhibition of key gluconeogenic enzyme, glucose-6-phosphatase. 133 43

Despite continuous exposure to gut-derived endotoxin (lipopolysaccharide) under normal conditions, Kupffer cells (KC) fail to generate detrimental cytokine responses. KC function within a unique microenvironment in which high hepatic arginase activities (25 times greater than those activities in the kidney) result in negligible local L-arginine levels. To evaluate the relevance of this profound arginine deficiency on the physiologic function of KC, the kinetics of tumor necrosis factor (TNF-alpha) production and autoregulatory eicosanoid prostaglandin E2 (PGE2) production were compared in lipopolysaccharide-stimulated KC cultured with (1200 mumol/L) and without (10 mumol/L) L-arginine media. In (+)arginine culture the KC TNF-alpha production peaked early before decreasing as PGE2 production increased. In (-)arginine culture, however, KC TNF-alpha production was significantly (p less than 0.01) reduced, whereas PGE2 production was amplified (p less than 0.01). When cyclooxygenase blockade with indomethacin completely prevented KC production of PGE2 in (-)arginine culture, TNF-alpha production was upregulated (p less than 0.001 vs (-)arginine; p not significant vs (+)arginine). These arginine-specific depression of TNF-alpha responses appeared unique to KC because both TNF-alpha and PGE2 levels increased when peritoneal, pleural, and alveolar macrophages were stimulated by lipopolysaccharide in (-)arginine medium. This PGE2-dependent autoregulation of potentially harmful lipopolysaccharide-induced TNF-alpha responses may reflect an evolutionary adaptation by KC to their local hepatic environment and strategic anatomic position in the portal circuit, which optimally removes endotoxin and naturally protects the host.
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PMID:A biologic basis for limited Kupffer cell reactivity to portal-derived endotoxin. 185 31

Rats fed a purified L-amino acid diet with 0.72, 1.50, 2.9 or 4.3% lysine excreted 117, 124, 237 and 628 micrograms/day orotic acid, respectively. Dietary arginine supplementation prevented the orotic aciduria induced by excess dietary lysine. Increased orotic acid excretion was accompanied by a significant depression in urinary urea in rats fed a diet containing 4.3% lysine compared to those fed a diet containing 0.72% lysine. As measured by incorporation of [14C]HCO3, lysine addition to liver slices or isolated hepatocytes resulted in a progressive increase in the rate of orotic acid biosynthesis. The minimum quantity of lysine tested that significantly increased the rate of orotic acid biosynthesis was 0.5 mM or 1 mM for studies with slices and hepatocytes, respectively. Ammonia at concentrations of 0, 0.75, or 5.0 mM NH4Cl linearly increased orotate and urea synthesis. Inhibition of urea biosynthesis resulting from lysine supplementation coincided with an increase in pyrimidine biosynthesis. Addition of 1 mM arginine to the liver incubation media prevented the increased rate of orotic acid biosynthesis caused by lysine. Arginine addition may overcome an approximate 90% competitive inhibition of arginase by excess lysine.
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PMID:The influence of excess lysine on urea cycle operation and pyrimidine biosynthesis. 681 6

Arginine metabolism plays an important role in many aspects of inflammation and wound healing. In this study, we tested the hypothesis that steroids and vitamin A have differential effects on arginine metabolism and thereby may provide a mechanism by which steroids impair wound healing, and vitamin A improves this impairment. Rats were treated with subcutaneous corticosterone pellets 2 days prior to wounding. Intraperitoneal injections of all-trans retinoic acid in peanut oil were administered at the same time and repeated 2 and 4 days later. Polyvinyl alcohol sponges were implanted subcutaneously through a dorsal incision. On Postwounding Days 1, 5, 10, and 15, wound fluid was recovered from the sponges and assayed for nitrite/nitrate (NOx), citrulline, arginine, and ornithine concentrations as well as arginase activity. Steroid treatment decreased the metabolism of arginine to nitric oxide in the early phase of wound healing, and retinoic acid did not change this relationship. Corticosterone also decreased metabolism of arginine to ornithine in the later wound. This depression was inhibited by concomitant administration of retinoic acid. Considering the importance of nitric oxide in host defense and ornithine as a precursor for polyamine and proline synthesis, these data provide a mechanism by which vitamin A improves wound strength, but does not improve wound infection rates in steroid-treated animals.
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PMID:Altered wound arginine metabolism by corticosterone and retinoic acid. 922 33

Manganese intake can vary greatly with food choices, water composition, and supplement use. Thus, individuals consuming Western diets consume from < 1 to > 10 mg Mn/d. The levels of manganese intake associated with adverse effects (both deficient and toxic) are debatable. Moreover, many of the symptoms of manganese deficiency (growth retardation, changes in circulating HDL cholesterol and glucose levels, reproductive failure) and manganese toxicity (growth depression, anemia) are non-specific. The bone deformities observed in manganese-deficient animals and neurological symptoms of individuals who have inhaled excess manganese are permanent and illustrate the need to identify sensitive biomarkers of manganese status that appear before these symptoms. Manganese balance and excretion data are not useful biomarkers of manganese exposure but demonstrate that the body is protected against manganese toxicity primarily by low absorption and/or rapid presystemic elimination of manganese by the liver. Serum manganese concentrations in combination with lymphocyte manganese-dependent superoxide dismutase (MnSOD) activity and perhaps blood arginase activity, appear to be the best ways to monitor ingestion of insufficient manganese. Serum manganese concentrations in combination with brain MRI (magnetic resonance imaging) scans, and perhaps a battery of neurofunctional tests, appear to be the best ways to monitor excessive exposure to manganese.
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PMID:Nutrition versus toxicology of manganese in humans: evaluation of potential biomarkers. 1038 84

1. Arginase, an important part of the arginine-regulating system modulates nitric oxide generation; a neuroregulatory agent, which has been implicated in various neuropathological conditions. 2. In this regard, the authors investigated the arginine-nitric oxide pathway by measuring serum arginase activity in drug free major (n=18) and minor depressed outpatients (n=12) and healthy control subjects (n=30) in order to make a contribution to the understanding of disease mechanism. 3. Major depressed patients were found to have significantly higher serum arginase activity compared to controls (p<0.001) and minor depressives (p=0.001). Moreover, there was significant positive correlation between arginase activity and severity of depression in patients (p<0.001). 4. Results suggest that the arginine-nitric oxide pathway is involved in depression. Enhanced arginase activity in major depressed patients possibly leading to a decrease in nitric oxide synthesis may contribute to the symptomatology of depression.
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PMID:Increased serum arginase activity in depressed patients. 1080 Jul 45

Post fertilization growth of tobacco ovary tissues treated with inhibitors of polyamine (PA) biosynthesis was examined in relation to endogenous PA titers and the activities of arginine decarboxylase (ADC, EC 4.1.1.19) and ornithine decarboxylase (ODC, EC 4.1.1.17). DL-alpha-Difluoromethylornithine (DFMO) and DL-alpha-difluoromethylarginine (DFMA), specific, irreversible ("suicide") inhibitors of ODC and ADC in vitro, were used to modulate PA biosynthesis in excised flowers. ODC represented >99% of the total decarboxylase activity in tobacco ovaries. In vivo inhibition of ODC with DFMO resulted in a significant decrease in PA titers, ovary fresh weight and protein content. Simultaneous inhibition of both decarboxylases by DFMO and DFMA produced only a marginally greater depression in growth and PA titers, indicating that ODC activity is rate-limiting for PA biosynthesis in these tissues. Paradoxically, DFMA alone inhibited PA biosynthesis, not as a result of a specific inhibition of ADC, but primarily through the inactivation of ODC. In vivo inhibition of ODC by DFMA appears to result from arginase-mediated hydrolysis of this inhibitor to urea and DFMO, the suicide substrate for ODC. Putrescine conjugates in tobacco appear to function as a storage form of this amine which, upon hydrolysis, may contribute to Put homeostasis during growth.
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PMID:In vivo inhibition of polyamine biosynthesis and growth in tobacco ovary tissues. 1153 96

There is a reciprocal regulation of arginase and nitric oxide synthase (NOS) in L-arginine-metabolizing pathways. Nitric oxide (NO) may be involved in some psychiatric disorders like schizophrenia, depression and bipolar affective disorder (BPAD). To our knowledge, there is no study in the literature in which the role of arginase, an important part of the arginine regulatory system affecting NOS activity, was investigated in BPAD. This study aims to investigate arginase, manganese (Mn) and total nitrite levels (a metabolite of NO) and their relationship to the arginine-NO pathway in patients with BPAD. Arginase activities, Mn and total nitrite levels were measured in plasma from forty-three patients with BPAD (Type one) and thirty-one healthy control subjects. Plasma arginase activities and Mn were found to be significantly lower and total nitrite level higher in patients with BPAD compared with controls. Our results suggest that the arginine-NO pathway is involved in the pathogenesis of BPAD.
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PMID:The role of the arginine-nitric oxide pathway in the pathogenesis of bipolar affective disorder. 1499 78


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