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)

In a series of 13 elderly patients with proven prealbumin-related senile systemic amyloidosis (SSA), depressed serum prealbumin values (110.7 +/- 14.1 micrograms/ml) were found as compared to an age-matched control group (175.1 +/- 20.3 micrograms/ml). As expected, there was a significant correlation between serum prealbumin and serum retinol-binding proteins in both groups of patients. Patients with reactive amyloid protein AA amyloidosis had slightly depressed serum prealbumin concentrations, whereas patients with prealbumin-related familial amyloidosis of Swedish type had prealbumin values within normal limits. Since the serum levels of the acute phase reactants, haptoglobin and amyloid-related serum protein AA, were higher in the group of patients with reactive amyloidosis than in patients with SSA, the depression of the prealbumin levels in SSA is not a result of inflammation. Since SSA is known to contain prealbumin, it is possible that a disturbed prealbumin metabolism in old age results in low prealbumin serum values and deposition of amyloid.
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PMID:Serum prealbumin and retinol-binding protein in the prealbumin-related senile and familial forms of systemic amyloidosis. 403 61

The concentration of the three components of the retinol circulating complex demonstrates in healthy male infants, but not in females, a transient elevation culminating at 5-6 months after birth. This trimolecular peak is significantly less elevated in bilateral cryptorchid babies. The rise of the retinol related parameters seems directly induced by the testosterone hypersecretion previously described in male infants at 2-3 months. The delay in the liver response in terms of retinol secretion appears to depend on a temporary functional immaturity and/or a transitory depression of the hepatic protein-synthesizing machinery. The surge of the retinol circulating complex could play a crucial role in the O-mannosylation of several glycoproteins involved in male sexual differentiation.
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PMID:Differences in the retinol circulating complex between healthy male and female infants. 611 51

Histidine metabolism was studied in rats fed 10% casein diets supplemented with 1000 IU of retinol/g concurrent with or previous to exposure to high levels of dietary histidine (1% or 2%). When a retinol-supplemented 10% casein + 1% histidine diet was fed ad libitum for 21 days, urinary excretion of formiminoglutamic acid (FIGLU) was decreased by 50-70% over the entire period and plasma histidine was reduced by 30-70% for 16 days compared to rats receiving 10% casein + 1% histidine with normal levels of retinol. Rats pretreated for 10 days with a 10% casein diet supplemented with high levels of retinol oxidized 30% more L-[ring-2-14C]histidine to 14CO2 and excreted 76% less of the administered dose as urinary FIGLU compared to control rats not pretreated with high levels of retinol. Depression in growth due to supplementation of a 10% casein diet with 1% histidine were also partially alleviated in rats that were first pretreated with retinol. Activities of histidase, urocanase, and formiminoglutamic acid formiminotransferase (FIGLU transferase) were unaffected by retinol supplementation. The results suggest that retinol supplementation enhances histidine catabolism by exerting a change on one-carbon metabolism.
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PMID:Enhancement of histidine and one-carbon metabolism in rats fed high levels of retinol. 612 Oct 19

Food intake and growth were depressed during the first week of feeding the anticarcinogenic retinoid N-(4-hydroxyphenyl) retinamide (HPR) at a concentration of 782 mg/kg diet to female rats. Food intake was normalized thereafter, but body weight did not reach that of control animals until 40 days later. The use of a pair-fed group demonstrated that weight depression in HPR fed animals was entirely due to reduced food intake. Mammary glands from HPR-fed animals showed decreased ductal branching and decreased end bud proliferation relative to control glands. Total hepatic retinol and retinol concentration were lower (P less than 0.05) for HPR fed animals than for controls. The effects of HPR on mammary development and retinol storage were attributable to dietary HPR per se. HPR was detected in mammary gland and body fat at concentrations of 27 and 53.7 nmol/g, respectively.
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PMID:Effect of N-(4-hydroxyphenyl) retinamide on food intake, growth, and mammary gland development in rats. 622 8

To study the possible hepatotoxicity of vitamin A supplementation and its potentiation by ethanol, rats were fed diets with either normal or fivefold increased vitamin A content, both with or without ethanol. Ethanol with a normal vitamin A diet produced the expected proliferation of the smooth endoplasmic reticulum and moderate mitochondrial lesions. Vitamin A supplementation by itself produced endoplasmic reticulum proliferation, slight enlargement of mitochondria, and moderate decrease in cytochrome oxidase activity and cytochrome aa3 content. The combination of high vitamin A and ethanol resulted in much more striking lesions, with giant mitochondria containing paracrystalline inclusions and depression of oxygen consumption in state-3 respiration with five different substrates, including palmitate and palmitoyl coA. The depression of fatty acid oxidation may have contributed to the lipid accumulation. The blood levels of vitamin A were unaffected whereas liver levels of vitamin A were increased by vitamin A supplementation and decreased by ethanol. As a net result the liver vitamin A content of the high-A-ethanol groups was not greater than that of the normal-A-control group, suggesting that a metabolite of vitamin A rather than vitamin A itself may have been responsible for the potentiation of vitamin A toxicity by ethanol. Mitochondrial toxicity reflected itself also in decreased content of various cytochromes and reduced activity of enzymes, including glutamate dehydrogenase. The activity of the latter was increased in the serum. Implications of these findings for the routine treatment of alcoholics with vitamin A and the monitoring for possible signs of toxicity are discussed.
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PMID:Hepatotoxicity of vitamin A and ethanol in the rat. 627 29

This report describes a series of experiments that attempt to characterize the lipidemia accompanying retinoic acid administration. After feeding young adult male Sprague-Dawley rats, 1.2 Retinol Equivalents (R.E.) retinyl acetate plus supplemental retinoic acid (100 microgram/g dry diet) for three days and fasting for 6-8 hr, triglyceride, cholesterol, and phospholipid content of various serum lipoprotein fractions were determined. When compared to unsupplemented controls, both the serum very low density lipoprotein (VLDL) and the high density lipoprotein (HDL) fractions of the retinoic acid-fed rats were found to harbor an elevated triglyceride content. While VLDL cholesterol and phospholipid content were also elevated, total serum cholesterol and phospholipids were not statistically altered. The detergent Triton WR-1339 was used to depress serum triglyceride clearance in order to assess the effects of retinoic acid feeding on serum triglyceride levels. Triglyceride accumulation started earlier after Triton treatment and was greater when rats were fed 100 microgram/g retinoic acid for three days prior to testing. Red and white gastrocnemius muscle, cardiac ventricular muscle, and perirenal adipose tissue were removed from rats following retinoic acid feeding. Analysis of these tissues for lipoprotein lipase (EC 3.1.1.3) activity showed a decrease in adipose tissue, a large depression in both areas of gastrocnemius muscle and no change in cardiac muscle as a result of retinoic acid feeding.
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PMID:Hyperlipidemia in rats fed retinoic acid. 727 11

The effects of neonatal vitamin A exposure on six behavioral parameters in adult Wistar rats were investigated. Newborn male rats were injected intraperitoneally with 80,000 IU/kg/day of retinol palmitate (vitamin A) dissolved in physiological saline or vehicle alone (controls) during 1-5 days after birth. The animals were examined using the open field test (at 36 weeks of age), the rotarod test (38 weeks), the Biel water-maze test (40 weeks), the conditioned avoidance test (42 weeks), the running-wheel activity with pentobarbital challenge test (44 weeks), and the tail flick test (45 weeks). The vitamin A-exposed rats made significantly more errors and took significantly longer times in the Biel water-maze test, and showed significantly slower responses in the tail flick test than the controls. No significant effects of treatment with vitamin A were observed in any of the other behavioral tests. These results indicate that a long-lasting defect in learning in water-maze task and depression of the heat-pain response are induced in rats exposed neonatally to vitamin A.
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PMID:Effects of the neonatal vitamin A exposure on behaviors of adult rats. 747 98

The retinoids are teratogenic in a wide variety of species. In the rat, 13-cis-retinoic acid and retinyl palmitate are significantly less potent teratogens than all-trans-retinoic acid. This investigation questioned whether differing teratogenic potencies of these moieties can be correlated with the concentrations of these drugs and/or metabolites in the embryonic compartment. Approximately equipotent teratogenic doses of these three retinoids were administered and the pharmacokinetics in maternal plasma and embryo of the most prevalent vitamin A metabolites were measured. The glucuronides of the respective retinoids were the predominant metabolites in the maternal plasma, but were not detected in the embryo. Also, the transport of 13-cis-retinoic acid across the placenta occurred to a much lesser extent than the transport of all-trans-retinoic acid. Administration of either all-trans- or 13-cis-retinoic acid causes a depression in the endogenous retinol concentration. This depression is more pronounced in the maternal plasma than in the embryo. The depression of the retinol level in both plasma and embryo after 13-cis-retinoic acid administration (75 mg/kg/day) was greater than the depression after all-trans-retinoic acid (6 mg/kg/day), corroborating the inferential teratological data that the 13-cis-retinoic acid dose was more embryotoxic than the all-trans-retinoic acid dose. Although the dose of all-trans-retinoic acid was less embryotoxic than that of either 13-cis-retinoic acid or retinyl palmitate, the embryonic exposure to all-trans-retinoic acid was considerably larger, as determined by maximum concentration or area under the concentration-versus-time curve, after administration of all-trans-retinoic acid than after either retinyl palmitate or 13-cis-retinoic acid application. These results suggest that embryonic retinoids other than all-trans-retinoic acid--including the administered substances themselves--are important in the teratogenic process induced by 13-cis-retinoic acid and retinyl palmitate.
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PMID:Comparative teratology and transplacental pharmacokinetics of all-trans-retinoic acid, 13-cis-retinoic acid, and retinyl palmitate following daily administrations in rats. 804 45

A survey on the nutritional status and cell-mediated immune function of 47 hospitalized patients with active pulmonary tuberculosis and healthy controls was conducted. In the patients group: 1) Anthropometric measurements, such as %ideal body weight (%IBW), %arm circumference (%AC), %arm muscle circumference (%AMC) and %triceps skin fold (%TSF), were significantly reduced. 2) Visceral proteins including serum albumin (Alb), transferrin (Tf), prealbumin (PA) and retinol binding protein (RBP) were significantly reduced. 3) The imbalance of plasma amino acids, which was characterized by the depression of Fischer ratio, a molar ratio of branched chain amino acids (BCAA) to aromatic amino acids (AAA), was observed. Fischer ratio was significantly correlated with anthropometric measurements (%IBW, %AC and %AMC). Delayed-type hypersensitivity to DNCB (2,4-dinitrochlorobenzene) and lymphocyte transformation to phytohemagglutinin (PHA) and concanavalin A (Con A) were significantly impaired in the patients group, whereas NK cell activity was higher than that of controls. Alb, PA, RBP and Fischer ratio were significantly lower in the patients with reduced DNCB reaction than in those with normal responses. Lymphocyte transformation was significantly correlated with Fischer ratio, and NK cell activity was significantly correlated with Alb, PA, RBP. These data may suggest that the imbalance of plasma amino acids represented by the reduction of Fischer ratio and the depletion of visceral proteins are closely related to the impairment of lymphocyte function in the patients with active pulmonary tuberculosis.
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PMID:[Relationship between nutritional depletion and cell-mediated immune function in active pulmonary tuberculosis]. 818 84

Vitamin A (VA) protects the small intestine from methotrexate (MTX)-induced damage. However, before VA can be used as a remedy to protect cancer patients from MTX-induced damage to the intestine, it is essential to clarify whether or not it disturbs the antitumor activity of MTX. This study investigated the effect of VA on the antitumor activity of MTX in vitro in L1210 murine leukemia cells. The incorporation of [6-3H]-thymidine and [6-3H]-uridine, [5-3H]-uridine, and [4,5-3H]-leucine into DNA, RNA, and proteins, respectively, was examined to evaluate this effect. The incorporation of thymidine, the uridines, and leucine decreased dose-dependently in MTX-treated L1210 cells and profoundly in the MTX plus VA-treated L1210 cells, since VA itself had a cell-killing activity. Thus, MTX depressed the growth of L1210 cells dose-dependently and this depression was not affected by the presence of VA. The present study proved in L1210 murine leukemia cells in vitro that VA did not disturb the antitumor activity of MTX.
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PMID:Effect of vitamin A on methotrexate cytotoxicity in L1210 murine leukemia cells in culture. 832 67


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