Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Levels of retinol-binding (RBP), the plasma transport protein for vitamin A, were measured by radioimmunoassay in sera and in a large number of tissues from both normal and vitamin A-deficient rats. The tissues included liver, kidney, fat, muscle, brain, eye, salivary gland, thymus, lung, heart, intestine, spleen, adrenal, testes, thyroid, and red blood cells. The RBP levels in tissues other than serum, liver, and kidneys varied from 12 mug/g of tissue for normal spleen to an undetectable level in red blood cells. Much of the RBP in the tissues with low levels may have been due to residual serum in the samples. In general, except for liver, RBP levels were lower in tissues from vitamin A-deficient rats than in those from normal rats. In normal rats, the liver, kidney, and serum levels were 30 plus or minus 4 (mean plus orminus SEM), 151 plus or minus 22, and 44 plus or minus 3 mug/g, respectively. In vitamin A-deficient rats, the liver RBP level was about three times the normal level whereas the kidney and serum levels were about one-fifth the normal values. When normal liver homogenates were fractionated by centrifugation, 67% of the RBP was recovered in the microsomal fraction and only 9% was found in the soluble 105,000 g supernate. In contrast, 76% of the RBP in homogenates of normal kidneys was in the soluble fraction. Similar results were obtained with deficient livers and kidneys. Incubation with deoxycholate released the liver RBP into the soluble fraction. RBP is produced in the liver and removed from the blood by the kidneys. The levels of RBP in normal and deficient liver, serum, and kidney appear to reflect the relative rates of RBP secretion and turnover.
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PMID:Tissue distribution and subcellular localization of retinol-binding protein in normal and vitamin A-deficient rats. 114 71

Two hundred eighty-four female adults (aged 40-70 years) were longitudinally studied to investigate the relationship between dietary supplemental vitamin A and serum biochemical markers of vitamin A toxicity. Serum retinol, retinyl esters, and retinol-binding protein (RBP), alkaline phosphatase and aspartate aminotransferase activities and bile acids were measured at baseline, 1 and 2 years. Fasting serum retinol and retinyl ester concentrations were determined by high-performance liquid chromatography, and dietary and supplemental intake of vitamin A were assessed by 3-day food records. There was no difference in dietary vitamin A intake between supplement users and nonusers. In supplemental users, the mean +/- SEM supplemental vitamin A intake was 952 +/- 81 IU/day (range 250-5000 retinol equivalents/day). Serum retinol, retinyl esters, and RBP concentrations were not different between the two groups during the 2-year period. For each group, serum retinyl esters significantly increased over time (p < 0.03), but the magnitude of the increase was not different between the groups. Serum levels of retinol, retinyl esters, and RBP were not correlated with vitamin A intake or age in either group. Biochemical measures of liver damage (serum alkaline phosphatase and aspartate aminotransferase activities and serum bile acids) were not related to serum retinol, retinyl esters or RBP concentrations, nor were they different between nonusers and users of supplemental vitamin A. This study provides evidence that long-term supplemental vitamin A in doses commonly found in multivitamin supplements does not present a risk for hypervitaminosis A.
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PMID:Lack of an effect of multivitamins containing vitamin A on serum retinyl esters and liver function tests in healthy women. 146 Jan 82

The concentrations of beta-carotene, retinol and retinyl esters in serum and selected tissues of ferrets fed diets supplemented with beta-carotene (80 micrograms/g wet diet) for 3 wk were determined. The initial concentration of serum beta-carotene was 0.011 +/- 0.006 mumol/L (mean +/- SEM); at the end of the experimental period it was 5.75 +/- 1.60 mumol/L. No significant differences in serum retinol and total retinyl esters were observed between beta-carotene-fed and control ferrets that had been fed an unsupplemented diet. The predominant retinyl esters in serum were retinyl stearate (53%) and retinyl palmitate (35%). Of the tissues analyzed after beta-carotene feeding, the liver contained the highest concentration of beta-carotene (78.8 +/- 18.8 nmol/g). Other tissues that contained beta-carotene in amounts ranging from 17 to 20 nmol/g were adrenals, small intestine, stomach and colon; lesser amounts (6.9 nmol/g) were found in kidneys. Amounts ranging from 1.2 to 2.3 nmol/g were found in muscle, bladder, adipose tissue, lungs and skin; only 0.37 and 0.34 nmol/g were present in brain and eyes, respectively. Thus, like humans, ferrets have the capacity to absorb intact beta-carotene and to store this compound in tissues, especially the liver. However, compared with humans, ferrets have elevated concentrations of retinyl esters in serum, liver and other tissues.
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PMID:Beta-carotene, retinol and retinyl ester concentrations in serum and selected tissues of ferrets fed beta-carotene. 151 40

Vitamin A status has been assessed by studying plasma vitamin A and retinol binding protein (RBP) levels in premature infants receiving 7,500 IU vitamin A/d (RDA 660-3,300 IU/d) and in control term babies during the 3 first months of life. Sampling was performed within the first week (D0-D7), between the 8th and the 30th day (D8-D30) and during the 2nd and the 3rd month of life (M2-M3). At D0-D7, vitamin A levels of the PTI group (28-32 weeks gestational age), PTII (33-36 weeks GA) and AT (control term newborn) were 242.1 +/- 20.5 (X +/- SEM), 176.1 +/- 12.3 and 213.1 +/- 17.1 micrograms/l respectively (P = 0.005). At D8-D30, these values were 264.2 +/- 26.0, 270.4 +/- 21.6 and 242.6 +/- 24.5 micrograms/l respectively (NS), and at M2-M3 234.2 +/- 21.6, 282.1 +/- 18.5 and 292.1 +/- 31.5 micrograms/l (NS). A significant difference was found between the values of the different dosage periods for PTII and AT groups; no difference in RBP levels was found either between groups or between dosage periods. At birth, our results show that the RBP synthesis is not closely linked to gestational age. The plasma vitamin A levels which rely on foetal stores and therefore on transplacental passage and on peripheral tissue requirements are low at 33-36 weeks gestational age. With a 7,500 IU daily supplement, excessively high vitamin A levels were not observed in premature infants; vitamin A and RBP levels in premature infants receiving supplement are not different from controls despite the 8-12-week term high vitamin A supply.
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PMID:[Vitamin A status in full-term and premature infants]. 217 49

The amount of vital cells recovered, their morphology (studied by SEM) and some of their biochemical aspects concerning the differentiation processes (aerobic glycolysis, cell production of cAMP and CEA) were investigated in a strain of H4 hepatoma cultured for 8 days in the presence of 5 microM retinol (R) or retinoic Acid (RA). Vital cell recovery is slightly reduced either by R or RA treatment. Flattening of the cell shape and reduction of the plasma membrane prolongations and of intercellular bonds are observed in the R-treated cells but to a greater extent in those treated with RA. Aerobic glycolysis is decreased in the R-treated cells but increased in those treated with RA. Such events could be related to the regressive processes observed in the RA-treated cells. cAMP cell content is increased to a greater extent in the R-treated cells than in those treated with RA. CEA cell content is greatly decreased in the RA-treated cells but only slightly in those treated with R. Therefore, the treatment of HA hepatoma cells with 5 microM R or RA, while reducing cell growth only slightly, does not cause evident and unequivocal morphological and biochemical events related to cell redifferentiation.
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PMID:[Actions of retinol and retinoic acid on hepatoma H4 cultures]. 256 Sep 25

Maintenance of vitamin A stores in the body is dependent on a number of basic metabolic processes. These processes, such as protein and carbohydrate metabolism, are disrupted in acute starvation, and, as a result, alterations in vitamin A status may result. We investigated this possibility in 8-week-old Sprague-Dawley male rats. The rats were starved for 24, 48, and 72 hr but had free access to water. At 24 hours of starvation, the plasma retinol concentration was depressed, but not significantly so. After 48 and 72 hours of starvation, however, the plasma retinol concentration decreased to less than half of the control values (61 +/- 4 vs 124 +/- 12 nmol/dl at 72 hours, mean +/- SEM, (p less than 0.005). The hepatic retinoid (retinyl esters + retinol) concentration (nmol/g liver) was increased at 24 and 48 hours of starvation compared to controls (p less than 0.05), and by 72 hours the concentration was 56% greater in starved rats than in fed controls (p less than 0.001). The total hepatic retinoid content (mumol/total liver) was decreased moderately at all periods of starvation compared to controls (p less than 0.05). In both starved and fed animals, the total hepatic content per 100 g body weight, a measure of total vitamin A reserves, was statistically the same. These results demonstrate that acute starvation in rats alters the vitamin A equilibrium between the plasma and hepatic stores without affecting the overall vitamin A reserves.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of acute starvation on vitamin A status in rats. 262 Dec 99

The purpose of this study was to explore the nature and time course of the functional effects of early retinol deficiency on the ocular surface epithelium. To this end, the conjunctival epithelial healing rate, mitotic rate, and goblet cell frequency were determined following experimental ocular surface epithelial wounding in 15 rabbits sustained on a retinol-deficient diet and in 12 pair-fed controls. The animals were sacrificed at 2, 7, and 14 days after wound closure. The mean serum retinol level (+/- SEM) prior to wounding was 6.0 +/- 0.9 microgram/dl for the group fed the deficient diet. The mean serum and liver retinol levels for this group following defect closure were 4.0 +/- 0.5 micrograms/dl and 0 micrograms/g, respectively. These values are all significantly less than the analogous respective control values of 83.2 +/- 2.4 micrograms/dl, 77.6 +/- 2.3 micrograms/dl and 35.1 +/- 3.0 micrograms/g (P less than 0.001 for each pair, student t-test). In the retinol-deficient animals, the unwounded eyes had an abnormally high rate of conjunctival epithelial cell mitosis, the earliest ocular surface cellular abnormality detected. Hypermitosis of the unwounded corneal epithelium was also noted, though somewhat later than in the conjunctiva. Epithelial wound healing was delayed considerably in the retinol-deficient group, with only 33% of eyes in this group healed within the same time period as the controls (P less than 0.05, Chi-square). Normal numbers of goblet cells were noted in the conjunctiva of retinol-deficient animals, despite at least 5, and up to 8 weeks of profoundly depleted retinol stores.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of ocular surface epithelium to corneal wounding in retinol-deficient rabbits. 318 2

Diurnal changes in human plasma levels of the fat-soluble vitamins retinol (R), alpha-tocopherol (E), and beta-carotene (CAR) have not been determined. Plasma levels of these three vitamins in 15 healthy volunteers were measured five times over a 24-hour period. Highly sensitive and specific HPLC assays were used. Mean +/- SEM levels for R, E, and CAR were 591 +/- 36 ng/mL, 10.3 +/- 0.6 micrograms/mL, and 271 +/- 28 ng/mL, respectively. Differences between subjects' mean levels were large and highly significant (p less than 0.0001). Relative to the first 8 AM fasting plasma sample, nonfasting plasma levels drawn over the next 24 hours showed no statistically significant or clinically important changes. The percent increases in standard deviation among subjects due to diurnal variation were 1.5%, 3.3%, and 2.3%, respectively, for R, E, and CAR. This implies that sample sizes for cross-sectional studies investigating differences between two treatments in these vitamin plasma levels would need to be increased by 3%, 7%, and 5%, respectively, if measurements are to be taken throughout the day. Plasma levels may be obtained at random during the day, and need not be 8 AM fasting levels. The small addition in variation introduced by diurnal fluctuations would have minimal impact upon the precision of estimates of treatment effect and sample sizes.
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PMID:Diurnal variation in plasma levels of retinol, tocopherol, and beta-carotene. 349 77

Prospective and retrospective studies have suggested that serum vitamin A and total cholesterol levels may be associated with cancer. Our study showed that the mean (+/- SEM) concentrations of serum vitamin A 489 +/- 33.28 (mean +/- SEM micrograms/liter and serum total cholesterol 174.7 +/- 8.96 (mean +/- SEM) mg/dl from ovarian cancer patients in Singapore were significantly lower than the respective values of 668 +/- 25.10 (mean +/- SEM) microgram/liter and 210.7 4.48 (mean +/- SEM) mg/dl from noncancerous control subjects (P less than 0.0001 for both compounds). In addition, ovarian cancer patients did not show significantly lower serum triglyceride levels than the control subjects. Age did not significantly correlate the serum vitamin A and total cholesterol concentrations, but there was correlation with respect to the serum triglyceride levels. There were moderate correlations between vitamin A and cholesterol levels (r = 0.36, P less than 0.0027) and between cholesterol and triglyceride levels (r = 0.37, P less than 0.0024) in the control subjects but not in the cancer patients. Vitamin A levels correlated moderately with triglyceride levels in both the cancer patients (r = 0.42, P less than 0.0258) and the control subjects (r = 0.33, P less than 0.0069). The inverse relationship between the incidence of ovarian cancer and serum vitamin A and serum total cholesterol concentrations may have distinct implications for preventive medicine and public health.
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PMID:The relationship of serum vitamin A, cholesterol, and triglycerides to the incidence of ovarian cancer. 359 92

Retinol and retinyl esters are measured in serum or plasma samples by gradient, normal-phase, adsorption "high-performance" liquid chromatography, with ultraviolet detection at 325 nm. The four major circulating retinyl esters in humans (esters of palmitate, stearate, oleate, and linoleate) are coeluted as a single peak. Retinyl acetate is included as an internal standard, to correct for variable recovery. Retinol values so measured correlated well (r = 0.88) with those by a widely used reversed-phase chromatographic technique (Clin Chem 1983;29:708-12). The mean retinol concentration was 570 (SEM 17) micrograms/L and the mean for retinyl esters was 33 (SEM 4) micrograms/L as determined in samples from 88 fasting young adults. Concentrations of retinol in plasma as low as 50 micrograms/L can be detected in 100-microL samples, as can 10 micrograms of retinyl esters per liter. Using this method, we measured absorption of low doses of vitamin A, which may provide a more physiological approach to assessment of fat malabsorption. Additionally, the procedure proved useful for quickly screening for vitamin A toxicity. Major advantages include small sample size, direct injection of the extract ed sample without evaporation, rapid elution pattern, co-elution of major retinyl esters as a single peak, and low limit of detection.
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PMID:Determination of retinyl esters and retinol in serum or plasma by normal-phase liquid chromatography: method and applications. 394 Jul 33


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