Disease relevance of Aquasol A

• Assay of serum levels of retinol, retinyl palmitate, alpha-carotene, and beta-carotene to assess nutritional status, to trials of retinol and/or beta-carotene to assess nutritional status, to monitor compliance with medication schedules, and to conduct toxicity surveillance [1].
• Six week-old male CBA/J mice fed a commercial powdered laboratory chow or the same chow supplemented with vitamin A palmitate (150,000 U/kg) were inoculated with either the Moloney strain of murine sarcoma virus (M-MuSV) or poxvirus [2].
• Similar results were obtained when BALB/c mice were inoculated sc with a syngeneic BALB/c Meth A fibrosarcoma and treated with RP (5,000 IU/kg/day) and FUra (20 mg/kg/every 3d day) [3].
• The retinyl palmitate absorption rate constants were similar in control and pancreatitis patients [4].
• These trials established that lung cancer was not prevented by alpha-tocopherol, beta-carotene, retinol, retinyl palmitate, N-acetylcysteine, or isotretinoin in smokers [5].

High impact information on Aquasol A

• The retinyl palmitate fat tolerance test was used to measure chylomicron remnant clearance in 10 normal subjects (apolipoprotein E [apo E] isotypes 3 or 4 only), 6 normolipidemic apo E2/2 homozygotes and 5 familial hypercholesterolemic homozygotes [6].
• We have examined the effect of the apo E polymorphism on dietary fat clearance using the vitamin A-fat loading test, which specifically labels intestinally derived lipoproteins with retinyl palmitate (RP) [7].
• Compared with E3/3 subjects, E3/2 subjects had a significantly higher nonchylomicron RP concentration (P less than 0.05) (peak heights and areas below the curves) indicating slower clearance and the E4/3, E4/4 group had a significantly lower nonchylomicron RP concentration (P less than 0.05) indicating faster clearance [7].
• Adjuvant effect of vitamin A palmitate and analogs on cell-mediated immunity [8].
• However, despite this effect on postprandial retinyl palmitate, the profile of postprandial triglyceride response was not significantly different among apo E genotypes [9].

Chemical compound and disease context of Aquasol A

• The retinyl palmitate content of the postnuclear membrane fraction from 10 Morris hepatomas, their host rat livers, one acetylaminofluorene-induced rat liver hepatoma, and the host liver and of regenerating rat liver was measured by reverse-phase high-pressure liquid chromatography of the chloroform:methanol extracts [10].
• Vitamin A status was examined in nine adult cystic fibrosis patients and six adult control subjects, together with an assessment of their ability to absorb 10,000 IU of retinyl palmitate from a test meal, taken with appropriate pancreatic enzyme supplements [11].
• Association of postprandial triglyceride and retinyl palmitate responses with newly diagnosed exercise-induced myocardial ischemia in middle-aged men and women [12].
• Enhanced numbers and sizes of vesicular stomatitis virus plaques occurred when Aquasol A or Tween 80 was added to the cell culture 30 min before virus adsorption but not when added after adsorption [13].
• The association between participant characteristics and serum concentrations of beta-carotene, retinol, retinyl palmitate, and alpha-tocopherol among participants in the Carotene and Retinol Efficacy Trial (CARET) for prevention of lung cancer [14].

Biological context of Aquasol A

• Hydrolysis of 11-cis- and all-trans-retinyl palmitate was protein- and time-dependent [15].
• With retinyl palmitate as substrate, the enzyme had a pH optimum of 7 and showed apparent saturation kinetics, with half-maximal activity achieved at substrate concentrations (Km) of approximately 70 microM [16].
• The vector-mediated expression of PPARgamma itself is sufficient to reverse the morphology of activated HSC to the quiescent phenotype with retracted cytoplasm, prominent dendritic processes, reduced stress fibers, and accumulation of retinyl palmitate [17].
• When microsomes were incubated with both [3H]retinol and [14C]palmitoyl-CoA of known specific radioactivities, the ratio of 14C to 3H in newly synthesized retinyl palmitate was essentially equal to that of its putative substrates, indicating that [14C]palmitate did not undergo significant isotope dilution prior to acylation of [3H]retinol [18].
• The product of retinyl ester synthesis from all-trans-retinol and palmitoyl-CoA is all-trans-retinyl palmitate, indicating that the stereochemical configuration is retained during esterification [19].

Anatomical context of Aquasol A

• Membranes from the hepatoma tissue contained less than detectable levels of retinyl acyl esters, whereas membranes from host liver tissue and regenerating liver contained levels of retinyl palmitate within normal ranges [10].
• Hydrolysis of 11-cis- and all-trans-retinyl palmitate by retinal pigment epithelium microsomes [15].
• Hydrolysis of 11-cis- and all-trans-retinyl palmitate by homogenates of human retinal epithelial cells [20].
• Following the oral dosing of deficient animals (T12) with 350 micrograms retinyl palmitate, all such changes were reversed within 6 days in the trachea and within 10 days in the submaxillary and sublingual glands [21].
• Hydrolysis of retinyl palmitate by enzymes of rat pancreas and liver. Differentiation of bile salt-dependent and bile salt-independent, neutral retinyl ester hydrolases in rat liver [22].

Associations of Aquasol A with other chemical compounds

• This retinol was enzymatically esterified to retinyl palmitate by rat pancreatic esterase with a retention time of 10 min on HPLC corresponding to authentic retinyl palmitate [23].
• Homogenates of LLC-PK1 cells converted retinol into retinoic acid and retinyl palmitate and hydrolyzed retinyl palmitate [24].
• The partially purified protein has an apparent molecular weight of 14,000 and high binding specificity for all-trans-[3H]retinol as only unlabeled all-trans-retinol but not retinal, retinoic acid, retinyl acetate, retinyl palmitate, or oleic acid could diminish binding of the 3H ligand under the conditions employed [25].
• Purified NREH shows a substrate preference for retinyl palmitate over triolein and did not catalyze the hydrolysis of cholesteryl oleate [16].
• Further characterization of 11-cis-retinyl palmitate hydrolysis involved monitoring formation of reaction products, 11-cis retinol and palmitic acid, which were found to be released in essentially a 1:1 stoichiometry [15].

Gene context of Aquasol A

• Here we show that Rpe65 specifically binds all-trans-retinyl palmitate but not 11-cis-retinyl palmitate by a spectral-shift assay, by co-elution during gel filtration, and by co-immunoprecipitation [26].
• In the present work, we show that purified RPE65 binds all-trans-retinyl palmitate (tRP) with a K(D) = 20 pM [27].
• Plasma total and chylomicron levels of retinyl palmitate were not affected by LCAT deficiency, while the removal of the vitamin from very low and intermediate density lipoproteins was clearly reduced so that the peak concentrations, values under the response curves and the time of the peak concentrations were markedly higher than in the controls [28].
• The retinyl palmitate concentrations in extracts of oral mucosa correlated to the retinol concentrations, both in plasma and mucosal extracts, but not to the CRBP content in mucosal extracts [29].
• Pancreatic lipase and pancreatic lipase-related protein 2, but not pancreatic lipase-related protein 1, hydrolyze retinyl palmitate in physiological conditions [30].

Analytical, diagnostic and therapeutic context of Aquasol A

• No statistically significant difference was observed in overall survival or event-free survival between patients who received retinyl palmitate and patients who did not [31].
• The 11-cis-retinyl palmitate hydrolase activity was maximally active with the addition of 1.0% sodium taurocholate at about pH 8.5, was abolished by incubation at 50 degrees C for 10 min, and was quantitatively recovered in the pellet after centrifugation at 100,000 X g for 1 h [20].
• We compared the effect of (i) 15 mg of retinyl palmitate, (ii) 2 microg of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], (iii) 15 mg of retinyl palmitate plus 2 microg of 1,25(OH)2D3, and (iv) placebo in a double-blind crossover study [32].
• In this nested case control study in older women (312 cases and 934 controls), serum retinol, retinyl palmitate, and beta-carotene were not associated with fracture risk, and there was no evidence of excess risk with multivitamin or cod liver oil supplementation [33].
• Relative to the low-vitamin A control group, the estimated mean changes in vitamin A stores were 0.029 mmol for sweet potato (P = 0.21), 0.041 mmol for Indian spinach (P = 0.033), 0.065 mmol for retinyl palmitate (P < 0.001), and 0.062 mmol for beta-carotene (P < 0.002) [34].

References