Folic Acid Conjugated Polyglutamic Acid Drug Vehicle Synthesis through Deep Eutectic Solvent for Targeted Release of Paclitaxel

2019 ◽  
Vol 4 (35) ◽  
pp. 10225-10235 ◽  
Author(s):  
Periyakaruppan Pradeepkumar ◽  
Ramalingam Sangeetha ◽  
Sathaiah Gunaseelan ◽  
Perumal Varalakshmi ◽  
Anil A Chuturgoon ◽  
...  
Keyword(s):  
Folic Acid ◽  
Deep Eutectic Solvent ◽  
Polyglutamic Acid ◽  
Targeted Release ◽  
Drug Vehicle

scholarly journals Mesoporous silica nanoparticles functionalized with folic acid for targeted release Cis-Pt to glioblastoma cells

2021 ◽  
Vol 60 (1) ◽  
pp. 25-37
Author(s):  
Emma Ortiz-Islas ◽  
Anahí Sosa-Arróniz ◽  
Ma Elena Manríquez-Ramírez ◽  
C. Ekaterina Rodríguez-Pérez ◽  
Francisco Tzompantzi ◽  
...  
Keyword(s):  
Folic Acid ◽  
Mesoporous Silica ◽  
Silica Nanoparticles ◽  
Mesoporous Silica Nanoparticles ◽  
High Surface ◽  
High Surface Area ◽  
Release Mechanism ◽  
Hexadecyltrimethylammonium Bromide ◽  
Targeted Release

Abstract This work reports the preparation, characterization, and a drug release study of mesoporous silica nanoparticles (MNPSiO2) functionalized with folic acid (FA) and loaded with Cis-Pt as a targeted release system to kill glioblastoma cancer cells. The MNPSiO2 were synthesized by the Stöber method using hexadecyltrimethylammonium bromide as the templating agent, which was finally removed by calcination at 550°C. The folic acid was chemically anchored to the silica nanoparticles surface by a carbodiimide reaction. Several physicochemical techniques were used for the MNPSiO2 characterization, and a triplicate in vitro Cis-Pt release test was carried out. The release Cis-Pt experimental values were fitted to different theoretical models to find the Cis-Pt release mechanism. The cytotoxicity evaluation of the MNPSiO2 was performed using LN 18 cells (human GBM cells). Homogeneous and well-defined nanoparticles with well-distributed and homogeneous porosity were obtained. The spectroscopic results show the proper functionalization of the mesoporous nanoparticles; besides, MNPSiO2 showed high surface area and large pore size. High correlation coefficients were obtained. Though the best fitted was the Korsmeyer-Peppas kinetic model, the Higuchi model adjusted better to the results obtained for our system. The MNPSiO2-FA were highly biocompatible, and they increased the cytotoxic effect of Cis-Pt loaded in them.

The Morphology of the Rat Kidney Following Folic Acid Administration

1970 ◽  
Vol 28 ◽  
pp. 200-201
Author(s):  
Aline Byrnes ◽  
Elsa E. Ramos ◽  
Minoru Suzuki ◽  
E.D. Mayfield
Keyword(s):  
Folic Acid ◽  
De Novo ◽  
Specific Activity ◽  
Rat Kidney ◽  
Present Report ◽  
Intracellular Localization ◽  
Male Rats ◽  
Renal Hypertrophy ◽  
Electron Microscopic ◽  
Biochemical Alterations

Renal hypertrophy was induced in 100 g male rats by the injection of 250 mg folic acid (FA) dissolved in 0.3 M NaHCO3/kg body weight (i.v.). Preliminary studies of the biochemical alterations in ribonucleic acid (RNA) metabolism of the renal tissue have been reported recently (1). They are: RNA content and concentration, orotic acid-c14 incorporation into RNA and acid soluble nucleotide pool, intracellular localization of the newly synthesized RNA, and the specific activity of enzymes of the de novo pyrimidine biosynthesis pathway. The present report describes the light and electron microscopic observations in these animals. For light microscopy, kidney slices were fixed in formalin, embedded, sectioned, and stained with H & E and PAS.

Efficacy of Adding Folic Acid to Foods

2012 ◽  
Vol 82 (3) ◽  
pp. 177-186 ◽  
Author(s):  
Violeta Fajardo ◽  
Gregorio Varela-Moreiras
Keyword(s):  
Folic Acid ◽  
Age Groups ◽  
Nutritional Deficiencies ◽  
Physiological Status ◽  
Food Fortification ◽  
Limited Information ◽  
Dietary Recommendations ◽  
Nutritional Education ◽  
Food Composition Tables ◽  
Staple Foods

In the past, food fortification along with nutritional education and the decrease in food costs relative to income have proven successful in eliminating common nutritional deficiencies. These deficiencies such as goiter, rickets, beriberi, and pellagra have been replaced with an entirely new set of “emergent deficiencies” that were not previously considered a problem [e.g., folate and neural tube defects (NTDs)]. In addition, the different nutrition surveys in so-called affluent countries have identified “shortfalls” of nutrients specific to various age groups and/or physiological status. Complex, multiple-etiology diseases, such as atherosclerosis, diabetes, cancer, and obesity have emerged. Food fortification has proven an effective tool for tackling nutritional deficiencies in populations; but today a more reasonable approach is to use food fortification as a means to support but not replace dietary improvement strategies (i. e. nutritional education campaigns). Folic acid (FA) is a potential relevant factor in the prevention of a number of pathologies. The evidence linking FA to NTD prevention led to the introduction of public health strategies to increase folate intakes: pharmacological supplementation, mandatory or voluntary fortification of staple foods with FA, and the advice to increase the intake of folate-rich foods. It is quite contradictory to observe that, regardless of these findings, there is only limited information on food folate and FA content. Data in Food Composition Tables and Databases are scarce or incomplete. Fortification of staple foods with FA has added difficulty to this task. Globally, the decision to fortify products is left up to individual food manufacturers. Voluntary fortification is a common practice in many countries. Therefore, the “worldwide map of vitamin fortification” may be analyzed. It is important to examine if fortification today really answers to vitamin requirements at different ages and/or physiological states. The real impact of vitamin fortification on some key biomarkers is also discussed. An important question also to be addressed: how much is too much? It is becoming more evident that chronic excessive intakes may be harmful and a wide margin of safety seems to be a mandatory practice in dietary recommendations. Finally, the “risk/benefit” dilemma is also considered in the “new” FA-fortified world.

Variations in the Lipid Profile of Patients with Chronic Renal Failure, Treated with Folic Acid

2003 ◽  
Vol 73 (3) ◽  
pp. 215-220 ◽  
Author(s):  
de Gómez Dumm ◽  
Giammona ◽  
Touceda
Keyword(s):  
Renal Failure ◽  
Folic Acid ◽  
Chronic Renal Failure ◽  
Density Lipoprotein ◽  
Plasma Homocysteine ◽  
Lipid Profiles ◽  
Erythrocyte Membranes ◽  
Favorable Effect ◽  
High Dose ◽  
Acid Therapy

Dyslipidemia and increases in plasma homocysteine usually occur at end-stage renal disease; both are recognized as risk factors for atherosclerosis. Folate administration reduces homocysteine concentration. In this study we determined the effect of a high dose of folic acid (40 mg intravenous injection three times a week) on plasma and red blood cell lipid profiles in twelve chronic renal failure patients on regular hemodialysis. Fasting blood samples were taken at the beginning of the study (baseline) and after 21, 42, and 64 days of treatment. Folic acid supplementation decreased plasma homocysteine. Plasma triglyceride levels decreased whereas polyunsaturated fatty acid values increased after 21 days; then they returned to baseline levels at the end of treatment. Total cholesterol and low-density lipoprotein (LDL) cholesterol were higher than those of the baseline during all the study, whereas high-density lipoprotein (HDL) cholesterol was reduced. In erythrocyte membranes, folic acid therapy enhanced cholesterol/phospholipid ratios and the fluorescence anisotropy of diphenyl-hexatriene. We conclude that large doses of folic acid produce a favorable effect, reducing plasma homocysteine levels and protecting patients from atherosclerosis. However, as this therapy induces significant alterations in both plasma and erythrocyte membrane lipid profiles, plasma lipid values should be controlled throughout the treatment of patients with renal failure.

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