Vitamin-loaded electrospun cellulose acetate nanofiber mats as transdermal and dermal therapeutic agents of vitamin A acid and vitamin E

This study aims to evaluate the influence of Vitamin A and E homologues toward acrylamide in equimolar asparagine-glucose model system. Vitamin A homologue as β-carotene (BC) and five Vitamin E homologues, i.e., α-tocopherol (AT), δ-tocopherol (DT), α-tocotrienol (ATT), γ-tocotrienol (GTT), and δ-tocotrienol (DTT), were tested at different concentrations (1 and 10 µmol) and subjected to heating at 160 °C for 20 min before acrylamide quantification. At lower concentrations (1 µmol; 431, 403, 411 ppm, respectively), AT, DT, and GTT significantly increase acrylamide. Except for DT, enhancing concentration to 10 µmol (5370, 4310, 4250, 3970, and 4110 ppm, respectively) caused significant acrylamide formation. From linear regression model, acrylamide concentration demonstrated significant depreciation over concentration increase in AT (Beta = −83.0, R2 = 0.652, p ≤ 0.05) and DT (Beta = −71.6, R2 = 0.930, p ≤ 0.05). This study indicates that different Vitamin A and E homologue concentrations could determine their functionality either as antioxidants or pro-oxidants.

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CFTR Modulator Therapy with Lumacaftor/Ivacaftor Alters Plasma Concentrations of Lipid-Soluble Vitamins A and E in Patients with Cystic Fibrosis

Antioxidants ◽

10.3390/antiox10030483 ◽

2021 ◽

Vol 10 (3) ◽

pp. 483

Author(s):

Olaf Sommerburg ◽

Susanne Hämmerling ◽

S. Philipp Schneider ◽

Jürgen Okun ◽

Claus-Dieter Langhans ◽

...

Keyword(s):

Cystic Fibrosis ◽

Vitamin E ◽

Vitamin A ◽

Clinical Chemistry ◽

Pancreatic Insufficiency ◽

Plasma Concentrations ◽

Plasma Vitamin ◽

Hypervitaminosis A ◽

Cholesterol Ratio ◽

Fat Soluble Vitamins

Rationale: Cystic fibrosis (CF), caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, leads to impaired pancreatic function and therefore reduced intestinal absorption of lipids and fat-soluble vitamins especially in patients with CF developing pancreatic insufficiency (PI). Previous studies showed that CFTR modulator therapy with lumacaftor-ivacaftor (LUM/IVA) in Phe508del-homozygous patients with CF results in improvement of pulmonary disease and thriving. However, the effects of LUM/IVA on plasma concentration of the lipid soluble vitamins A and E remain unknown. Objectives: To investigate the course of plasma vitamin A and E in patients with CF under LUM/IVA therapy. Methods: Data from annual follow-up examinations of patients with CF were obtained to assess clinical outcomes including pulmonary function status, body mass index (BMI), and clinical chemistry as well as fat-soluble vitamins in Phe508del-homozygous CF patients before initiation and during LUM/IVA therapy. Results: Patients with CF receiving LUM/IVA improved substantially, including improvement in pulmonary inflammation, associated with a decrease in blood immunoglobulin G (IgG) from 9.4 to 8.2 g/L after two years (p < 0.001). During the same time, plasma vitamin A increased significantly from 1.2 to 1.6 µmol/L (p < 0.05), however, levels above the upper limit of normal were not detected in any of the patients. In contrast, plasma vitamin E as vitamin E/cholesterol ratio decreased moderately over the same time from 6.2 to 5.5 µmol/L (p < 0.01). Conclusions: CFTR modulator therapy with LUM/IVA alters concentrations of vitamins A and vitamin E in plasma. The increase of vitamin A must be monitored critically to avoid hypervitaminosis A in patients with CF.

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