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Results for “Coenzyme Q10”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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5 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2020

Crystalline Loading of Lipophilic Coenzyme Q10 Pharmaceuticals within Conjugated Carbon Aerogel Derivatives

Low-density aerogel materials currently are being considered for applications in controlling the rate of release for small-molecule pharmaceuticals in vivo. In particular, silica (SiO2) aerogels are an intriguing platform for controlling both the absolute amount of drug loading, but also the crystalline state of small molecule pharmaceuticals has been shown to affect drug release kinetics. To date, loading silica aerogel materials with crystalline pharmaceuticals typically require dissolving small molecules in a supercritical solvent (i.e., CO2) before drying to recover the aerogel/drug composite. Here we demonstrate a simple and low-cost method for controlling the crystallinity of the model drug coenzyme Q10 (CoQ10) within carbon aerogel materials by rationally controlling the chemical microstructure of the aerogel to exhibit ?-conjugated (sp2) chemical bonding. In particular, both pyrolyzed graphene and nanodiamond aerogels exhibit enhanced intrinsic drug loading capacity and CoQ10 crystallinity over a broad range of sp2 surface-curvature. In contrast, amorphous carbon aerogel materials are observed to load CoQ10 pharmaceuticals with strictly amorphous microstructure.

Lim, Mathew↗
DOE OSTI2012

Mixture-process variable approach to optimize a microemulsion electrokinetic chromatography method for the quality control of a nutraceutical based on coenzyme Q10

In recent years, multivariate optimization has played an increasing role in analytical method development. ICH guidelines recommend using statistical design of experiments to identify the design space, in which multivariate combinations of composition variables and process variables have been demonstrated to provide quality results. Considering a microemulsion electrokinetic chromatography method (MEEKC), the performance of the electrophoretic run depends on the proportions of mixture components (MCs) of the microemulsion and on the values of process variables (PVs). In the present work, for the first time in the literature, a mixture-process variable (MPV) approach was applied to optimize a MEEKC method for the analysis of coenzyme Q10 (Q10), ascorbic acid (AA), and folic acid (FA) contained in nutraceuticals. The MCs (buffer, surfactant-cosurfactant, oil) and the PVs (voltage, buffer concentration, buffer pH) were simultaneously changed according to a MPV experimental design. A 62-run MPV design was generated using the I-optimality criterion, assuming a 46-term MPV model allowing for special-cubic blending of the MCs, quadratic effects of the PVs, and some MC-PV interactions. The obtained data were used to develop MPV models that express the performance of an electrophoretic run (measured as peak efficiencies of Q10, AA, and FA) in terms of the MCs and PVs. Contour and perturbation plots were drawn for each of the responses. Finally, the MPV models and criteria for the peak efficiencies were used to develop the design space and an optimal subregion (i.e., the settings of the mixture MCs and PVs that satisfy the respective criteria), as well as a unique optimal combination of MCs and PVs.

Coenzyme Q10↗
DOE OSTI2018

Ubiquinol promotes retinal ganglion cell survival and blocks the apoptotic pathway in ischemic retinal degeneration

Highlights: • Ubiquinol treatment promotes RGC survival in the ischemic retina. • Ubiquinol treatment blocks astroglial and microglial activation in the ischemic retina. • Ubiquinol treatment prevents apoptotic cell death by modulating the Bax/Bad/Bcl-xL pathway in the ischemic retina. Coenzyme Q10 (CoQ{sub 10}) protects retinal ganglion cells (RGCs) in experimental retinal ischemia and glaucoma by scavenging reactive oxygen species. We tested whether a diet supplemented with ubiquinol, the reduced form of CoQ{sub 10}, promotes RGC survival and blocks the apoptotic pathway in ischemic mouse retina induced by acute high intraocular pressure (IOP) elevation. Ubiquinol (1%) treatment significantly promoted RGC survival at 2 weeks after ischemia/reperfusion. The ubiquinol treatment significantly blocked activation of astroglial and microglial cells in the ischemic retina at 2 weeks. While the ubiquinol treatment significantly decreased active Bax protein expression in the ischemic retina, phosphorylation of Bad at serine 112 and Bcl-xL protein expression were preserved in the ubiquinol-treated ischemic retina at 12 h. Consistently, the ubiquinol treatment prevented apoptotic cell death by blocking caspase-3 cleavage. These results suggest that the ubiquinol enhances RGC survival by modulating the Bax/Bad/Bcl-xL-mediated apoptotic pathway in the ischemic retina. Ubiquinol has therapeutic potential for ameliorating elevated IOP-induced ischemic retinal degeneration.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

A novel ADCK4 mutation in a Chinese family with ADCK4-Associated glomerulopathy

Highlights: • ADCK4 is located on human chromosome 19q13.2 and encodes the ADCK4 protein, which interacts with members of the CoQ10 biosynthesis pathway. • Mutations in the ADCK4 gene can cause CoQ10 deficiency and mitochondrial nephropathy (ADCK4-associated glomerulopathy, ADCK4-GN). • ADCK4-GN mainly manifests as steroid resistant nephrotic syndrome clinically and focal segmental glomerulosclerosis pathologically. • The C-terminal portion in ADCK4 is important and indispensable. The upstream nonsense/frameshift mutations should be considered deleterious. • CoQ10 treatment may reduce proteinuria and postpone ADCK4-GN progression. AarF domain-containing kinase 4 (ADCK4)-associated glomerulopathy (ADCK4-GN) is an inherited mitochondrial nephropathy caused by mutations in the ADCK4 gene. Herein, we report a case of ADCK4-GN. The patient, a 14-year-old Chinese male, presented with asymptomatic proteinuria and steroid resistance. A renal biopsy showed focal segmental glomerulosclerosis (FSGS) and dysmorphic mitochondria in podocytes. Coenzyme Q10 treatment was partially effective. No adverse events were observed. Next generation and Sanger sequencing analyses revealed compound heterozygous mutations (c.625C > G, p.D209H and c.918G > T, p.C306X). Both inherited mutations are located in the highly conserved ABC1 domain. The unreported nonsense mutation causes a loss of 197 amino acids from the C-terminal portion of ADCK4, suggesting a deleterious effect of the truncating mutation by abolishing ADCK4 function. In conclusion, we identified a novel ABC1 domain-localized pathogenic mutation responsible for ADCK4-GN, further supporting the importance of the C-terminal portion of ADCK4. Next generation sequencing facilitated the early diagnosis. CoQ{sub 10} treatment may reduce proteinuria and postpone ADCK4-GN progression.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2019

Niacin for Parkinson's disease

Abstract Parkinson's disease (PD) is a neurodegenerative disease associated with progressive loss of motor function and cognitive decline occurring in 1% of the USA population. There is no cure for PD, and current treatment regimens are directed towards treating symptoms and not treating the underlying cause of the disease. Chronic neuroinflammation is associated with loss of neuronal cells, leading to motor and cognitive decline. Current clinical trials on drugs and nutraceuticals, such as coenzyme Q10 and niacin, are being carried out to delay progression and reduce damage by inflammatory molecules, such as reactive oxygen species and cytokines, in PD patients. In this review, we present available clinical trials and the role of niacin in reducing neuroinflammation in PD.

Seamon, Marissa↗