Coenzyme Q10

Two simple, preciseand stability-indicating densitometric HPTLC method were developed and validated for qualitative and quantitative analysis of Coenzyme Q10in pharmaceutical formulations using normal-phase (Method I) and reversed phase (Method II) silica gel TLC plates. Both methods were developed and validated with 10×20cm glass-backed plates coated with 0.2mm layers of either silica gel 60 F254 (E-Merck, Germany) using hexane-ethyl acetate (8.5:1.5v/v) as developing system (Method I) or RP-18 silica gel 60 F254 (E-Merck, Germany) using methanol-acetone (4:6v/v) as mobile phase (Method II). Both analyses were scanned with a densitometer at 282 nm. Linearity was found in the ranges 50-800ng/spot (r(¬¬2)=0.9989) and 50-800ng/spot (r¬¬(2)=0.9987) for Method I and Method II respectively. Stability of Coenzyme Q10 was explored by the two methods using acid, base, hydrogen peroxide, temperature and different solvents. Due to the efficiency of the method in separating Coenzyme Q10 from other ingredients including its degradation products, it can be applied for quality control, standardization of different pharmaceutical formulations and stability study.

This study explored effects of ubiquinol-10 and ubiquinone-10, two different forms of coenzyme Q10, in diabetic rats. Oxidative stress is characterized by the depletion of antioxidant defenses and overproduction of free radicals that might contribute to, and even accelerate, the development of diabetes mellitus (DM) complications. Coenzyme Q10 was administered orally to diabetic rats and oxidative stress markers were then assessed. Bioavailability in normal rats was additionally assessed in various tissues and subcellular fractions after short-term and long-term coenzyme Q10 supplementation. Elevated nonfasting blood glucose and blood pressure in diabetic rats were decreased by ubiquinone-10. Both ubiquinol-10 and ubiquinone-10 ameliorated oxidative stress, based on assays for reactive oxygen metabolites and malondialdehyde. Coenzyme Q10 levels increased with both treatments and liver nicotinamide adenine dinucleotide phosphate (NADPH) coenzyme Q reductase with ubiquinone-10.

Coenzyme Q10 (CoQ10) is a lipophilic redox molecule that is present in membranes of almost all cells in human tissues. CoQ10 is, amongst other functions, essential for the respiratory transport chain and is a modulator of inflammatory processes and gene expression. Rare monogenetic CoQ10 deficiencies show noticeable symptoms in tissues (e.g. kidney) and cell types (e.g. neurons) with a high energy demand. To identify common genetic variants influencing serum CoQ10 levels, we performed a fixed effects meta-analysis in two independent cross-sectional Northern German cohorts comprising 1,300 individuals in total. We identified two genome wide significant susceptibility loci. The best associated single nucleotide polymorphism (SNP) was rs9952641 (P-value= 1.31 x 10-8, BETA = 0.063, CI0.95 [0.041, 0.085]) within the COLEC12 gene on chromosome 18. The SNP rs933585 within the NRXN-1 gene on chromosome 2 also showed genome wide significance (P-value= 3.