• Title/Summary/Keyword: Coenzyme A

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Bioaccessibility of β-Lactoglobulin Nanoemulsions Containing Coenzyme Q10: Impact of Droplet Size on the Bioaccessibility of Coenzyme Q10

  • Ha, Ho-Kyung;Lee, Mee-Ryung;Lee, Won-Jae
    • Food Science of Animal Resources
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    • v.38 no.6
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    • pp.1294-1304
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    • 2018
  • The aims of this research were to examine the effect of heating temperature (65, 75, and $85^{\circ}C$) and $CaCl_2$ concentration level (3, 4, and 5 mM) on the physicochemical properties of ${\beta}$-lactoglobulin (${\beta}$-lg) nanoemulsions (NEs) and to study how the droplet size of NEs affects the bioaccessibility (BA) of coenzyme $Q_{10}$ ($CoQ_{10}$). The droplet size of NEs and BA of $CoQ_{10}$ was assessed by particle size analyzer and UV-Vis spectrophotometer, respectively. An increase in heating temperature and $CaCl_2$ concentration level resulted in a significant (p<0.05) increase in the droplet size of NEs while there were no significant differences in polydispersity index and zeta-potential of NEs. When NEs containing $CoQ_{10}$ were incubated in simulated small intestinal phases, an increase in the droplet size and polydispersity index of NEs was observed. This indicated that NEs were not stable in small intestine and digestion of NEs occurred. As heating temperature and $CaCl_2$ concentration level were decreased, a significant (p<0.05) increase in BA of $CoQ_{10}$ was observed. There was a significant (p<0.05) increase in BA of $CoQ_{10}$ with a decrease in the droplet size of NEs. In conclusion, heating temperature and $CaCl_2$ concentration level were key-parameters affecting the initial droplet size of NEs and BA of $CoQ_{10}$ was negatively correlated with initial droplet size of NEs.

Coenzyme Q10, oxidative stress markers, and sperm DNA damage in men with idiopathic oligoasthenoteratospermia

  • Alahmar, Ahmed T;Sengupta, Pallav;Dutta, Sulagna;Calogero, Aldo E.
    • Clinical and Experimental Reproductive Medicine
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    • v.48 no.2
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    • pp.150-155
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    • 2021
  • Objective: Oxidative stress (OS) plays a key role in the etiology of unexplained male infertility. Coenzyme Q10 (CoQ10) is a potent antioxidant that may improve semen quality and OS in infertile men with idiopathic oligoasthenoteratospermia (OAT), but the underlying mechanism is unknown. Therefore, the present study was undertaken to investigate the effect of CoQ10 on OS markers and sperm DNA damage in infertile patients with idiopathic OAT. Methods: This prospective controlled study included 50 patients with idiopathic OAT and 50 fertile men who served as controls. All patients underwent a comprehensive medical assessment. Patients and controls received 200 mg of oral CoQ10 once daily for 3 months. Semen and blood were collected and analyzed for sperm parameters, seminal CoQ10 levels, reactive oxygen species (ROS) levels, total antioxidant capacity, catalase, sperm DNA fragmentation (SDF), and serum hormonal profile. Results: The administration of CoQ10 to patients with idiopathic OAT significantly improved sperm quality and seminal antioxidant status and significantly reduced total ROS and SDF levels compared to pretreatment values. Conclusion: CoQ10, at a dose of 200 mg/day for 3 months, may be a potential therapy for infertile patients with idiopathic OAT, as it improved sperm parameters and reduced OS and SDF in these patients.

Differential Effects of Typical and Atypical Neuroleptics on Mitochondrial Function In Vitro

  • Josephine, S.;Napolitano, Modica;Lagace, Christopher-J.;Brennan, William-A.;Aprille, June-R.
    • Archives of Pharmacal Research
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    • v.26 no.11
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    • pp.951-959
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    • 2003
  • A series of typical (chlorpromazine, haloperidol and thioridazine) and atypical (risperidone, quetiapine, clozapine and olanzapine) antipsychotics were tested for effects on integrated bioenergetic functions of isolated rat liver mitochondria. Polarographic measurement of oxygen consumption in freshly isolated mitochondria showed that electron transfer activity at respiratory complex I is inhibited by chlorpromazine, haloperidol, risperidone, and quetiapine, but not by clozapine, olanzapine, or thioridazine. Chlorpromazine and thioridazine act as modest uncouplers of oxidative phosphorylation. The typical neuroleptics inhibited NADH-coenzyme Q reductase in freeze-thawed mitochondria, which is a direct measure of complex I enzyme activity. The inhibition of NADH-coenzyme Q reductase activity by the atypicals risperidone and quetiapine was 2-4 fold less than that for the typical neuroleptics. Clozapine and olanzapine had only slight effects on NADH-coenzyme Q reductase activity, even at 200 $\mu$ M. The relative potencies of these neuroleptic drugs as inhibitors of mitochondrial bioenergetic function is similar to their relative potencies as risk factors in the reported incidence of extrapyramidal symptoms, including tardive dyskinesia (TD). This suggests that compromised bioenergetic function may be involved in the cellular pathology underlying TD.

Production of Coenzyme $Q_{10}$ by Recombinant E. coli Harboring the Decaprenyl Diphosphate Synthase Gene from Sinorhizobium meliloti

  • Seo Myung-Ji;Im Eun-Mi;Hur Jin-Haeng;Nam Jung-Yeon;Hyun Chang-Gu;Pyun Yu-Ryang;Kim Soon-Ok
    • Journal of Microbiology and Biotechnology
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    • v.16 no.6
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    • pp.933-938
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    • 2006
  • Decaprenyl diphosphate synthase (DPS) is the key enzyme for the production of coenzyme $Q_{10}$ ($CoQ_{10}$). A dps gene from Sinorhizobium meliioti KCCM 11232 (IFO 14782) was isolated by PCR and then cloned in Escherichia coli. DNA sequencing analysis revealed an open reading frame of 1,017 bp encoding a 338-amino-acid protein. The protein was identical at the 98% level to the putative octaprenyl diphosphate synthase (IspB) of S. meliloti 1021. The deduced amino acid sequence included the DDxxD domains conserved in the majority of the prenyl diphosphate synthases. Heterologous expression in E. coli BL21 (DE3) was carried out, and the $CoQ_{10}$ produced was then analyzed by HPLC. E. coli BL21 (DE3) harboring the dps gene from S. melioti produced CoQ$_{10}$ in addition to endogenous coenzyme Q$_8$ (CoQ$_8$), whereas wild-type E. coli BL21 (DE3) host did not have the ability of producing CoQ$_{10}$. The results suggest that the putative dps from S. meliloti KCTC 2353 encoded the DPS.

Mutations in the PPE Genes that Confer Resistance to a Nitroimidazopyran Drug on Mycobacterium bovis Strains (Mycobacterium bovis 균주들이 nitroimidazopyran 항생제에 내성을 갖게 해주는 PPE 유전자들의 돌연변이들)

  • Bae Young-Min;Daniels Lacy
    • Journal of Life Science
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    • v.15 no.2 s.69
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    • pp.182-185
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    • 2005
  • We used the IS1096 transposon to construct Mycobacterium bovis BCG mutants resistant to an antituberculosis drug PA-824 and isolated several different mutants. We identified the locations of the insertions and found that the insertions were at various sites including the genes for the PPE proteins. HPLC analyses of the extracts of these five PPE mutant cells showed that three mutants produced only F0, and intermediate for the synthetic pathway of coenzyme $F^{420}$, and the remaining two neither F0 nor $F^{420}$. These data suggest that the products of these PPE genes are somehow involved in the biosynthesis of the coenzyme $F^{420}$.

New evidences of neurotoxicity of aroclor 1254 in mice brain: potential of coenzyme q10 in abating the detrimental outcomes

  • Majumdar, Anuradha;Nirwane, Abhijit;Kamble, Rahul
    • Environmental Analysis Health and Toxicology
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    • v.29
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    • pp.1.1-1.7
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    • 2014
  • Objectives The present subacute study was designed to evaluate the effect of coenzyme Q 10 (CoQ10) in the 28 days aroclor 1254 exposure induced oxidative stress in mice brain. Methods Biochemical estimations of brain lipid peroxidation (LPO), reduced glutathione (GSH), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetyl cholinesterase (AChE), and histopathological investigations of brain tissue were carried out. Results Oral exposure of aroclor 1254 (5 mg/kg) led to significant decrease in levels of GSH, and activities of SOD, CAT, GPx, and AChE, and increase in LPO. These aberrations were restored by CoQ10 (10 mg/kg, intraperitoneal injection [IP]). This protection offered was comparable to that of L-deprenyl (1 mg/kg, IP) which served as a reference standard. Conclusions Aroclor 1254 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in the brains of Swiss albino mice. Supplementation of CoQ10 abrogates these deleterious effects of aroclor 1254. CoQ10 also apparently enhanced acetyl cholinesterase activity which reflects its influence on the cholinergic system.

Very Long Chain Acyl-coenzyme A Dehydrogenase Deficiency: A Review of Pathophysiology, Clinical Manifestations, Diagnosis, and Treatment (장쇄 수산화 아세틸코에이 탈수소효소 결핍증에 대한 고찰)

  • Kang, Seokjin
    • Journal of The Korean Society of Inherited Metabolic disease
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    • v.22 no.1
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    • pp.21-27
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    • 2022
  • Very long-chain acyl-coenzyme A dehydrogenase (VLCAD) deficiency (VLCADD) leads to a defective 𝛽-oxidation, specifically during prolonged fasting, infection, or exercise. Patients with VLCADD usually suffer from cardiomyopathy, hypoketotic hypoglycemia, hepatic dysfunction, exercise intolerance, muscle pain, and rhabdomyolysis, and sometimes succumb to sudden death. VLCADD is generally classified into three phenotypes: severe early-onset cardiac and multiorgan failure, hypoketotic hypoglycemia, and later-onset episodic myopathy. Diagnostic evaluation comprises acylcarnitine analysis, genetic analysis, and VLCAD activity assay. In the acylcarnitine analysis, the key metabolites are C14:1, C14:2, C14, and C12:1. A C14:1 level >1 mmol/L strongly suggests VLCADD. Various treatment recommendations are available for this condition. Dietary management includes decreasing fat content, increasing medium-chain triglyceride levels, and decreasing fasting periods. Supplementation with L-carnitine is controversial. Triheptanoin (a seven-carbon fatty acid triglyceride) treatment demonstrates improvement of cardiac functions. Bezafibrate may improve the quality of life of patients with VLCAD.

Genome of Betaproteobacterium Caenimonas sp. Strain SL110 Contains a Coenzyme $F_{420}$ Biosynthesis Gene Cluster

  • Li, Xiuling;Feng, Fuying;Zeng, Yonghui
    • Journal of Microbiology and Biotechnology
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    • v.24 no.11
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    • pp.1490-1494
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    • 2014
  • To probe the genomic properties of microbes thriving in desert lakes, we sequenced the full genome of a betaproteobacterial strain (SL110) belonging to the understudied genus Caenimonas of the family Comamonadaceae. This strain was isolated from a freshwater lake in the western Gobi Desert, Northern China. Its genome contains genes encoding carbon monoxide dehydrogenase, nitrate reductase, nitrite reductase, nitric oxide reductase, and sulfur oxidation enzymes, highlighting the potentially important contribution of this group of bacteria to the cycling of inorganic elements in nature. Unexpectedly, a coenzyme $F_{420}$ biosynthesis gene cluster was identified. A further search for $F_{420}$ biosynthesis gene homologs in genomic databases suggests the possible widespread presence of $F_{420}$ biosynthesis gene clusters in proteobacterial genomes.

Enhanced Dissolution of Coenzyme Q10 using Solid Dispersions Prepared by Low Temperature Melting Method

  • Kang, Jun-Heok;Yan, Yi-Dong;Kim, Hyun-Chan;Lee, Sung-Neung;Yong, Chul-Soon;Choi, Han-Gon
    • Journal of Pharmaceutical Investigation
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    • v.40 no.5
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    • pp.277-283
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    • 2010
  • CoQ with low melting temperature was exploited to improve its solubility by preparing its solid dispersions (SDs) with a meltable polymer, poloxamer 407 (P 407). P407 can be utilized for a relatively simple, quick, inexpensive, reproducible and potentially scalable manner in the low temperature melting method. CoQ 10 solubility and dissolution increased with increasing concentrations of P 407 in SDs. Comparison of the enhanced dissolution of CoQ 10 from different poloxamers suggested that the preparation of CoQ 10 SDs using P 407 as a meltable hydrophilic polymer carrier could be a promising approach to improve its dissolution.

Studies on the possible role of thiamine in the central nervous system

  • Iwata, Heitaroh
    • Archives of Pharmacal Research
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    • v.3 no.1
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    • pp.51-55
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    • 1980
  • Thiamine, in the form of its diphosphate (TDP), is well known to act as a coenzyme, and during the early stage in the study of thiamine it had been believed that the symptoms of thiamine-deficiency were resulted secondarily from the disturbance of metabolic processes in which TDP participated as a coenzyme. However, the neurological symptoms in thiamine deficiency are now separated from the metabolic disturbances in thiamine deficiency. On the other hand, the specific involvement of phosphorylated thiamine in nerve conduction has been suggested by von Muralt, but nature of this involvement has not been elucidated at a molecular level. Recently the possible significance of thiamine triphosphate (TTP) in nervous tissue was suggested by the demonstration that TTP is not present in the brain of patients with subacute necrotizing encephalomyelitis, a fatal disease associated with an abnormality in thiamine metabolism. Furthermore, the studies using membrane fragments of rat brain strongly indicated that ion movement across the nerve membrane is associated with dephosphorylation of phosphorylated thiamine.

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