Aims: The white rot fungus Pycnoporus cinnabarinus MUCL 39533 is able to reduce vanillic acid to vanillin. Reduction of vanillic acid to vanillin catalysed by the key enzyme aryl-aldehyde dehydrogenase has been reported. Here we report the isolation and cloning of aryl-aldehyde dehydrogenase from P. cinnabarinus strain MUCL 39533. Methodology and results: An aryl-aldehyde dehydrogenase gene (PcALDH) was isolated from P. cinnabarinus by producing a partial cDNA sequence fragment of an aryl-aldehyde dehydrogenase gene through PCR. Degenerate PCR primers were designed based on codons corresponding to conserved amino acid regions of aryl-aldehyde dehydrogenases of several fungi and bacteria. The full-length PcALDH cDNA was obtained through ReverseTranscription-Polymerase Chain Reaction (RT-PCR) and Rapid Amplification cDNA Ends (RACE) PCR. PcALDH cDNA comprises an open reading frame of 1,506 bp that encodes a protein of 501 amino acids. The PcALDH predicted protein showed the highest amino acid sequence identity (84%) to ALDH from Trametes versicolor. In silico analysis of PcALDH indicated that it belongs to the ALDH super-family and Class 3 ALDH. Conclusion, significance and impact study: PcALDH cDNA was successfully isolated and characterized. Important motifs identified from the highly conserved PcALDH protein indicated that it belongs to the aldehyde dehydrogenase superfamily. The cDNA clone will be used in expression studies to confirm the catalytic function of the enzyme.
Vanillic Acid ; Flavoring Agents

High intake of added sugars increases the risk for obesity, type 2 diabetes, and cardiovascular disease. Non-nutritive sweeteners (NNS) are widely used in many beverages and food products to reduce calories and sugar content. NNS have higher intensity of sweetness per gram than caloric sweeteners such as sucrose, corn syrup, and fruit juice concentrates. NNS approved for use have been tested and determined to be safe at levels that are within acceptable daily intake by the Joint Food Agriculture Organization/World Health Organization Expert Committee on Food Additives. The eight items of sweeteners are regulated as food additives in Korea. Dietary intake of the sweeteners was suggested as safety level by the ministry of Food and Drug Safety in 2012. If substituted for caloric sweeteners without intake of additional calories from other food sources, NNS may help consumers limit carbohydrate and energy intake as a strategy to manage blood glucose and weight. Dietitians can provide guidance on the use of NNS that give the desired results in food preparation and use at the table.
Agriculture ; Blood Glucose ; Carbohydrates ; Cardiovascular Diseases ; Diabetes Mellitus ; Energy Intake ; Food Additives ; Food and Beverages ; Fruit ; Joints ; Korea ; No-Observed-Adverse-Effect Level ; Non-Nutritive Sweeteners* ; Nutritionists ; Obesity ; Sucrose ; Sweetening Agents ; Zea mays

OBJECTIVETo estimate the daily intake of DEHP among workers in flavoring factories.

METHODS71 workers in two flavoring manufacturers, 27 administrators in those factories and 31 laboratory technicians in a research institute were recruited and assigned to exposure group, control group 1 and control group 2 respectively. Their urinary DEHP metabolites, mono(2-ethylhexyl) phthalate (MEHP), mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), were detected by isotope dilution-ultra performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS). The urinary metabolites concentrations were converted into DEHP intake levels using two pharmacokinetic models: the urine creatinine-excretion (UCE) one and the urine volume (UV) one.

RESULTSNo significant differences were found among the three groups. Based on the urinary concentrations of Σ₃MEHP, we got a median daily DEHP intake of 3.22 or 1.85 μg/kg body-weight/day applying the UV or UCE models respectively. Depending on the UV model, three subjects (2.34%) exceeded the RfD value given by US EPA and the P₅₀ of estimate daily DEHP intakes accounted for 16.10% of the RfD value. No subjects exceeded the limitation depending on the UCE model.

CONCLUSIONThe workers in flavoring factories were not supposed to be the high DEHP exposure ones and their exposure level remained at a low risk.

Curcumin is a widely used flavoring agent in food, and it has been reported to inhibit cell growth, to induce apoptosis, and to have antitumor activity in many cancers. Cisplatin is one of the most potent known anticancer agents and shows significant clinical activity against a variety of solid tumors. This study was undertaken to investigate the synergistic apoptotic effects of co-treatment with curcumin and cisplatin on human tongue SCC25 cells. To investigate whether the co-treatment efficiently reduced the viability of the SCC25 cells compared with the two treatments separately, an MTT assay was conducted. The induction and the augmentation of apoptosis were confirmed by DNA electrophoresis, Hoechst staining, and an analysis of DNA hypoploidy. Western blot, MMP and immunofluorescence tests were also performed to evaluate the expression levels and the translocation of apoptosis-related proteins following the co-treatment. In this study, following the co-treatment with curcumin and cisplatin, the SCC25 cells showed several forms of apoptotic manifestation, such as nuclear condensation, DNA fragmentation, reduction of MMP, increased levels of Bax, decreased levels of Bcl-2, and decreased DNA content. In addition, they showed a release of cytochrome c into the cytosol, translocation of AIF and DFF40 (CAD) to the nuclei, and activation of caspase-7, caspase-3, PARP, and DFF45 (ICAD). In contrast, separate treatments of 5 microM of curcumin or 4 microg/ml of cisplatin, for 24 hours, did not induce apoptosis. Therefore, our data suggest that combination therapy with curcumin and cisplatin could be considered as a novel therapeutic strategy for human oral squamous cell carcinoma.
Antineoplastic Agents ; Apoptosis ; Blotting, Western ; Carcinoma, Squamous Cell* ; Caspase 3 ; Caspase 7 ; Cell Line* ; Cisplatin* ; Curcumin* ; Cytochromes c ; Cytosol ; DNA ; DNA Fragmentation ; Electrophoresis ; Flavoring Agents ; Fluorescent Antibody Technique ; Humans ; Tongue*

This study was designed to determine whether acute fructose or sucrose administration at different levels (0.05 g/kg, 0.1 g/kg or 0.4 g/kg body weight) might affect oral glucose tolerance test (OGTT) in normal and type 2 diabetic rats. In OGTT, there were no significant differences in glucose responses between acute fructose- and sucrose-administered groups. However, in normal rats, the AUCs of the blood glucose response for the fructose-administered groups tended to be lower than those of the control and sucrose-administered groups. The AUCs of the lower levels fructoseor sucrose-administered groups tended to be smaller than those of higher levels fructose- or sucrose-administered groups. In type 2 diabetic rats, only the AUC of the lowest level of fructose-administered (0.05 g/kg body weight) group was slightly smaller than that of the control group. The AUCs of fructose-administered groups tended to be smaller than those of the sucrose-administered groups, and the AUCs of lower levels fructose-administered groups tended to be smaller than those fed higher levels of fructose. We concluded from this experiment that fructose has tendency to be more effective in blood glucose regulation than sucrose, and moreover, that smaller amount of fructose is preferred to larger amount. Specifically, our experiments indicated that the fructose level of 0.05 g/kg body weight as dietary supplement was the most effective amount for blood glucose regulation from the pool of 0.05 g/kg, 0.1 g/kg and 0.4 g/kg body weights. Therefore, our results suggest the use of fructose as the substitute sweetener for sucrose, which may be beneficial for blood glucose regulation.
Animals ; Area Under Curve ; Blood Glucose ; Body Weight ; Dietary Supplements ; Fructose ; Glucose ; Glucose Tolerance Test ; Rats ; Sucrose ; Sweetening Agents

PURPOSE: Maltol (3-hydroxy-2-methyl-4-pyrone), formed by the thermal degradation of starch, is found in coffee, caramelized foods, and Korean ginseng root. This study investigated whether maltol could rescue neuroretinal cells from oxidative injury in vitro. METHODS: R28 cells, which are rat embryonic precursor neuroretinal cells, were exposed to hydrogen peroxide (H2O2, 0.0 to 1.5 mM) as an oxidative stress with or without maltol (0.0 to 1.0 mM). Cell viability was monitored with the lactate dehydrogenase assay and apoptosis was examined by the terminal deoxynucleotide transferase-mediated terminal uridine deoxynucleotidyl transferase nick end-labeling (TUNEL) method. To investigate the neuroprotective mechanism of maltol, the expression and phosphorylation of nuclear factor-kappa B (NF-kappaB), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 were evaluated by Western immunoblot analysis. RESULTS: R28 cells exposed to H2O2 were found to have decreased viability in a dose- and time-dependent manner. However, H2O2-induced cytotoxicity was decreased with the addition of maltol. When R28 cells were exposed to 1.0 mM H2O2 for 24 hours, the cytotoxicity was 60.69 ± 5.71%. However, the cytotoxicity was reduced in the presence of 1.0 mM maltol. This H2O2-induced cytotoxicity caused apoptosis of R28 cells, characterized by DNA fragmentation. Apoptosis of oxidatively-stressed R28 cells with 1.0 mM H2O2 was decreased with 1.0 mM maltol, as determined by the TUNEL method. Western blot analysis showed that treatment with maltol reduced phosphorylation of NF-kappaB, ERK, and JNK, but not p38. The neuroprotective effects of maltol seemed to be related to attenuated expression of NF-kappaB, ERK, and JNK. CONCLUSIONS: Maltol not only increased cell viability but also attenuated DNA fragmentation. The results obtained here show that maltol has neuroprotective effects against hypoxia-induced neuroretinal cell damage in R28 cells, and its effects may act through the NF-kappaB and mitogen-activated protein kinase signaling pathways.
Animals ; *Apoptosis ; Blotting, Western ; Cell Survival ; Cells, Cultured ; Disease Models, Animal ; Flavoring Agents/pharmacology ; In Situ Nick-End Labeling ; Oxidative Stress/*drug effects ; Pyrones/*pharmacology ; Rats ; Retinal Ganglion Cells/drug effects/metabolism/*pathology

Electronic cigarettes (ECs) are a device that aerosolize liquid nicotine by heating a solution of nicotine, glycerol and flavoring agents. The awareness and the usage of ECs has increased in many countries. Due to the online sales and the absence of EC regulations, the prevalence of EC usage is especially high in adolescents and young adults. Due to the large amount and the high nicotine concentration of EC liquid, the ingestion for suicide can lead to cardiac death. We had two patients, a 27-year-old male who ingested about 23 mg/kg of nicotine and a 17-year-old female who ingested about 30 mg/kg of nicotine. Both patients presented seizure-like movement and cardiac arrest. They had metabolic acidosis and transient cardiomyopathy. They were ultimately discharged with a cerebral performance category of 2 and 4, respectively. Increasing EC use may produce more cases of medical problems or suicide by nicotine intoxication.
Acidosis ; Adolescent ; Adult ; Cardiomyopathies ; Commerce ; Death ; Eating ; Electronic Cigarettes* ; Female ; Flavoring Agents ; Glycerol ; Heart Arrest ; Heating ; Hot Temperature ; Humans ; Male ; Methods* ; Nicotine ; Poisoning ; Prevalence ; Social Control, Formal ; Suicide* ; Young Adult

No abstract available.
Sweetening Agents*

Many different additives are added to the food which we consume and the number of additives are estimated ranges from 2,000 to 20,000. These substances include preservatives, stabilizers, conditioners, thickeners, colorings, flavorings, sweeteners, and antioxidants. Despite the multitude of additives known, only a surprisingly small number have been associated with hypersensitivity reactions.
Antioxidants ; Dermatitis, Atopic ; Food Additives ; Food Hypersensitivity ; Hypersensitivity ; Sweetening Agents

Carbohydrates are a primary source of energy and a major component of the structure of living things-; there are many different kinds. As eating behavior is a part of life, it was usually not described in addiction. However, sometimes it seems aspects of addiction. This eating behavior can also appear with regard to other food. A bio-psycho-social model is required for complex analysis of addiction. When highly addictive agents are excluded, we can usually identify a key factor related to the vulnerability of the individual to addictive behavior. Considering that every source of happiness can potentially lead to addictive behaviors, we need to be cautious about the controlling. Not every carbohydrate can be connected with addictive behavior. Addictive behavior could be associated with a variety of ingredients other than carbohydrates. Until recently, sweet substances were thought to be the primary culprit behind addictive behavior. It is necessary to identify the food component or other factors associated with a specific craving. A multidimensional approach to the psychology of addictive behaviors might be more useful than opposing carbohydrate consumption in general.
Behavior, Addictive ; Carbohydrates ; Craving ; Feeding Behavior ; Happiness ; Psychology ; Sweetening Agents