Objective: This study aimed to determine the threshold of $anti-M{\ddot{u}}llerian$ hormone (AMH) as predictor of follicular growth failure in polycystic ovary syndrome (PCOS) patients treated with clomiphene citrate (CC). Methods: Fifty female subjects with PCOS were recruited and divided into two groups based on successful and unsuccessful follicular growth. Related variables such as age, infertility duration, cigarette smoking, use of Moslem hijab, sunlight exposure, fiber intake, body mass index, waist circumference, AMH level, 25-hydroxy vitamin D level, and growth of dominant follicles were obtained, assessed, and statistically analyzed. Results: The AMH levels of patients with successful follicular growth were significantly lower (p= 0.001) than those with unsuccessful follicular growth ($6.10{\pm}3.52$ vs. $10.43{\pm}4.78ng/mL$). A higher volume of fiber intake was also observed in the successful follicular growth group compared to unsuccessful follicular growth group (p= 0.001). Our study found the probability of successful follicle growth was a function of AMH level and the amount of fiber intake, expressed as Y =-2.35+($-0.312{\times}AMH\;level$)+($0.464{\times}fiber\;intake$) (area under the curve, 0.88; 95% confidence interval, 0.79-0.98; p< 0.001). Conclusion: The optimal threshold of AMH level in predicting the failure of follicle growth in patients with PCOS treated with CC was 8.58 ng/mL.
The effect of long-term ginseng (Panax ginseng C.A. Meyer) administration on the clearance of carboxyhemoglobin (CO-Hb) and the property of blood gases was investigated in rats. Rats were received ginseng water extract (0.025% in drinking water) for 42 weeks starting at the age of 6 weeks. They were exposed to the diluted mainstream smoke generated from 15 filter cigarettes for 20 min in a round polycarbonate chamber (D37 cmXH13 cm). Under this condition, the mean CO-Hb content of control and the ginseng-treated rats immediately after the exposure was nearly the same as 13.8$\pm$2.9 f) and 13.9$\pm$1.6%, respectively. However, CO-Hb was more rapidly removed from blood in the ginseng treated rats than in untreatEd control with the laps of time, namely, its biological half life In the former was 36.9$\pm$1.5 min and in the latter was 56.9$\pm$13.2 min. Although long-term ginseng treatment did not affect the content of hemoglobin and blood pH of rats, it slightly increased blood oxygen content and its partial pressure value, and decreased levels of carbon dioxide and bicarbonate. These results suggest that long-term administration of rats with ginseng extract accelerate the elimination of CO from the blood. This effect seems to be related to the enhancement of oxygen consumption of the rat by a certain action of ginseng components as previously reported.
Objectives : Polycyclic aromatic hydrocarbons (PAHs), which are risk factors for lung cancer, have been reported to induce oxidative DNA damage. The paraoxonase (PON) plays a significant role in the detoxification of a variety of organophosphorous compounds, with paraoxonase-1 (PON1) being one of the endogenous free-radical scavenging systems in the human body. The aim of this case-control study was to investigate the effects of PAH exposure, oxidative stress and the Q192R polymorphism of PON1 genes, and their interactions in the carcinogenesis of lung cancer. Methods : One hundred and seventy seven lung cancer patients and 177 age- and sex-matched controls were enrolled in this study. Each subject was asked to complete a questionnaire concerning their smoking habits and environmental exposure to PAHs. The Q192R genotypes of the PON1 gene was examined, and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8-hydroxydeoxyguanosine (8-OH-dG) measured. Results : Cigarette smoking was found to be a significant risk factor for lung cancer. The urinary 8-OH-dG level was higher in the patients, whereas the urinary 1-OHP and 2-naphthol levels were higher in the controls. There was a significant correlation between the urinary levels of 8-OHdG and 1-OHP in both the cases and controls. The PON1 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Q/Q genotype of the PON1 gene were found to be at higher risk of developing lung cancer. There was a significant correlation between the urinary levels of 8-OH-dG and 1-OHP in those with the PON1 Q/Q genotype. Conclusions : These results lead to the conclusion that PAHs would induce oxidative DNA damage, especially in individuals with the PON1 Q/Q genotype. Therefore, people with the PON1 Q/Q genotype would be more susceptible to lung cancer than those with the R/R or Q/R genotypes of the PON1 gene.
Objectives: The purpose of this study was to assess the validity of self-reported cigarette smoking status and investigate factors associated with the accuracy self-reported and measured urinary cotinine in Korean adults. Methods: We used data from the $1^{st}$ Korean National Environmental Health Survey (2009-2011) among adults aged ${\geq}19$ years (N=6,246). The survey examined self-reported smoking status, and urinary cotinine was regarded as the biomarker of exposure to tobacco smoke. Urinary cotinine was analyzed using a gas chromatography-mass spectrometry (GC/MS) and data analysis was conducted using IBM SPSS version 20.0, which uses the sample weight and calculates variance estimates to adjust for the unequal probability of selection into the survey. Results: We calculated a cut-off point (53.3 ug/L) by using a ROC (Receiver Operating Characteristic) curve. The smoking prevalence was 24.6% based on self-reported data and 28.2% based on urinary cotinine concentrations. When we assessed the agreement between self-reported and urinary cotinine, we found an average agreement of 97.7% among self-reported smokers and 94.5% among self-reported non-smokers. Among self-reported smokers, factors affected the discrepancy were age, household economic status and average number of cigarettes smoked per day. On the other hand, gender, former smoking experience, and exposure to SHS (second hand smoke) were associated with discrepancies among self-reported non-smokers. Conclusion: These results suggest that self-reported data on smoking status provide a valid estimate of actual smoking status. In future research, we will conduct a continuous monitoring study for reliability verification of the data to reduce potential interpretation errors.
This study was to evaluate the biological activity of flavor components extracted from E. ciliata and E. splendens in order to survey the possibility applicable to tobacco and food industry. Flavor components were extracted with dividing into three parts; essential oil, absolute, oleoresin. In the nonenzymatic lipid peroxidation system, the inhibition rate($\%$) of essential oil were $67.3\;\pm\;20.7\%,\;58.1\;\pm\;19.3\%$ at the concentration of 50 ${\mu}g/mL$ of E. ciliata and E. splendens, respectively. The inhibition rate($\%$) of the oleoresin in E. ciliata was higher than one in E. splendens. In the enzymatic lipid peroxidation system, the inhibition rate($\%$) of essential oil and oleoresin was$14.28\;\pm\;2.38\%,\;and\;65.93\;\pm\;0.01\%,\;and\;was\;22.58\;\pm\;2.84\%\;and\;40.73\;pm\;6.04\%$. The oleoresin of two species were showed above $90\%$ of the inhibition rate($90\%$) against autooxidative lipid peroxidation system. $EC_{50}$ values in neutral red uptake assays 24 h of exposure times were $23.3\;{\mu}g/mL,\;341.0\;{\mu}g/mL\;and\;17.2\;{\mu}g/mL$ in essential oil, absolute and oleoresin from E. ciliata respectively, and were $46.4\;{\mu}g/mL,\;681.7\;{\mu}g/mL\;17.6\;{\mu}g/mL$ in three extractions of E. splendens. Oleoresin of two species showed high rate in the cytotoxic effect by neutral red uptake assay. Absolute and oleoresin did not show antibiotic and mutagenic activity. On the contrary, essential oil with over 500 ug/plate showed antibiotic and mutagenic activity in Ames test. Essential oil and oleoresin have a prolongating effect the ciliostasis of rat trachea. This results indicate that flavor components extracted from E. ciliata and E. splendens can be considered to be toxicological safe and to be the possibility applicable the cigarette, food and drug industry as a flavor for expectoration.
This study has done to investigate the relationship between the icreased lipid oncentration caused by smoking and plama levels of vitamin A and vitamin E, antiodative enzyme activity, and lipid peroxidation , in 52 male smokers and 32 non-smokers, Dietary vitamin A and vitamin E intake was imilar in both smokers and non-smokers. Absolute plasma concentrations of vitamin A and vitamin E were not significantly different between two groups, whereas vitamin E/cholesterol ration in plasma was low or in smokers than in that of non-smokers(p<0.05). It was considered that this lowered effect was due to the elevated plasma lipid concentration rather than oxidant stress derived from smoking, in view of the fact that smokers had higher cholesterol (15.2%) adn LDL-C(26.6%) levels than non-smokers. In non-smokers, plasma thiobarbiturin acid reactive substances(TBARS) conrrelated positively with total cholesterol(r=0.63466, p<0.001), LDL-C level(r=0.57166, p<0.01) , and LDL-C/HDL-C ratio(r=0.45926, p<0.05) . Activities of glutathione perosidase(GSH-Px) , superoside dismutase(SOD), and catalse made no difference in both groups. However, it was observed in non-smokers that GSH-Px activity had negative correlations with total cholesterol(r=-0.67293, p<0.001), LDL-C level(r=-0.62878, p<0.001), and LDL-C/HDL-C ratio (r=-0.58824, p<0.01), indicating that there was a dependent relationship between lipid perosidation and plasma lipid level. The smokers also showed negative correlations for GSH-Px activity with total cholesterol (r=-0.29946, p<0.05) and LDL-c level (r=0.45914, p<0.001), and LDL-C/HDL-c ratio(r=-0.35438, p<0.05). It seemed that the lipid that the lipid level elevated by sustaines smoking resulted in reducing vitamin E/cholesterol ratio and proportion of antioxidant to oxidant load, and then GSH-Px activity, with insufficient removal of free radicals(TBARS 2.43$\pm$0.51 and 1.81$\pm$0.15nmol/ml in smokers and non-smokers, respectively). These findings suggest that higher plasma lipid levels may play a more important role in perturbing the antioxidant defense system including vitamin E status and GSH-Px activity, at least in circumstances that increase lipid concentration . In addition, in exposure to free radicals like those in cigarette smoke. In those cases the ratio of vitamin E/lipid in plasma can be a more indicator of vitamin E status than plasma levels of vitamin E alone.
Cigarette smoking is the leading cause of the lung cancer. However, mechanism of action underlying the carcinogenesis in the lung still remains to be elucidated. The present study attempted to look into the carcinogenic potential of tobacco-specific nitrosamine, NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) and the effects of protein kinase C (PKC) isoforms in an immortalized human epithelial cell model. Material and Method: Immortalized human epithelial cells were exposed with NNK and examined for its carcinogenic potential as measured by saturation density, soft-agar colony formation, and cell aggregation assay. The specific isoform of PKCs involved in the cellular transformation was analysed through western blot with monoclonal antibody and measured separately in cytosolic fraction and membrane fraction. Result: Human epithelial cells exposed with NNK showed prominent carcinogenic potential in saturation density, soft agar colony formation, and cell aggregation assay. PKC isoform analysis results are as follows: PKC- $\alpha$ showed significant translocation of protein levels from cytosolic fraction to membrane fraction, as analyzed by immunoblot. PKC- $\varepsilon$ showed a dose-dependent increase of translocation. PKC- λ was not affected by NNK treatment. Conclusion: The study demonstrated that there was a certain specificity in the patterns of isoform induction following chemical carcinogen exposure. Thus, it is suggested that identification of specific isoform be a clue to find target molecules in the carcinogenesis.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
/
v.34
no.5
/
pp.509-517
/
2008
DNA damage accumulates in cells as a result of exposure to exogenous agents such as benzopyrene, cigarette smoke, ultraviolet light, X-ray, and endogenous chemicals including reactive oxygen species produced from normal metabolic byproducts. DNA damage can also occur during aberrant DNA processing reactions such as DNA replication, recombination, and repair. The major of DNA damage affects the primary structure of the double helix; that is, the bases are chemically modified. These modification can disrupt the molecules'regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. DNA repair genes and proteins scan the global genome to detect and remove DNA damage and damage to single nucleotides. Direct reversal of DNA damage, base excision repair, double strand break. DNA repair are known relevant DNA repair mechanisms. Four different mechanisms are distinguished within excision repair: direct reversal, base excision repair, nucleotide excision repair, and mismatch repair. Genetic variation in DNA repair genes can modulate DNA repair capacity and alter cancer risk. The instability of a cell to properly regulate its proliferation in the presence of DNA damage increase risk of gene mutation and carcinogenesis. This article aimed to review mechanism of excision repair and to understand the relationship between genetic variation of excision repair genes and head and neck cancer.
Journal of the Korean Applied Science and Technology
/
v.31
no.1
/
pp.120-129
/
2014
The structure and physiological function of human skin continuously weaken due to growing older. The reasons of aging from external conditions are long term exposure to sun, wind, heat, cigarette smoke, and etc. This also palmitoyl oligopeptide or ceramide oligopeptide are known asc ingredient stimulating collagens and have the effect of reproducing the upper level of skin. Acetyl hexapeptide is an ingredient that makes the skin and muscle suppler and reduces wrinkles. It is a major high function beauty ingredient that substitutes botox. After dividing 7%, 14%, and 20% Acetyl hexapeptide experimental groups as groups A, B, and C the control group and experiment groups' change of wrinkles, hair follicles, moisture content, and dead skin cells was analyzed. According to the results, Acetyl hexapeptide seems to affect wrinkles, hair follicles and moisture content contrasting to the control group. Experimental groups and control group showed similar change in dead skin cells. In contrast to the control group satisfaction of examines was affected in wrinkles, hair follicles and moisture but removing dead skin cells had similar result in experimental groups and control group.
Journal of the Korean Society of Food Science and Nutrition
/
v.38
no.7
/
pp.852-861
/
2009
This study was performed to assess the risk factors associated with hypertension from Jan/2003 to Feb/2003. The subjects were 1,296 people (496 males, 800 females) aged 40 years and over living in Andong rural area. The hypertensive group was composed of 602 people (272 males, 330 females), who were diagnosed as hypertension ($SBP{\geq}140\;mmHg$ or $DBP{\geq}90\;mmHg$) for the first time at this health examination. The mean anthropometric values of body weight, body fat (%), body mass index (BMI) and waist circumference were significantly higher in hypertensive group than those in normal group. However, the biochemical measurements such as total-cholesterol (TC), triglyceride (TG), HDL-C, LDL-C and fasting blood glucose (FBG) levels did not show any difference between two groups except TG in female. The risk factors of interest in the development of hypertension were analyzed using the multiple logistic regression and expressed as odds ratio (OR) and 95% confidential interval (CI). The results showed that age, sex, obesity, waist circumference, alcohol drinking and meat intakes were risk factors for hypertension. In contrast, cigarette smoking, exercise and the increased fish, fruit and vegetable (except Kimchi) consumption, blood lipid levels and FBG were not linked with the development of hypertension. Nutrient intakes were not associated with hypertension, either. In conclusion, we cannot assert that this study established the existence of the cause-and-effect relationship between nutrient intakes and risk of hypertension in the subjects, but it does suggest that this is a question worth investigating further using a larger scale of case-control study to determine how the past exposure to some nutrient or dietary component relates to the development of the disease.
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