Kim, Seo-Yun;Lee, Su-Hwan;Lee, In-Seon;Kim, Sae-Byol;Moon, Chan-Soo;Jung, Sung-Mo;Kim, Se-Kyu;Kim, Young-Sam
Tuberculosis and Respiratory Diseases
/
v.72
no.2
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pp.163-168
/
2012
Background: Cigarette smoke induced release of iron could alter iron metabolism in the lungs of chronic smokers and contribute to the increase in the total oxidative burden on the lungs of smokers. In previous studies, ferritin levels of bronchoalveolar lavage fluid in smokers were elevated. The aim of the present study was to investigate the relationship between serum ferritin concentration, smoking and lung function in Korean people. Methods: This study was based on the data acquired in the second year (2008) of the Forth National Health and Nutrition Examination Survey that was conducted from 2007 to 2009. The analysis included 2,244 subjects who were older than 20 years and had complete data from both lung function test and serum ferritin concentration. Among participants, 1,076 were male and 1,168 were female. Results: Mean serum ferritin concentrations in males were $120.3{\pm}80.1{\mu}g/L$ and $47.9{\pm}39.8{\mu}g/L$ in females. There were no differences in serum ferritin concentrations between non-smokers and smokers after adjusting for age, body mass index, and amounts of alcohol. Serum ferritin concentrations were associated with smoking amounts by simple linear regression but not associated with smoking amounts after adjustment with age, body mass index, and amounts of alcohol in both males and females. Lung function was not associated with serum ferritin concentrations. Conclusion: Our data suggested that serum ferritin concentrations are not related with smoking and lung function.
Lee, Jeong Yoon;An, Yeon Ju;Kim, Ji Won;Choi, Hyo-Kyoung;Lee, Yoo-Hyun
Journal of the Korean Society of Food Science and Nutrition
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v.45
no.10
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pp.1391-1397
/
2016
We investigated the hepatoprotective effects of Angelica keiskei Koidzumi extract (AK) in HepG2-overexpressing cytochrome P4502E1 (CYP2E1) and C57BL/6J mice. In HepG2 cells expressing CYP2E1, cell viability and catalase activity in the ethanol-AK co-treated group significantly increased compared to those in the ethanol-treated group. In the in vivo study with C57BL/6J mice, the AK-supplemented group with ethanol liquid diet showed significantly reduced hepatic markers, including serum aspartate aminotransferase, alanine aminotransferase, and ${\gamma}$-glutamyl transferase, compared to the ethanol group without AK supplementation. AK supplementation (20 mg/kg BW/d) also significantly attenuated reactive oxygen species generation and malondialdehyde level. Notably, a low dose of AK supplementation (20 mg/kg BW/d) suppressed expression of hepatic CYP2E1 and inhibited CYP2E1 enzyme activity. These data indicate that a low dose of AK supplementation could restrain alcohol-induced hepatic damage mediated by CYP2E1.
The purpose of this study was to investigate the effects of dietary Indongcho(L. japonica Thunb) powder on blood glucose, serum lipid levels and antioxidative enzymes in normal and streptozotocin(STZ)-induced diabetic rats. Four groups of rats(3-week-old inbred Sprague-Dawley male rats) were normal rats fed control diet(NC), diabetic rats fed control diet(DC), normal rats fed Indongcho powder diet(NI), and diabetic rats fed Indongcho powder diet(DI). Diabetes was induced by single injection of streptozotocin(60mg/kg B.W., i.p.). The animals were fed ad libium each of the experimental diet for 5 weeks. Food and water intakes were determined everyday. Blood glucose and serum total cholesterol levels were determined every week. After 5 weeks the animals were sacrificed and activities of antioxidant enzymes and lipid peroxidation products were determined in their liver and kidney homogenates. We also determined serum concentrations of total lipid(TL), total cholesterol(TC), triglycerides(TG) and HDL-cholesterol(HDL-C). Blood sugar and water intake were higher in diabetic group(DC and DI group) than normal group(NC and NI group) and were not significantly decreased by dietary Indongcho intake. Body weight gain and FER(feed efficiency ratio) were reduced by STZ treatment. But, Final body weight was recovered by Indongcho-contained diet. LHR(LDL-cholesterol/HDL-cholesterol) of the DI g re up was significantly lower than the other experimental groups(NC, NI and DC groups). The hepatic glucose 6-phosphatase(G6Pase) activity of the groups fed Indongcho diet(NI and DI group) was lower than the groups fed control diet(NC and DC group) and the G6Pase activity of NI group was recovered to the normal levels(p<0.05). However, The glutathione peroxidase(GPx) and glutathione reductase(GR) activities in liver and G6Pase activity in kidney were not statistically different between the control and diabetic control groups. Renal GST activity of the DI group was recovered by Indongcho intake. In conclusion, these results confirm oxidative stress in the liver and kidney of rats with STZ diabetes and antioxidative effect of Indongcho.
Biofilm media was equipped in two-compartmented wastewater treatment bioreactor which was separated by porcelain septum. DC 2.0 volt of electric potential was charged to anodic (oxidative) biofilm media (ABM) to induce oxidation potential but not to that of carbon (neutral) biofilm media (CBM) that was used for control test. Biofilm structure, biomass variation, Off variation and wastewater treatment efficiency in the bioreactor equipped with ABM (ABM-bioreactor) and CBM (CBM-bioreactor). Time-coursed variation of biofilm structure forming on surface of ABM and CBM was observed by scanning electron microscopy. The biofilm growing on ABM was dispersed on surface and was not completely covered the media but the biofilm growing on CBM was continuously increased and finally covered the media. The ORP of CBM was decreased to 100 mV, which was reciprocally proportional to the biomass growth. However, the ORP of ABM was about 800 mV, which was maintained during operation for about 60 days. The treatment efficiency of COD in the ABM bioreactor was 2 times higher than those in the CBM bioreactor. From these results, we proposed that electrochemical oxidation potential charged to biofilm media may inhibit formation of biofilm extremely condensed and activate bacterial cell metabolism.
It has been well documented that animals exposed to cold show increased activity of thyroid gland. The calorigenic action of thyroid hormone has been demonstrated by a variety of in vivo and in vitro studies. According to Edelman et al., the thyroid thermogenesis is due to activation of energy consuming processes, especially the active sodium transport by the hormone in target tissues. If so, the increase in thyroid activity during cold exposure should induce increased capacity of sodium transport in target tissue and the change in tissue metabolism should be precisely correlated with the change in Na+_K+_ATPase activity of the tissue. This possibility was tested in the present study: in one series, changes in oxygen consumption and Na+_K+_-ATPase activity of liver preparations were measured in rats as a function of thyroid status, in order to establish the effect of thyroid hormone on the tissue respiration and enzyme system in another series, the effect of cold stimulus on the serum thyroid hormone level, hepatic tissue oxygen consumption and Na+_K+_ATPase activity in rats. The results obtained are as follows: 1. The Na+_dependent oxygen consumption of liver slices, the oxygen consumption of liver mitochondria and the Na+_K+_ATPase activity of liver preparations were significantly inhibited in hypothyroidism and activated in hyperthyroidism. Kinetic analysis indicated that the Vmax. of Na+_K+_ATPase was decreased in hypothyroidism and increased in hyperth)'roidism. 2. In cold exposed rats, the serum triiodothyronine (T₃) level increased rapidly during the initial one day of cold exposure, then declined slowly to the control level after two weeks. The serum thyroxine (T₄) level decreased gradually throughout the cold exposure. Accordingly the T₃/T₄ratio increased. The mitochondrial oxygen consumption and the Na+_dependent oxygen consumption of liver slices increased during the first two days and then remained unchanged thereafter The activity of the Na+_K+_ATPase in liver preparations increased during cold exposure with a time course similar to that of oxygen consumption. Kinetic analysis indicated that the Vmax. of Na+_K+_ATPase increased. 3. Once the animal was adapted to cold, induction of hypothyroidism did not significantly alter the hepatic oxygen consumption and Na+_K+_ATPase activity. These results indicate that: 1) thyroid hormone increases capacities of mitochondrial respiration and active sodium transport in target tissues such as liver; 2) the increased T₃level during the initial period of cold exposure facilitates biosynthesis of Na+_K+_ATPase and mitochondrial enzymes for oxidative phosphorylation, leading to enhanced production and utilization of ATP, hence heat production.
Pyracantha is a genus of thorny evergreen large shrubs in the family of Rosaceae, with common names Firethorn or Pyracantha. It's extract has also been used in cosmetics as a skin-whitening agent and functioning through tyrosinase inhibition. Recent studies have shown that pyracantha extract possesses antioxidant activities and may significantly improve lipoprotein metabolism in rats. Although the mode of action of Pyracantha extract is not fully understood, a strong relationship was observed between antioxidant and apoptosis in some types of cells. Thus, the aim of this study was to evaluated the effect of pyracantha extract on blastocysts formation and their quality of the porcine parthenogenetic embryos. After parthenogenetic activation by chemicals, presumptive porcine parthenogenetic embryos were cultured in PZM-3 medium supplemented with extracts of pyracantha leaf, stalk and root for 6 day (1, 5 and $10{\mu}g/ml$, respectively). In our results, the frequency of blastocyst formation in pyracantha root extract ($5{\mu}g/ml$) treated group had increased that of other groups. Furthermore, blastocysts derived from pyracantha root extract ($5{\mu}g/ml$) treated group had increased the total cell numbers and reduced apoptotic index. Blastocyst development was significantly improved in the pyracantha root extract ($5{\mu}g/ml$) treated group when compared with the $H_2O_2$ treated group (p<0.05). Subsequent evaluation of the intracellular levels of ROS in pyracantha root extract ($5{\mu}g/ml$) treated groups under $H_2O_2$ induced oxidative stress were decreased (p<0.05). In conclusion, our results indicate that treatment of pyracantha root extract may improve in vitro development of porcine parthenogenetic embryos through its antioxidative and antiapoptotic effects.
Li, Chengcheng;Peng, Meng;Liao, Man;Guo, Shuangshuang;Hou, Yongqing;Ding, Binying;Wu, Tao;Yi, Dan
Asian-Australasian Journal of Animal Sciences
/
v.33
no.9
/
pp.1444-1454
/
2020
Objective: Cold stress induces oxidative damage and impairs energy status of broilers. N-acetylcysteine (NAC) exhibits antioxidant properties and modulates energy metabolism of animals. This study was conducted to investigate the effects of NAC on energy status and antioxidant capacity of heart and liver in the cold-stressed broilers. Methods: The experiment consisted of 4 treatments in a 2×2 factorial arrangement with two diets (basal diet or plus 0.1% NAC) and two ambient temperatures (thermoneutral [conventional ambient temperature] or cold stress [10℃±1℃ during days 15 to 42]). Results: No ascites were seen in cold-stressed broilers. NAC did not attenuate the impaired growth performance of stressed birds. However, NAC decreased plasma asparagine but increased aspartate levels in cold-stressed birds (p<0.05). NAC reduced hepatic adenosine triphosphate (ATP) but elevated adenosine diphosphate contents in unstressed birds (p<0.05). The hepatic ratio of adenosine monophosphate (AMP) to ATP was increased in birds fed NAC (p<0.05). NAC decreased plasma malondialdehyde (MDA) level and cardiac total superoxide dismutase (T-SOD) activity in unstressed birds, but increased hepatic activities of T-SOD, catalase and glutathione peroxidase in stressed birds (p<0.05). NAC down-regulated hepatic AMP-activated protein kinase but up-regulated cardiac heme-oxigenase mRNA expression in stressed birds, and decreased expression of hepatic peroxisome proliferator-activated receptor coactivator-1α as well as hypoxia-inducible factor-1α in liver and heart of birds. Conclusion: Dietary NAC did not affect energy status but enhanced the hepatic antioxidant capacity by increasing the activities of antioxidant enzymes in cold-stressed broilers.
Brominated flame retardants (BFRs) are present in many consumer products ranging from fabrics to plastics and electronics. Wide use of flame retardants can pose an environmental hazard, which makes it important to determine the mechanism of their toxicity. In the present study, dose-dependent toxicity of tetrabromobisphenol A (TBBPA), a flame retardant, was examined in male prepubertal rats (postnatal day 18) treated orally with TBBPA at 0, 125, 250 or 500 mg/kg for 30 days. There were no differences in body weight gain between the control and TBBPA-treated groups. However, absolute and relative liver weights were significantly increased in high dose of TBBPA-treated groups. TBBPA treatment led to significant induction of CYP2B1 and constitutive androstane receptor (CAR) expression in the liver. In addition, serum thyroxin (T4) concentration was significantly reduced in the TBBPA treated group. These results indicate that repeated exposure to TBBPA induces drug-metabolising enzymes in rats through the CAR signaling pathway. In particular, TBBPA efficiently produced reactive oxygen species (ROS) through CYP2B1 induction in rats. We measured 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of DNA oxidative damage, in the kidney, liver and testes of rats following TBBPA treatment. As expected, TBBPA strongly induced the production of 8-OHdG in the testis and kidney. These observations suggest that TBBPA-induced target organ toxicity may be due to ROS produced by metabolism of TBBPA in Sprague-Dawley rats.
Park, Chan Jin;Kim, Dae Han;Han, Sang Ho;Gye, Myung Chan
Korean Journal of Environmental Biology
/
v.32
no.4
/
pp.271-285
/
2014
Aluminum flows into the river from the abandoned mine leachate, industrial wastewater, and sewage and is responsible for acute toxicity in aquatic organisms. Recently, the number of reports have indicated the increased toxicity in a variety of aquatic organisms' due to the aluminum toxicity. In this study, we reviewed the toxicity of aluminum on aquatic invertebrates, fishes and amphibians and suggested the guideline for management of aluminum residues in aquatic environment and strategies for aluminum toxicity evaluation. In aquatic animals aluminum complexes evoke gill dysfunction primarily, the cytotoxicity, genotoxicity, oxidative stress, disruption of endocrine function, reproductive success, metabolism and homeostasis. Notably, at environmentally relevant concentration, aluminum complex can alter the hormone levels in fish in acidic condition. Further, since the solubility of aluminum is higher in the acidic and basic conditions, thus it is likely that the toxic effects of aluminum may not only occur in acidic water near the abandoned mines but also in lakes and rivers, where pH is raised by algal bloom.
The oxidative metabolism of ibuprofen in healthy male urine collected at 3, 6, 9, 12 and 15 h after oral administration of ibuprofen was studied by GC/MS assay. To detect conjugated metabolites of ibuprofen, urine sample was acid-hydrolyzed with 6 M HCl at $100^{\circ}C$ for 30 min. To effectively extract ibuprofen and its metabolites, liquid-liquid extraction (LLE) was conducted at pH 3, 5, and 7, respectively. As a result, LLE at pH 3 was shown to be the best extraction condition. For the determination of trace amounts of ibuprofen and its metabolites in extract, trimethylsilylation (TMS) with BSTFA was applied and followed by GC/MS analysis. In this study, main 5 metabolites including parent drug were detected and these metabolites were assigned as three hydroxylated forms and one carboxylated form. Each metabolite was tentatively identified by both interpretation of mass spectrum and comparison with previously reported results. In addition, time profile of urinary excretion rate for parent drugs and metabolites was studied. Finally, the metabolic pathways of ibuprofen were suggested on the basis of the structural elucidation of its metabolites and excretion profiles.
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