An important factor in the transition from an open to a closed circulatory system was a change in vessel wall that are dynamic structure composed of cells and extracellular matrix. The component of arterial wall in vertebrates that accounts for these properties is the elastic fiber network organized by medial smooth muscle cells. Elastin and elastin associated protein are synthesized and secreted by vascular smooth muscle cells and are the major extracellular matrix component deposited in the vascular wall. Pathological states related to hypertension or atherosclerosis is associated with vascular wall remodeling, which is deleterious for cardiovascular function. Elastic fiber may be key factors in the pathophysiology of hypertensive or atherosclerotic vascular remodeling. The well-known effects of cardiovascular disease on the deterioration and the promoted degradation of elastic fiber result to loss of arterial wall resilience. Recently, several studies have highlighted new roles for individual components of elastic fiber and their degraded products. This review describes current knowledge regarding components of elastic fibers and discusses relationship between their structural abnormalities and cardiovascular diseases.
We isolated and characterized a pathogenicity-related protein in Salmonella Enteritidis (SE) from poultry farms, and designated it as SEp22, which was identified later as Salmonella Dps, a DNA-binding protein from starved cells. Expression of SEp22 was regulated by bacterial growth in Luria-Bertani (LB) medium, showing reduced expression in the logarithmic phase but increased expression from the late logarithmic to stationary phases, which was linked to the expression of σS both in protein as well as mRNA levels. In addition, induction of SEp22 required nutritional factors in LB or casamino acids during overnight incubation in M9 minimal medium, or even through short-term exposure to H2O2 for 5-15 min. Induction of SEp22 was also remarkable after sudden addition of H2O2 and exposure of the bacteria to the drying protocol. The roles of SEp22 in the pathogenicity of Salmonella in mice, the survival of Salmonella exposed to H2O2, or that under dry-stress were proved not only by the difference among Salmonella clones from environmental isolates with different levels of SEp22 expression, but also by sep22-gene-depleted mutants that originated from SECl#15-1, a wild type virulent strain with high levels of SEp22. These results suggest that SEp22 is a key molecule that is responsible for pathogenesis as well as environmental stress-resistance. In this review, the diverse roles of SEp22/Dps in Salmonella are also described, suggesting the importance of this protein in the bacterial stress responses in infection and survival, as well as in the regulation of bacterial growth through aerobic metabolism. Recent progress in SEp22/Dps research at the molecular levels is also discussed.
Recent reports of the analysis of drugs of abuse in biological specimens are reviewed herein. Different perspectives from reviews so far published and the need for and the background of drug analysis in biological specimens, and difficulty of drug testing in biological specimens are introduced. Comprehensive biological specimens for the analysis of drugs of abuse in forensic science, including oral fluid (saliva), hair, umbilical cord, placenta, meconium, cadaver tissue (brain, adipose), sweat, breath, and nail clippings, in addition to the commonly used blood and urine specimens in clinical chemistry, are described along with their outlines, advantages/disadvantages, and actual examples. Today, liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the method of choice for the analysis of drugs of abuse. A simultaneous screening method for multiple types of drugs has also become popular recently. However, because qualitative determination remains important in forensic science, gas chromatography-mass spectrometry (GC-MS) is still in use even if it requires complicated specimen preparation and derivatization procedures. This is because GC-MS is reliable and has been employed ever since for the appraisal of trials.
Allergic diseases have been increasing worldwide in industrialized countries. The interplay of genetic and environmental factors is involved in the induction and progression of several types of allergic diseases. Recently, there have been many reports that the increase and spread of allergic diseases are related to chronic exposure to several environmental pollutants, such as diesel exhaust particles and formaldehyde. Trichloroethylene (TCE) and tetrachloroethylene (PCE) are categorized into chlorinated organic compounds, and are the most widely used extensively in various industrial processes. As a consequence of their widespread use, TCE and PCE are becoming environmental pollutants. Generally, TCE and PCE exposure causes organ toxicological effects on the liver, kidney, and the central nervous system; however, studies of TCE and PCE exposure-induced immune modulations are limited. In this review, we summarize research into immunotoxic effects, such as allergy hypersensitivity, autoimmune disease, and immunosuppression, of TCE and PCE from experimental animal studies and human epidemiological studies.
Phthalate esters (PEs) are plasticizers used in many plastic products, food packaging materials, and medical bags. The widespread use of PEs has led to ubiquitous environmental contamination and human-exposure. Several epidemiological studies have indicated that exposure to PEs, especially during the prenatal period, induces adverse effects, including developmental and behavioral abnormalities, suggesting that PEs are endocrine-disrupters. Although the endocrine-disrupting effect of PEs is thought to be estrogen receptor (ER)-mediated, the ER-binding affinity of PEs is quite low, indicating that other mechanisms should be considered. In this review, we demonstrate that alkyl chain length and hydroxylation of PEs have a significant impact on binding to ERs and peroxisome proliferator-activated receptors. In addition, we discuss recent results from our laboratory that suggest additional risks may arise from environmental and metabolic processing of PEs through microbial transformation, microsomal metabolism, and sunlight exposure.
Polycyclic aromatic compounds are ubiquitous atmospheric pollutants with toxic, mutagenic, and carcinogenic properties. They are produced from chemical reactions of their parent compounds in the atmosphere as well as from a wide variety of anthropogenic sources such as fuel combustions. The present review is mainly concerned with several reaction pathways regarding secondary formation of atmospheric polycyclic aromatic hydrocarbon (PAH) derivatives, i.e., formation of mutagenic nitrated PAHs, 1- and 2-nitrotriphenylene, via gas-phase OH or NO3 radical-initiated reactions of the parent triphenylene, atmospheric formation of hydroxynitropyrenes from a photochemical reaction of 1-nitropyrene, and photochemical degradation of selected nitrated and oxygenated PAHs on airborne particles under simulated solar UV-irradiation.
Alcoholic fatty liver (AFL) is the most common liver disease among Korean men, and Korean red ginseng has been used as a folk medicine to diverse diseases in Korea. Therefore, we examined if Korean red ginseng extract (KRG) could be a suppressive agent on AFL in a rat model or not. Experimental rats were fed the Lieber DeCarli diet with 36% of energy intake from ethanol, and divided into three groups which daily co-administered KRG 0, 700 and 1400 mg/kg for six weeks, respectively. Naive rats were fed iso-caloric control diet without ethanol and KRG. We investigated histopathological hepatic characteristics, hepatic and plasma lipid concentrations, hepatic hydroxyproline contents, heart/liver radioactivity ratio of 201Thallium and liver/body weight of the rats at the end point. Ethanol intake brought about steatotic, inflammatory, necrotic and fibrotic changes of livers significantly, and it also lead the rats to increase hepatic triglyceride and hydroxyproline contents, plasma total cholesterol and low density lipoprotein cholesterol levels, and liver/body weight. However, co-administration of KRG 1400 mg/kg suppressed fat accumulation and fibrotic initiation in AFL rat model significantly. It was also inclined to attenuate inflammatory cell infiltration, hydroxyproline accumulation, and increasing liver/body weight, even though plasma lipid levels and heart/liver ratios were not successfully improved by six-week-long intakes of KRG. In conclusions, co-administration of KRG 1400 mg/kg could significantly suppress steatosis in AFL rat model, and it might need longer ingestion of KRG than six weeks to improve plasma lipid imbalance.
This research is preliminary study to examine whether puerariae flos extract (PFE) makes any action to body fat of man or not. We conducted the double-blind placebo controlled study on eighty mildly obese subjects for 8 weeks. The subjects were randomly divided into 4 groups: I, II, III, and IV. Subjects in groups I, II, and III consumed test food containing 100, 200, and 300 mg PFE, respectively, while those in group IV were given placebo food for 8 weeks. All subjects were instructed to restrict their total-energy intake to within 2650 kcal/day in the case of males and 2300 kcal/day in the case of females during the test period. Haematological and biochemical markers of blood, urinary markers, and physical markers were examined at 0, 4, and 8 weeks during the test period. As a result, no adverse effects were noted in any of the groups. For physical examinations, we analysed only males whose initial body mass index (BMI) values were over 24. BMI value and body weights of the subjects in group III were significantly reduced, and total fat area and subcutaneous fat area of the subjects in groups II and III were significantly reduced over the 8-week test period. Moreover, as a result of comparison among groups by unpaired t-test, significant difference appeared between group III and group IV in BMI. Total fat area in group III tend to decrease compared with group IV. By these results, the reduction of BMI in group III may reflect fat area reduction. To confirm the anti-obesity effect of PFE, we need to research particularly by extensive studies hereafter.
The aim of this study was to obtain data on the safety of yeast hydrolysate with below 10 kDa molecular weight. The acute [at a single dose of 5000 mg/kg body weight (BW)] and subacute (at a dose of 1000 mg/kg BW for 14 consecutive days) oral toxicity of yeast hydrolysate from Saccharomyces cerevisiae was assessed in Sprague-Dawley (SD) rats. The yeast hydrolysate acute treatment via the oral route at the dose of up to 5000 mg/kg did not produce any signs of toxicity or death in the rats. The yeast hydrolysate with below 10 kDa molecular weight did not induce any damage to the internal organs of the rats as examined by hematological and biochemical parameters. The macroscopic analysis of the treated animals did not show significant changes in color and texture. These results show that yeast hydrolysate with below 10 kDa molecular weight possesses very low toxicity as indicated in this SD rat model.
Triclosan is an antibacterial agent used in household items and personal care products. Because wild animals and humans can harbor this compound in their systems, the toxic effects of triclosan are a possibility and are suspected. Therefore, we examined the effects of triclosan on intracellular Ca2+ concentration in rat thymocytes by cytometric techniques using fluorescent probes. Triclosan doses of 1-10 μM significantly increased the intensity of Ca2+-detecting Fluo-3 fluorescence, indicating an increase in intra-cellular Ca2+ concentrations. The augmentation of Fluo-3 fluorescence became more profound in a dose-dependent manner after the addition of an external source of Ca2+. Conversely, the removal of external Ca2+ greatly attenuated the triclosan-induced augmentation of Fluo-3 fluorescence. These results suggest that triclosan treatment allows external Ca2+ to pass through cell membranes. This phenomenon was not specific for Ca2+ because external Mn2+ quenched the triclosan-induced augmentation of Fluo-3 fluo-rescence, indicating that triclosan can also mediate Mn2+ permeation across membranes. Therefore, these results suggest that triclosan increases membrane permeability to divalent metal cations. Furthermore, triclosan induces Ca2+ release from intracellular stores because the Fluo-3 fluorescence intensitystill increased slightly after triclosan treatment, even under conditions free from external Ca2+. Additionally, triclosan did not increase the intensity of Fluo-3 fluorescence when Ca2+ was depleted from intracellular Ca2+ stores by A23187 under the external Ca2+-free condition. Taken together, these data suggest that micromolar concentrations of triclosan affect intracellular Ca2+ homeostasis in thymocytes, possibly resulting in cellular malfunction.
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