In order to develop a new type of natural seasoning material combining fish meat with seaweed, a processing method of the mixture of enzyme treated mackerel meat and Laminaria powder was studied. Mackerel meat previously boiled and deboned was treated with proteolytic enzyme to enhance taste of meat by proper hydrolysis. The enzyme-treated meat was dried at $100{\pm}2^{\circ}C$ for 4 hrs, and finally mixed with kelp power, moistened in advance, plus binding agents (0.02% calcium carbonate) to aid the formation of pellets by extrusion. Boiled mackerel meat of enzyme treated (0.03% Protease-A) at $50^{\circ}C$ for 90 min was adequate to result an increase in 6 times of total free amino acid content and about 10% increase of taste-enhancing amino acids such as glutamic acid, glycine, arginine, lysine.
The uptake of cadmium in animals is mainly accumulated in and affected to the liver and kidney by binding with red blood cells and serum albumin. The process accounts for more than 50% of the total accumulated cadmium in the body. The kidneys may be damaged without regarding the pathway uptake of cadmium. In a group of rats on supplements of 1% chlorella and 40 ppm cadmium, the concentration of cadmium in urine greatly decreased by 66% compared to control group, and the total synthesis of metallothionein decreased by 48.6% compared to control group. However, no previous study has assessed the protective effect on kidney damage induced by cadmium uptake through supplementation with chlorella. This study analyzed the biochemical marker for kidney damage in the rats after uptake of 40 ppm $CdCl_2$ and supplementation of the diet of Sprague Dawley (SD) rats with 1%, 5%, and 10% chlorella during 4 weeks. In a group of SD rats on supplementation with 1% chlorella and uptake of 40 ppm $CdCl_2,\;\beta_2$ microglobulin in the urine was found to be $3.1\pm0.6\;{\mu}g/L$, a decrease of 58% compared to a group of Sp rats on uptake of $CdCl_2$ only, in which the $\beta_2$ microglobulin was found to be $4.9\pm0.7\;{\mu}g/L$. According to the results of histopathological observation, the accumulation of mild and localized chronic inflammatory cells in kidney tissues was observed in 50% of the SD rats on uptake of cadmium only. In contrast, only 30% of the SD rats on supplementation with 1% chlorella and uptake of 40ppm $CdCl_2$, representing a histopathological abnormality, and there were no histopathological abnormalities at all in groups of SD rats on supplementation with 5% or 10% chlorella and uptake of 40 ppm $CdCl_2$. In conclusion, protein, calcium, and iron, which account for more than 50% of the total dried chlorella composition, may contribute to the reduction nephrotoxicity by stimulating both inhibited absorption of cadium and increased excretion of accumulated cadmium in kidneys.
Neutrophil elastases were purified by a three step procedure consiting of one Sephadex G-75 and two HPLC elutions. The elastases cross-reacted with antibodies to human neutrophil elastase. Three bands with molecular weights between 26,000 and 29,700 were observed by gel electrophoresis. At each stage of purification the quantity of Zn increased, reaching molar ratio of 2:1 with elastase in the most purified samples. Calcium content. was seletively elevated during the earlier stages of purification but decreased to a ratio of 0.25 to 1 with elastase at the final step of purfication. Neutrophil elastase could be inhibited by EDTA, EGTA and 1,10-phenanthroline. EGTA inhbition was noncompetitive inhibition and reversible only if the time of preincubation was relatively short, indicating the instability of the apoenzyme. The concentration of chelator required to show significant inhibition of elastase was also dependent upon the stage of purity and the ionic strength of the reaction mixture. Inhibition by EGTA, followed by the removal of EGTA, could be reversed by Zn. In the presence of EGTA the enzyme could be returened to full activity by the addition of Zn, Mn and Ca, but not Mg or Na. All of the above evidence strongly supports human neturophil elastase could be a metalloenzyme as well as a serine protease.
In this study sodium dodecyl sulfate (SDS), which was anionic surfactant, was added for forming micelles to remove iron ion that could be contained with small amount in industrial water. Then aggregates binding between iron ions and micelles were rejected by a ceramic microfiltration membrane. As result of SDS concentration effect on removal rates of iron and SDS in modified iron solution, the removal rate of iron was the highest value of 92.26% and the removal rate of SDS was 61.10% a little higher than the result of calcium ion at 8 mM which was CMC (Critical micelle concentration) of SDS. As final resistance of membrane fouling $R_f$ increased the more at the higher SDS concentration, it showed the highest value at 4 mM and the lowest at 10 mM of SDS. The final permeate flux $J_{180}$ had the highest value and the largest total permeate volume could be finally acquired at SDS 10 mM. In case of CMC 8 mM, low $R_f$ was shown as same as that of 10 mM until 80 minutes of operation, and tended to increase dramatically to 120 minutes and increase slowly again until 180 minutes.
Background: The physiological role of vitamin D extends beyond bone health and calcium-phosphate homeostasis to effects on cancer risk, mainly for colorectal cancer. Vitamin D may have an anticancer effect in colorectal cancer mediated by binding of the active form $1,25(OH)_2D$ to the vitamin D receptor (VDR). The Taq1 VDR gene polymorphism, a C-to-T base substitution (rs731236) in exon 9 may influence its expression and function. The aim of this study wass to determine the 25(OH)D vitamin D level and to investigate the association between circulating vitamin D level and Taq1VDR gene polymorphism among Jordanian colorectal cancer patients. Materials and Methods: This case control study enrolled ninety-three patients and one hundred and two healthy Jordanian volunteers from AL-Basheer Hospital/Amman (2012-2013). Ethical approval and signed consent forms were obtained from all participants before sample collection. 25(OH)D levels were determined by competitive immunoassay Elecsys (Roche Diagnostic, France). DNA was extracted (Promega, USA) and amplified by PCR followed by VDR Taq1 restriction enzyme digestion. The genotype distribution was evaluated by paired t-test and chi-square. Comparison between vitamin D levels among CRC and control were assessed by odds ratio with 95% confidence interval. Results: The vitamin D serum level was significantly lower among colorectal cancer patients (8.34 ng/ml) compared to the healthy control group (21.02ng/ml). Patients deficient in vitamin D (less than 10.0 ng/ml) had increased colorectal cancer risk 19.2 fold compared to control. Only 2.2% of CRC patients had optimal vitamin D compared to 23.5% among healthy control. TT, Tt and tt Taq1 genotype frequencies among CRC cases was 35.5%, 50.5% and 14% compared to 43.1%, 41.2% and 15.7% among healthy control; respectively. CRC patients had lower mean vitamin D level among TT ($8.91{\pm}4.31$) and Tt ($9.15{\pm}5.25$) genotypes compared to control ($21.3{\pm}8.31$) and ($19.3{\pm}7.68$); respectively. Conclusions: There is significant association between low 25(OH)D serum level and colorectal cancer risk. The VDRTaq1 polymorphism was associated with increased colorectal cancer risk among patient with VDRTaq1 TT and Tt genotypes. Understanding the functional mechanism of VDRTaq1 TT and Tt may provide a strategy for colorectal cancer prevention and treatment.
This study was designed to investigate the effect of iron supplementation on the iron nutritional status and anemia of high school girls in Korea. One hundred thirty-five female students residing in Ulian metropolitan city in Korea diagnosed as having anemia or iron deficiency participated in this study. One or two tablets of iron medicine(80-160 mg Fe as ferrous sulfate/day) were administered to all participants for 3 months. Subjects were evaluated with a questionaire, measurement of hematological indices before and after iron supplementation. The average height and weight of respondents were 161.62 $\pm$ 4.68 cm and 53.87 $\pm$ 6.10 kg, respectively. Daily intakes of energy were 1597.8 $\pm$ 302.35 kcal(76.0% RDA). Iron intakes were 13.72 $\pm$ 4.17 mg (76.3% of RDA) and calcium intakes were 580.74 $\pm$ 177.21(72.5% of RDA) before iron supp]ementation. At baseline, 63% of all participants had depleted store(serum ferritin 12 ug/ml and/or transferrin saturation(TS) < 14%). After iron supplementation, this proportion declined to 19.3%. 55.6% of subjects had 12 ug/m1 of basal ferritin concentration before iron supplementation, and this proportion declined to 16.3% after iron supplementation. The basal hemoglobin(Hb) concentrations were 12.13 $\pm$ 1.01 g/dl and they increased to 12.79 $\pm$ 0.81 g/dl, which showed significant difference artier iron supplementation(p < 0.001). The basal ferritin and TS(%) were 13.24 $\pm$ 11.66 ng/ml, 18.42 $\pm$ 10.12% and they significantly increased to 32.95 $\pm$ 21.14 ng/ml, 33.53 $\pm$ 16.64%, respectively(p < 0.001). The basal total iron binding protein(TIBC) were 467.81 $\pm$ 97.24 ug/dl and they significantly decreased to 325.05 $\pm$ 48.89 ug/dl(p < 0.001) after iron supplementation. The number of tablets administered was positively correlated with serum iron(t = 0.553, p < 0.01), serum ferritin(t = 0.557, p < 0.01), TS(%)(t = 0.588, p < 0.01) and negatively correlated with TIBC(t= -0.409, p <0.01). The anemia symptoms such as ‘Shortening of breath when going upstairs(p < 0.01)’, ‘Tired out easily(p < 0.01)’, ‘Feeling blue(p < 0.001)’, ‘Decreased ability to concentrate(p < 0.01)’, and ‘Poor memory(p < 0.001)’improved significantly after iron supplementation. In this study, daily iron supplementations were efficacious in improving the iron status and anemic symptoms of female high school students. Regular check-ups and nutrition education for adolescents are necessary because of their vulnerability to iron deficiency. Further studies are needed to determine the minimum effective dose of iron and to examine the adverse effect of long-term iron supplementation.
To prepare edible skin gelatin of conger eel such as material fur quality improvement of surimi gel, the defatted skin was limed with 1% calcium hydroxide at $5^{\circ}C$ for 2 days, washed thoroughly with tap water, extracted with 8 volumes of distilled water to dehydrated skin for 2 hours at $50^{\circ}C$. The gelatin extract was centrifuged, filtered and then passed through anion(Amberlite 200C) and cation (Amberlite IR 900) resins. The purified gelatin solution was evaporated and dried by hot-air blast$(40^{\circ}C)$. The gelatin prepared by above condition had the highest quality as revealed by physical property values i.e. 240.5 g in gel strength, $28.0^{\circ}C$ in melting point and $28.0^{\circ}C$ in gelling point. Funtional property values were 56.8% in solubility, 1.8 ml/g in oil binding capacity, 55.0% in emulsifying capacity and 48.5% in emulsifying stability. jelly strength and senso교 evaluation of surimi gel from fish with red muscle were not improved by addition of emulsifying curd from conger eel skin gelatin as emulsifier. Therefore, the conger eel skin gelatin requires a suitable modification of functional group and improvement of processing operation to utilize as a material for quality Improvement of surimi gel.
Lee, Sung Ryul;Noh, Su Jin;Pronto, Julius Ryan;Jeong, Yu Jeong;Kim, Hyoung Kyu;Song, In Sung;Xu, Zhelong;Kwon, Hyog Young;Kang, Se Chan;Sohn, Eun-Hwa;Ko, Kyung Soo;Rhee, Byoung Doo;Kim, Nari;Han, Jin
The Korean Journal of Physiology and Pharmacology
/
v.19
no.5
/
pp.389-399
/
2015
Zinc has been considered as a vital constituent of proteins, including enzymes. Mobile reactive zinc ($Zn^{2+}$) is the key form of zinc involved in signal transductions, which are mainly driven by its binding to proteins or the release of zinc from proteins, possibly via a redox switch. There has been growing evidence of zinc's critical role in cell signaling, due to its flexible coordination geometry and rapid shifts in protein conformation to perform biological reactions. The importance and complexity of $Zn^{2+}$ activity has been presumed to parallel the degree of calcium's participation in cellular processes. Whole body and cellular $Zn^{2+}$ levels are largely regulated by metallothioneins (MTs), $Zn^{2+}$ importers (ZIPs), and $Zn^{2+}$ transporters (ZnTs). Numerous proteins involved in signaling pathways, mitochondrial metabolism, and ion channels that play a pivotal role in controlling cardiac contractility are common targets of $Zn^{2+}$. However, these regulatory actions of $Zn^{2+}$ are not limited to the function of the heart, but also extend to numerous other organ systems, such as the central nervous system, immune system, cardiovascular tissue, and secretory glands, such as the pancreas, prostate, and mammary glands. In this review, the regulation of cellular $Zn^{2+}$ levels, $Zn^{2+}$-mediated signal transduction, impacts of $Zn^{2+}$ on ion channels and mitochondrial metabolism, and finally, the implications of $Zn^{2+}$ in health and disease development were outlined to help widen the current understanding of the versatile and complex roles of $Zn^{2+}$.
The calcium-activated $K^+$ ($BK_{Ca}$) channel is one of the potassium-selective ion channels that are present in the nervous and vascular systems. $Ca^{2+}$ is the main regulator of $BK_{Ca}$ channel activation. The $BK_{Ca}$ channel contains two high affinity $Ca^{2+}$ binding sites, namely, regulators of $K^+$ conductance, RCK1 and the $Ca^{2+}$ bowl. Lysophosphatidic acid (LPA, 1-radyl-2-hydroxy-sn-glycero-3-phosphate) is one of the neurolipids. LPA affects diverse cellular functions on many cell types through G protein-coupled LPA receptor subtypes. The activation of LPA receptors induces transient elevation of intracellular $Ca^{2+}$ levels through diverse G proteins such as $G{\alpha}_{q/11}$, $G{\alpha}_i$, $G{\alpha}_{12/13}$, and $G{\alpha}s$ and the related signal transduction pathway. In the present study, we examined LPA effects on $BK_{Ca}$ channel activity expressed in Xenopus oocytes, which are known to endogenously express the LPA receptor. Treatment with LPA induced a large outward current in a reversible and concentration-dependent manner. However, repeated treatment with LPA induced a rapid desensitization, and the LPA receptor antagonist Ki16425 blocked LPA action. LPA-mediated $BK_{Ca}$ channel activation was also attenuated by the PLC inhibitor U-73122, $IP_3$ inhibitor 2-APB, $Ca^{2+}$ chelator BAPTA, or PKC inhibitor calphostin. In addition, mutations in RCK1 and RCK2 also attenuated LPA-mediated $BK_{Ca}$ channel activation. The present study indicates that LPA-mediated activation of the $BK_{Ca}$ channel is achieved through the PLC, $IP_3$, $Ca^{2+}$, and PKC pathway and that LPA-mediated activation of the $BK_{Ca}$ channel could be one of the biological effects of LPA in the nervous and vascular systems.
It has been reported that the luteal function may be regulated by the intracellular calcium in luteal cells (Higuchi et al, 1976; Dorflinger et at, 1984; Gore and Behrman, 1984) which is adjusted partially by $Ca^{++}-ATPase$ activities in luteal cell membranes (Verma and Pennistion, 1981). However, the physicochemical and kinetic properties of $Ca^{++}-ATPase$ in luteal membranes were not fully characterized. This study was, therefore, undertaken to partially characterize the physicochemical and kinetic properties of $Ca^{++}-ATPase$ system in luteal membranes and microsomal fractions, known as an one of the major $Ca^{++}$ storge sites (Moore and Pastan, 1978), from the highly luteinized ovary Highly luteinized ovaries were obtained from PMSG-hCG injected immautre female rats. Light membrane and heavy membrane fractions and microsomal fractions were prepared by the differential and discontinuous sucrose density gradient centrifugation method desribed by Bramley and Ryan (1980). Light membrane and heavy membrane fractions and microsomal fractions from highly luteinized ovaries are composed of the two different kinds of $Ca^{++}-ATPase$ system. One is the high affinity $Ca^{++}-ATPase$ which is activated in low $Ca^{++}$ concentration (Km, 10-30 nM), the other is low affinity $Ca^{++}-ATPase$ activated in higher $Ca^{++}$ concentration $(K_{1/2},\;40\;{\mu}M)$. At certain $Ca^{++}$ concentrations, activities of high and low affinity $Ca^{++}-ATPase$ are the highest in light membrane fractions and are the lowest in microsomal fractions. It appeares that high affinity $Ca^{++}-ATPase$ system have 2 binding sites for ATP (Hill's coefficient; around 2 in all membrane fractions measured) and the positive cooperativity of ATP bindings obviously existed in each membrane fractions. The optimum pH for high affinity $Ca^{++}-ATPase$ activation is around S in all membrane fractions measured. The lipid phase transition temperature measured by Arrhenius plots of high affinity $Ca^{++}-ATPase$ activity is around $25^{\circ}C$. The activation energies of high affinity $Ca^{++}-ATPase$ below the transition temperature are similar in each membrane fractions, but at the above transition temperature, it is the hightest in heavy membrane fractions and the lowest in microsomal fractions. According to the above results, it is suggested that intracellular $Ca^{++}$ level, which may regulate the luteal function, may be adjusted primarily by the high affinity $Ca^{++}-ATPase$ system activated in intracellular $Ca^{++}$ concentration range $(below\;0.1\;{\mu}M)$.
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