• Title/Summary/Keyword: Nitro

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Nitric oxide 화합물 첨가가 한우 체외수정란의 체외발육에 미치는 효과

  • 장현용;박동헌;박춘근;정희태;김정익;양부근
    • Proceedings of the KSAR Conference
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    • 2001.03a
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    • pp.88-88
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    • 2001
  • 소 난포란을 체외에서 성숙, 수정시킨 후, 2~8 세포기 수정란을 체외배양액인 CR$_1$aa에 일정량의 nitric oxide scavenger, Hb와, inhibitor인 L-nitro - L- arginine methyl ester (L-NAME)를 첨가 배양하여 체외발육에 미치는 영향을 검토하고자 실시하였다. 체외수정 후 체외배양 48시간에 난구세포의 제거 유.무에 따라 CR$_1$aa 배양액에 hemoglobin을 0, 1, 5$\mu\textrm{g}$/$m\ell$를 첨가한 구의 상실배기이상 체외발육성적은 난구세포를 제거한 구에서 23.8%, 33.3% 및 26.8%였으며, 난구세포를 제거하지 않은 구에서는 각각 39.5%, 54.8% 및 48.8%로써 난구세포를 제거하지 않은 구에 Hb를 1$\mu\textrm{g}$/$m\ell$를 첨가한 구가 여타구 보다 통계적으로 높은 결과를 얻었다(P<0.05). 체외수정 후 체외배양 96시간 후 난구세포를 제거 유.무에 따라 Hb를 0, 1, 5$\mu\textrm{g}$/$m\ell$를 첨가하였을 때, 상실배기 이상 체외발육성적은 난구세포를 제거한 구에서 각각 28.6%, 46.2% 및 39.1%였으며, 난구세포를 제거하지 않은 구에서는 각각 33.9%, 67.2% 및 46.0%로써, 난구세포를 제거하지 않은 구에 Hb를 1$\mu\textrm{g}$/$m\ell$첨가구가 여타구에 비해 통계적으로 유의하게 높게 나타났다( P<0.05).CR$_1$aa배양액에 L-NAME를 0, 10, 50 및 100mM을 첨가한 구에서 상실배이상 발육된 체외발육성적은 각각 55.6%, 64.9%, 58.8% 및 66.7%로써 L-NAME 첨가구가 무첨가구에 비해 커다란 차이가 나타나지 않았다(P>0.05). 본 실험의 결과로 볼 때, nitric oxide scavenger인 hemoglobin의 첨가는 체외수정 후 체외배양 96시간에 1$\mu\textrm{g}$/$m\ell$ 첨가하는 것이 체외수정란의 체외 발육율을 향상시켰으며, nitric oxide inhibitor인 L-NAME는 첨가 농도에 관계없이 체외수정란의 체외발육율에 영향을 미치지 않는 것으로 나타났다. 본 실험에서 생산된 배반포기 체외수정란의 세포수에는 커다란 차이가 인정되지 않았다.

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Antiapoptotic Effect of Paricalcitol in Gentamicin-induced Kidney Injury

  • Suh, Sang Heon;Lee, Ko Eun;Park, Jeong Woo;Kim, In Jin;Kim, Ok;Kim, Chang Seong;Choi, Joon Seok;Bae, Eun Hui;Ma, Seong Kwon;Lee, Jong Un;Kim, Soo Wan
    • The Korean Journal of Physiology and Pharmacology
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    • v.17 no.5
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    • pp.435-440
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    • 2013
  • While the anti-apoptotic effect of paricalcitol has been demonstrated in various animal models, it is not yet clear whether paricalcitol attenuates the apoptosis in gentamicin (GM)-induced kidney injury. We investigated the effect of paricalcitol on apoptotic pathways in rat kidneys damaged by GM. Rats were randomly divided into three groups: 1) Control group (n=8), where only vehicle was delivered, 2) GM group (n=10), where rats were treated with GM (150 mg/kg/day) for 7 days, 3) PARI group (n=10), where rats were co-treated with paricalcitol (0.2 ${\mu}g/kg/day$) and GM for 7 days. Paricalcitol attenuated renal dysfunction by GM administration in biochemical profiles. In terminal deoxynucleotidyl transferase dUTP nick end labeling staining, increased apoptosis was observed in GM group, which was reversed by paricalcitol co-treatment. Immunoblotting using protein samples from rat cortex/outer stripe of outer medulla showed increased Bax/Bcl-2 ratio and cleaved form of caspase-3 in GM group, both of which were reversed by paricalcitol. The phosphorylated Jun-N-terminal kinase (JNK) expression was increase in GM, which was counteracted by paricalcitol. The protein expression of p-Akt and nitro-tyrosine was also enhanced in GM-treated rats compared with control rats, which was reversed by paricalcitol co-treatment. Paricalcitol protects GM-induced renal injury by antiapoptotic mechanisms, including inhibition of intrinsic apoptosis pathway and JNK.

Isolation and characteristics of yellow-pigment producing mutants of Monascus anka. (Monascus anka로부터 황색소 생성 변이주의 분리 및 특성)

  • 이호재;이형주
    • Microbiology and Biotechnology Letters
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    • v.30 no.2
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    • pp.111-115
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    • 2002
  • To produce yellow pigment selectively, mutants were induced from Monascus anka Nakazawa et Sato IFO 4478 (KCCM 11832 strain), and their characteristics were evaluated. Five kinds of auxotrophic mutants which required amino acids for growth and pigmentation, were isolated through a series of mutagenic treatments. Especially, asparagine auxotroph Y7 produced high ratio of yellow pigment. This mutant showed all the morphological characteristics of Monascuceae but the shape of colony and the diameter of conidia. Mutant Y7 was propagated by sexual reproduction more often than asexual reproduction, which could be effective in production of pigments. Yellow pigment produced extracellularly by the mutant Y7 was more soluble in polar solvents such as ethanol and water than in nonpolar solvents. Its productivity of yellow pigment was 2.2 times higher in the mutant Y7 than in parents. In addition, its yellow pigment showed characteristics of maximum absorption at 373 nm. Moreover, the hue of pigment produced by the mutant Y7 was bright yellow, and it was stable through the subculture over 10 generations.

The Effect of Carbon Monoxide on L-type Calcium Channel Currents in Human Intestinal Smooth Muscle Cells

  • Lim, In-Ja
    • The Korean Journal of Physiology and Pharmacology
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    • v.7 no.6
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    • pp.357-362
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    • 2003
  • Carbon monoxide (CO) is low molecular weight oxide gas that is endogenously produced under physiological conditions and interacts with another gas, nitric oxide (NO), to act as a gastrointestinal messenger. The aim of this study was to determine the effects of exogenous CO on L-type calcium channel currents of human jejunal circular smooth muscle cells. Cells were voltage clamped with 10 mM barium ($Ba^{2+}$) as the charge carrier, and CO was directly applied into the bath to avoid perfusion induced effects on the recorded currents. 0.2% CO was increased barium current ($I_{Ba}$) by $15{\pm}2$% ($mean{\pm}S.E.$, p<0.01, n=11) in the cells. To determine if the effects of CO on barium current were mediated through the cGMP pathway, cells were pretreated with 1-H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, $10{mu}M$), a soluble guanylyl cyclase inhibitor, and exogenous CO (0.2%) had no effect on barium currents in the presence of ODQ ($2{\pm}1$% increase, n=6, p>0.05). CO mediates inhibitory neurotransmission through the nitric oxide pathway. Therefore, to determine if the effects of CO on L-calcium channels were also mediated through NO, cells were incubated with $N^G-nitro-L-arginine$ (L-NNA, 1 mM), a nitric oxide synthase inhibitor. After L-NNA pretreatment, 0.2 % CO did not increase barium current ($4{\pm}2$% increase, n=6, p>0.05). NO donor, SNAP ($20{\mu}M$) increased barium current by $13{\pm}2$% (n=6, p<0.05) in human jejunal smooth muscle cells. These data suggest that CO activates L-type calcium channels through NO/cGMP dependant mechanism.

Characteristics of Diprophylline-Induced Bidirectional Modulation on Rat Jejunal Contractility

  • Liu, Fang-Fei;Chen, Da-Peng;Xiong, Yong-Jian;Lv, Bo-Chao;Lin, Yuan
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.1
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    • pp.47-53
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    • 2014
  • In this study, we propose that diprophylline exerts bidirectional modulation (BM) on the isolated rat jejunal segment depending on its contractile state. The results supported the hypothesis. Diprophylline ($20{\mu}M$) exerted stimulatory effects on the contractility of jejunal segment in six low contractile states while inhibitory effects in six high contractile states, showing the characteristics of BM. Diprophylline-induced stimulatory effect was significantly blocked by atropine, indicating the correlation with cholinergic activation. Diprophylline-induced inhibitory effect was partially blocked by phentolamine, propranolol, and L-N-Nitro-Arginine respectively, indicating their correlation with sympathetic activation and nitric oxide-mediated relaxing mechanisms. Diprophylline-induced BM was abolished by tetrodotoxin or in a $Ca^{2+}$ free condition or pretreated with tyrosine kinase inhibitor imatinib, suggesting that diprophylline-induced BM is $Ca^{2+}$ dependent, and that it requires the presence of enteric nervous system as well as pacemaker activity of interstitial cells of Cajal. Diprophylline significantly increased the reduced MLCK expression and myosin extent in constipation-prominent rats and significantly decreased the increased MLCK expression and myosin extent in diarrhea-prominent rats, suggesting that the change of MLCK expression may also be involved in diprophylline-induced BM on rat jejunal contractility. In summary, diprophylline-exerted BM depends on the contractile states of the jejunal segments, requires the presence of $Ca^{2+}$, enteric nervous system, pacemaker activity of interstitial cells of Cajal, and MLCK-correlated myosin phosphorylation. The results suggest the potential implication of diprophylline in relieving alternative hypo/hyper intestinal motility.

Mechanism of Acetylcholine-induced Endothelium-dependent Relaxation in the Rabbit Carotid Artery by M3-receptor Activation

  • Song, Yong-Jin;Kwon, Seong-Chun
    • The Korean Journal of Physiology and Pharmacology
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    • v.8 no.6
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    • pp.313-317
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    • 2004
  • The present study were designed to characterize the action mechanisms of acetylcholine (ACh)-induced endothelium-dependent relaxation in arteries precontracted with high $K^+$(70 mM). For this, we simultaneously measured both muscle tension and cytosolic free $Ca^{2+}$ concentration $([Ca^{2+}]_i)$, using fura-2, in endothelium-intact, rabbit carotid arterial strips. In the artery with endothelium, high $K^+$ increased both $[Ca^{2+}]_i$ and muscle tension whereas ACh $(10{\mu}M)$ significantly relaxed the muscle and increased $[Ca^{2+}]_i$. In the presence of $N^G$-nitro-L-arginine (L-NAME, 0.1 mM), ACh increased $[Ca^{2+}]_i$ without relaxing the muscle. In the artery without endothelium, high $K^+$ increased both $[Ca^{2+}]_i$ and muscle tension although ACh was ineffective. 4-DAMP (10 nM) or atropine $(0.1{\mu}M)$ abolished ACh-induced increase in $[Ca^{2+}]_i$ and relaxation. The increase of $[Ca^{2+}]_i$ and vasorelaxation by ACh was siginificantly reduced by either $3{\mu}M$ gadolinium, $10{\mu}M$ lanthanum, or by $10{\mu}M$ SKF 96365. These results suggest that in rabbit carotid artery, ACh-evoked relaxation of 70 mM $K^+$-induced contractions appears to be mediated by the release of NO. ACh-evoked vasorelaxation is mediated via the $M_3$ subtype, and activation of the $M_3$ subtype is suggested to stimulate nonselective cation channels, leading to increase of $[Ca^{2+}]_i$ in endothelial cells.

Effect of Lutein on L-NAME-Induced Hypertensive Rats

  • Sung, Ji Hoon;Jo, Young Soo;Kim, Su Jin;Ryu, Jeong Soo;Kim, Myung Chul;Ko, Hyun Ju;Sim, Sang Soo
    • The Korean Journal of Physiology and Pharmacology
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    • v.17 no.4
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    • pp.339-345
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    • 2013
  • We investigated the antihypertensive effect of lutein on $N^G$-nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Daily oral administration of L-NAME (40 mg/kg)-induced a rapid progressive increase in mean arterial pressure (MAP). L-NAME significantly increased MAP from the first week compared to that in the control and reached $193.3{\pm}9.6$ mmHg at the end of treatment. MAP in the lutein groups was dose-dependently lower than that in the L-NAME group. Similar results were observed for systolic and diastolic blood pressure of L-NAME-induced hypertensive rats. The control group showed little change in heart rate for 3 weeks, whereas L-NAME significantly reduced heart rate from $434{\pm}26$ to $376{\pm}33$ beats/min. Lutein (2 mg/kg) significantly prevented the reduced heart rate induced by L-NAME. L-NAME caused hypertrophy of heart and kidney, and increased plasma lipid peroxidation four-fold but significantly reduced plasma nitrite and glutathione concentrations, which were significantly prevented by lutein in a dose-dependent manner. These findings suggest that lutein affords significant antihypertensive and antioxidant effects against L-NAME-induced hypertension in rats.

Effect of OQ21 and Melatonin on Lipopolysaccharide-Induced Oxidative Stress in Rat Brain (흰쥐 뇌에서의 Lipopolysaccharide-유도 산화적 스트레스에 대한 OQ21과 Melatonin의 작용)

  • Bae Mee Kyung;Choi Shinkyu;Ko Moon-Jeong;Ha Hun-Joo;Kim Hwa-Jung
    • YAKHAK HOEJI
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    • v.49 no.4
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    • pp.347-354
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    • 2005
  • Lipopolysaccharide (LPS) induces synthesis of several inflammatory cytokines and nitric oxide (NO). NO in brain is involved not only in the regulation of important metabolic pathways via intracellular cyclic GMP-dependent path­ways, but also in neurotoxic damage by reacting with superoxide ion leading to form peroxynitrite radical. Oxidative stress has suggested to be related to the inhibition of NO synthase/cyclic GMP pathway. OQ21 is a new fluorinated quinone compound that is recently known to have inhibitory effects on both NO synthase (NOS) and guanylyl cyclase (GC). In this study, we examined effects of OQ21, other known NOS or GC inhibitors, or an antioxidant, melatonin, on the oxidative stress produced by LPS in rat brain. Oxidative stress was observed by using the 2',7'-dichlorofluorescin diacetate to measure intra-cellular reactive oxygen species (ROS) production and by measuring the formation of thiobarbituric acid reactive substances to measure lipid peroxidation. LPS induced significant increase in both ROS produdction and lipid peroxidation in all brain regions tested (striatum, hippocampus and cortex), which were dissected 6hr after intraperitoneal administration of LPS to rats. Direct striatal injection of two NOS inhibitors, N-nitro-L-arginine methyl ester and diphenyleneiodonium, or a GC inhibitor, IH-[1,2,4]oxadiazolo[4,3-a]quinoxaline-l-one, produced no significant ROS increase. However, OQ21 enhanced ROS formation in striatal tissues from LPS-treated rats. Melatonin decreased LPS-induced ROS formation and decreased ROS formation increased by OQ21 in striatum of LPS-treated rats.

The Role of Nitric Oxide in Non-adrenergic Non-cholinergic Relaxation in the Rabbit Penile Corpus Cavernosum (토끼 음경해면체의 비-아드레날린 비-콜린성 이완반응에서 산화질소의 역할)

  • Park, Mi-Sun;Kim, Jin-Bo;Hong, Eun-Ju;Hong, Sung-Cheul
    • YAKHAK HOEJI
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    • v.41 no.3
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    • pp.370-380
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    • 1997
  • The role of nitric oxide (NO) on the non-adrenergic non-cholinergic (NANC) relaxations induced by the short and prolonged electrical field stimulation (EFS) has been studied in the rabbit corpus cavernosum. In the presence of atropine and guanethidine the prolonged EFS (2-16 Hz) of corpus cavernosal strips precontracted with phenylephrine produced frequency-dependent relaxations, which were abolished by tetrodotoxin as shown in the relaxations induced gy the short EFS, indicating that their orgin is NANC nerve stimulation. $N^G$-nitro-L-arginine (L-NNA), inhibitor of nitirc oxide synthase, caused a concentration-dependent inhibition to the NANC relaxation, and at 100 M L-NNA the relaxation were virtually abolished. The inhibitory effect of L-NNA was reversed by L-arginine. Hemoglobin abolished the relaxations to NO and also caused a concentration-dependent inhibition of the NANC relaxation. The hemoglobin-resistant relaxation induced by EFS was eliminated by L-NNA. Methylene blue significantly reduced the NANC relaxation in a conentration-dependent manner. The NANC relaxation was not affected by a VIP-inactivating pepridase, alpha0chymotrypsin, whereas VIP-induced relaxation was completely abolished. NO- and VIP-induced relaxation were not affected by L-NNA. These results indicate that the NANC relaxation induced by prolonged EFS of the rabbit corpus cavernosum is mediated by NO-guanosine 3',5'-cyclic monophosphate pathway as shown in the relaxation induced by the short EFS, and that VIP release is not essential for the NANC relaxation of the rabbit corpus cavernosum and VIP is not involved the generation fo NO.

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Kinetics of 2, 4, 6-Trinitrotoluene reduction by zero valent iron (금속 철을 이용한 TNT 환원시의 동역학 산정)

  • 배범한
    • Journal of Korea Soil Environment Society
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    • v.4 no.1
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    • pp.97-108
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    • 1999
  • Reduction 2, 4, 6-trinitrotoluene by zero valent iron was studied in a batch reactor under anoxic conditions. Results showed that the removal of trinitrotoluene (TNT)followed a pseudo-first order reaction and the rate was linearly dependent on the available reactive surfau area of the zero valent iron surface area, resulting a rate constant of 0.0981min$^{1}m$$^{-2}m$. High concentrations of the final product, presumably triaminotoluene which needs to be treated by other means, accumulated in the solution. However , little amount of TAT was extracted from the metal surface by using acetonitrile or phosphate buffered water (pH 7.0). Other common major intermediate in biological TNT degradation, a group of aminodinitrotoluenes, was not detected in the solution. Therefore, it is postulated that the reduction of nitro group by $Fe^0$ occurs simultaneously in all three positions and a TNT reduction model by zero valent iron was suggested.

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