• Title/Summary/Keyword: Hepatic cells

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Regulation of Tumor Neceosis Factor-${\alpha}$ Receptors and Signal Transduction Pathways

  • Han, Hyung-Mee
    • Toxicological Research
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    • v.8 no.2
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    • pp.343-357
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    • 1992
  • Tumor necrosis factor-${\alpha}$(TNF), a polypeptide hormone secreted primarily by activated macrophages, was originally identified on the basis of its ability to cause hemorrhagic necrosis and tumor regression in vivo. Subsequently, TNF has been shown to be an important component of the host responses to infection and cancer and may mediate the wasting syndrome known as cachexia. These systemic actions of TNF are reflected in its diverse effects on target cells in vitro. TNF initiates its diverse cellular actions by binding to specific cell surface receptors. Although TNF receptors have been identified on most of animal cells, regulation of these receptors and the mechanisms which transduce TNF receptor binding into cellular responses are not well understood. Therefore, in the present study, the mechanisms how TNF receptors are being regulated and how TNF receptor binding is being transduced into cellular responses were investigated in rat liver plasma membranes (PM) and ME-180 human cervical carcinoma cell lines. $^{125}I$-TNF bound to high ($K_d=1.51{\pm}0.35nM$)affinity receptors in rat liver PM. Solubilization of PM with 1% Triton X-100 increased both high affinity (from $0.33{\pm}0.04\;to\;1.67{\pm}0.05$ pmoles/mg protein) and low affinity (from $1.92{\pm}0.16\;to\;7.57{\pm}0.50$ pmoles/mg protein) TNF binding without affecting the affinities for TNF, suggesting the presence of a large latent pool of TNF receptors. Affinity labeling of receptors whether from PM or solubilized PM resulted in cross-linking of $^{125}I$-TNF into $M_r$ 130 kDa, 90 kDa and 66kDa complexes. Thus, the properties of the latent TNF receptors were similar to those initially accessible to TNF. To determine if exposure of latent receptors is regulated by TNF, $^{125}I$-TNF binding to control and TNF-pretreated membranes were assayed. Specific binding was increased by pretreatment with TNF (P<0.05), demonstrating that hepatic PM contains latent TNF receptors whose exposure is promoted by TNF. Homologous up-regulation of TNF receptors may, in part, be responsible for sustained hepatic responsiveness during chronic exposure to TNF. As a next step, the post-receptor events induced by TNF were examined. Although the signal transduction pathways for TNF have not been delineated clearly, the actions of many other hormones are mediated by the reversible phosphorylation of specific enzymes or target proteins. The present study demonstrated that TNF induces phosphorylation of 28 kDa protein (p28). Two dimensional soidum dodecyl sulfate-polyacrylamide gel electrophoresis(SDS-PAGE) resolved the 28kDa phosphoprotein into two isoforms having pIs of 6.2 and 6.1. The pIs and relative molecular weight of p28 were consistent with those of a previously characterized mRNA cap binding protein. mRNA cap binding proteins are a class of translation initiation factors that recognize the 7-methylguanosine cap structure found on the 5' end of eukaryotic mRNAs. In vitro, these proteins are defined by their specific elution from affinity columns composed of 7-methylguanosine 5'-triphosphate($m^7$GTP)-Sepharose. Affinity purification of mRNA cap binding proteins from control and TNF treated ME-180 cells proved that TNF rapidly stimulates phosphorylation of an mRNA cap binding protein. Phosphorylation occurred in several cell types that are important in vitro models of TNF action. The mRNA cap binding protein phosphorylated in response to TNF treatment was purifice, sequenced, and identified as the proto-oncogene product eukaryotic initiation factor-4E(eIF-4E). These data show that phosphorylation of a key component of the cellular translational machinery is a common early event in the diverse cellular actions of TNF.

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Immunocytochemistry of Metallothionein Expression in Developing Rat Liver (발생중인 흰쥐 간에서의 Metallothionein 발현에 관한 면역세포화학적 연구)

  • Oh, Seung-Han;Ahn, Young-Mo;Shin, Kil-Sang;Kim, Wan-Jong
    • Applied Microscopy
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    • v.34 no.3
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    • pp.171-178
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    • 2004
  • Metallothionein (MT) is a family of ubiquitous, low molecular weight (6-7 kDa), cysteine-rich protein with a high affinity to metal ions and has no aromatic amino acids and histidine. Some of the known functions of MT include detoxification of heavy metals and alkylating agents and neutralization of free radicals. Also, this protein may affect a number of cellular processes including gene expression, apoptosis, proliferation and differentiation. But, its actual functions are still not clear. The present study was undertaken to examine immunocytochemically the localization of MT in developing rat liver. On the day 11 of gestation, the fetal rat liver has already been formed and contained numerous oval cells with high nuclear cytoplasmic ratio, which were the progenitors of hepatic parenchymal cells, but no reaction products of MT were detected at this time. And then, positive reactions against MT started to appear predominantly in the parenchymal cells of liver from the 13th day after gestation. Reaction products, immunogold particles or brown coloration, were localized at both the nucleus and the cytoplasm of the parenchymal cells, except mitochondria. The intensity of this reaction gradually increased, and exhibited the strongest at birth. The intensity of MT staining and immunogold labelling diminished with growth, and by the 15th day after birth weak positive reaction was observed in the cells. In brief, positive reactions for MT were observed in the oval cells and the parenchymal cells during fetal stage, meanwhile they were present only in the parenchymal cells after birth. The present results suggest that MT possibly involves parechymal cell proliferation and differentiation through the storage or the supply of various metal ions in the developing rat liver.

Definition of the peptide mimotope of cellular receptor for hepatitis C virus E2 protein using random peptide library (Random peptide library를 이용한 C형 간염바이러스 E2 단백질 세포막 수용체의 peptide mimotope 규명)

  • Lee, In-Hee;Paik, Jae-Eun;Seol, Sang-Yong;Seog, Dae-Hyun;Park, Sae-Gwang;Choi, In-Hak
    • IMMUNE NETWORK
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    • v.1 no.1
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    • pp.77-86
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    • 2001
  • Background: Hepatitis C virus(HCV), a family of Flaviviridae, has a host cell-derived envelope containing a positive-stranded RNA genome, and has been known as the maj or etiological agent for chronic hepatitis, hepatic cirrhosis, and hepatocellular carcinoma. There remains a need to dissect a molecular mechanism of pathogenesis for the development of therapeutic and effective preventive measure for HCV. Identification of cellular receptor is of central importance not only to understand the viral pathogenesis, but also to exploit strategies for prevention of HCV. This study was aimed at identifying peptide mimotopes inhibiting the binding of E2 protein of HCV to MOLT-4 cell. Methods: In this study, phage peptide library displaying a random peptides consisting of 7 or 12 random peptides was employed in order to pan against E2 protein. Free HCV particles were separated from the immune complex forms by immunoprecipitation using anti-human IgG antibody, and used for HCV-capture ELISA. To identify the peptides inhibiting E2-binding to MOLT-4 cells, E2 protein was subj ect to bind to MOLT-4 cells under the competition with phage peptides. Results: Several phage peptides were selected for their specific binding to E2 protein, which showed the conserved sequence of SHFWRAP from 3 different peptide sequences. They were also able to recognize the HCV particles in the sera of HCV patients captured by monoclonal antibody against E2 protein. Two of them, showing peptide sequence of HLGPWMSHWFQR and WAPPLERSSLFY respectively, were revealed to inhibit the binding of E2 protein to MOLT-4 cell efficiently in dose dependent mode. However, few membrane-associated receptor candidates were seen using Fasta3 programe for homology search with these peptides. Conclusion: Phage peptides containing HLGPWMSHWFQR and WAPPLERSSLFY respectively, showed the inhibition of E2-binding to MOLT-4 cells. However, they did not reveal any homologues to cellular receptors from GenBank database. In further study, cellular receptor could be identified through the screening of cDNA library from MOLT-4 or hepatocytes using antibodies against these peptide mimotopes.

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Red Ginseng Extract Improves Liver Fibrosis in Mice Treated with the Endocrine Disruptor Bisphenol A (내분비교란물질 비스페놀 A를 처리한 마우스에서 홍삼 추출물의 간 섬유화 개선)

  • Choi, Jehun;Park, Chun Geon;Seo, Kyoung Hee;Kim, Hyung Don;Yoon, Ji Hye;Ahn, Young Sup;Kim, Jin Seong
    • Korean Journal of Plant Resources
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    • v.30 no.2
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    • pp.125-132
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    • 2017
  • Bisphenol A (BPA), a known endocrine disruptor, induces toxicity in cells and in experimental animals. Ginseng extracts were evaluated to determine whether they can inhibit BPA-induced toxicity. The antioxidant activity of fresh ginseng extract (WGE), dried white ginseng extract (DGE), and dried red ginseng extract (RGE) was measured using the DPPH assay. WGE and RGE increased DPPH free radical scavenging activity. Cell viability was measured in HepG2 cells following treatment with BPA and ginseng extracts using the MTT assay. DGE and RGE increased HepG2 cell viability following treatment with $200{\mu}M$ BPA. RGE reduced levels of biochemical markers of liver damage, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) that increased in mice following treatment with BPA. In addition, the regeneration and proliferation of damaged liver cells were significantly increased in RGE-treated mice. Moreover, RGE inhibited hepatic fibrosis in the surrounding area and in the central vein of the liver microstructure. RGE also significantly inhibited BPA-induced cytotoxicity. In addition, RGE protected liver damage and regenerated liver tissues in BPA-treated animals. These results show that RGE may represent a potential candidate drug for the treatment and prevention of liver damage caused by environmental toxins.

The Protective Activity of Soeumin Bojungykgi-tang Water Extract Against Oxidative Stress-induced Hepato-Toxicity (산화적 스트레스로 유도된 간손상에 대한 소음인보중익기탕 열수추출물의 간세포보호효과)

  • Son, Jin Won;Jung, Ji Yun;Kim, Kwang-Youn;Hwangbo, Min;Park, Chung A;Cho, IL Je;Back, Young Doo;Jung, Tae Young;Kim, Sang Chan;Jee, Seon Young
    • Herbal Formula Science
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    • v.25 no.4
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    • pp.509-526
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    • 2017
  • Background and objectives : Soeumin Bojungykgi-tang (seBYTE) has been used to supplement qi in Korean medicine. It has been demonstrated to possess various biological functions such as anti-cancer, anti-aging and anti-inflammatory effects. The present study evaluated the protective roles of seBYTE in hepatotoxic in vitro and in vivo model. Methods : To investigate cytoprotective effect of seBYTE, HepG2 cells were pretreated with seBYTE and then subsequently exposed to $10{\mu}m$ AA for 12 h, followed by $5{\mu}m$ iron. Cell viability was examined by MTT assay, and expression of apoptosis-related proteins was evaluated by immunoblot analysis. For responsible molecular mechanisms, ROS production, GSH contents, and mitochondrial membrane potential were measured. In addition, hepatoprotective effect of seBYTE in vivo was assessed in $CCl_4$-induced animal model. Results : seBYTE prevented AA + iron-induced cytotoxicity in concentration dependent manner. In addition, ROS production, GSH depletion, and mitochondrial dysfunction induced by AA + iron were significantly reduced by seBYTE pretreatment. Furthermore, seBYTE recovered expression of the pro-apoptotic proteins such as PARP and pro-caspase-3. In animal experiment, plasma ALT and AST levels were significantly elevated in $CCl_4$ treatment, but seBYTE significantly decreased the ALT and AST levels. Moreover, seBYTE alleviated the numbers of histological activity index, percentages of degenerative regions, degenerated hepatocytes, infiltrated inflammatory cells, nitrotyrosine- and 4-hydroxynonenal-positive cells in liver. Conclusions : These results showed that hepatoprotective effect of seBYTE against on $CCl_4$-induced hepatic damages is partly due to antioxidative and anti-apoptotic process.

Effects of miR-152 on Cell Growth Inhibition, Motility Suppression and Apoptosis Induction in Hepatocellular Carcinoma Cells

  • Dang, Yi-Wu;Zeng, Jing;He, Rong-Quan;Rong, Min-Hua;Luo, Dian-Zhong;Chen, Gang
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.12
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    • pp.4969-4976
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    • 2014
  • Background: miR-152 is involved in the genesis and development of several malignancies. However, its role in HCC has not been fully clarified. The aim of this study was to investigate the clinicopathological significance of miR-152 and its effect on the malignant phenotype of HCC cells. Methods: miR-152 expression was detected using real-time quantitative RT-PCR in 89 pairs of HCC formalin-fixed paraffin-embedded and their adjacent tissues. Functionally, in vitro effects and mechanisms of action of miR-152 on proliferation, viability, caspase activity, apoptosis and motility were explored in HepG2, HepB3 and SNU449 cells, as assessed by spectrophotometry, fluorimetry, fluorescence microscopy, wound-healing and Western blotting, respectively. Results: miR-152 expression in HCC was downregulated remarkably compared to that in adjacent hepatic tissues. miR-152 levels in groups of advanced clinical stage, larger tumor size and positive HBV infection, were significantly lower than in other groups. A miR-152 mimic could suppress cell growth, inhibit cell motility and increase caspase activity and apoptosis in HCC cell lines. Furthermore, Western blotting showed that the miR-152 mimic downregulated Wnt-1, DNMT1, ERK1/2, AKT and TNFRS6B signaling. Intriguingly, inverse correlation of TNFRF6B and miR-152 expression was found in HCC and bioinformatics confirmed that TNFRF6B might be a target of miR-152. Conclusions: Underexpression of miR-152 plays a vital role in hepatocarcinogenesis and lack of miR-152 is related to the progression of HCC through deregulation of cell proliferation, motility and apoptosis. miR-152 may act as a tumor suppressor miRNA by also targeting TNFRSF6B and is therefore a potential candidate biomarker for HCC diagnosis, prognosis and molecular therapy.

Different Regulation of p53 Expression by Cadmium Exposure in Kidney, Liver, Intestine, Vasculature, and Brain Astrocytes

  • Lee, Jin-Yong;Tokumoto, Maki;Hattori, Yuta;Fujiwara, Yasuyuki;Shimada, Akinori;Satoh, Masahiko
    • Toxicological Research
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    • v.32 no.1
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    • pp.73-80
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    • 2016
  • Chronic exposure to cadmium (Cd) is known to adversely affect renal function. Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells. In this study, the effects of Cd on protein expression of p53 and apoptotic signals in the kidney and liver of mice exposed to Cd for 12 months were examined, as well as the effects of Cd on p53 protein levels and gene expression of the Ube2d family in various cell lines. Results showed that in the kidney of mice exposed to 300 ppm Cd for 12 months, there was overaccumulation of p53 proteins in addition to the induction of apoptosis, which was triggered specifically in the proximal tubules. Interestingly, the site of apoptosis was the same as that of p53 accumulation in the proximal tubules. In the liver of mice chronically exposed to Cd, gene expression of the Ube2d family tended to be slightly decreased, together with slight apoptosis without the accumulation of p53 protein. In rat small intestine epithelial (IEC-6) cells, Cd decreased not only the p53 protein level but also gene expression of Ube2d1, Ube2d2 and Ube2d4. In human brain microvascular endothelial cells (HBMECs), Cd did not suppress gene expression of the Ube2d family, but increased the p53 protein level. In human brain astrocytes (HBASTs), Cd only increased gene expression of UBE2D3. These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.

Role of stearyl-coenzyme A desaturase 1 in mediating the effects of palmitic acid on endoplasmic reticulum stress, inflammation, and apoptosis in goose primary hepatocytes

  • Tang, Bincheng;Qiu, Jiamin;Hu, Shenqiang;Li, Liang;Wang, Jiwen
    • Animal Bioscience
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    • v.34 no.7
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    • pp.1210-1220
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    • 2021
  • Objective: Unlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid (PA) tolerance of goose primary hepatocytes. Methods: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide was examined to reflect the effect of PA on hepatocytes viability, and quantitative polymerase chain reaction was used to detect the mRNA levels of several genes related to endoplasmic reticulum (ER) stress, inflammation, and apoptosis, and the role of SCD1 in PA tolerance of goose hepatocytes was explored using RNA interfere. Results: Our results indicated that goose hepatocytes exhibited a higher tolerant capacity to PA than human hepatic cell line (LO2 cells). In goose primary hepatocytes, the mRNA levels of fatty acid desaturation-related genes (SCD1 and fatty acid desaturase 2) and fatty acid elongate enzyme-related gene (elongase of very long chain fatty acids 6) were significantly upregulated with 0.6 mM PA treatment. However, in LO2 cells, expression of ER stress-related genes (x box-binding protein, binding immunoglobulin protein, and activating transcription factor 6), inflammatory response-related genes (interleukin-6 [IL-6], interleukin-1β [IL-1β], and interferon-γ) and apoptosis-related genes (bcl-2-associated X protein, b-cell lymphoma 2, Caspase-3, and Caspase-9) was significantly enhanced with 0.6 mM PA treatment. Additionally, small interfering RNA (siRNA) mediated downregulation of SCD1 significantly reduced the PA tolerance of goose primary hepatocytes under the treatment of 0.6 mM PA; meanwhile, the mRNA levels of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), forkhead box O1 (FoxO1), mammalian target of rapamycin and AMPK pathways (AKT1, AKT2, FoxO1, and sirtuin 1), as well as the protein expression of cytochrome C and the apoptosis rate were upregulated. Conclusion: In conclusion, our data suggested that SCD1 was involved in enhancing the PA tolerance of goose primary hepatocytes by regulating inflammation- and apoptosis-related genes expression.

Effect of Ginseng on Visceral Nucleic Acid Content of Rats (고려인삼이 흰쥐의 장기조직 핵산 함유량에 미치는 영향)

  • Kim, Chul;Choi, Hyun;Kim, Chung-Chin;Kim, Jong-Kyu;Kim, Myung-Suk;Huh, Man-Kyung
    • The Korean Journal of Physiology
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    • v.5 no.1
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    • pp.23-42
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    • 1971
  • I. Chemical analysis A study was planned to see if administration of ginseng extract has any influence upon the adrenal, the hepatic, the splenic, and the pancreatic nucleic acid contents of rats, and to estimate the effect of ACTH administration as a substitute for stress reaction upon these nucleic acid contents of rats previously primed with ginseng. Ninety male rats$(body\;weight:\;150{\sim}200gm)$ were divided into the ginseng, the saline, and the normal control groups, which received for 5 days 0.5ml/100 gm body weight of ginseng extract solution (4 mg of ginseng alcohol extract in 1 ml of saline), same amount of saline, or no medication, respectively. On the 5th experimental day, each of the 3 groups was further divided into 2 subgroups yielding the ginseng, the ginseng-ACTIT, the saline, the saline-ACTH, the normal control, and the normal-ACTH subgroups. The ginseng, the saline, and the normal control subgroups were sacrificed 3 hours after the last medication, while the ginseng-ACTH, the saline·ACTH, and the normal-ACTH subgroups received ACTH(0.1 unit/subject) 1 hour after the last medication and were sacrificed after 1 more hour. The adrenal gland, the liver, the spleen and the pancreas of each rat were measured for RNA and DNA contents using the chemical method of Schmidt-Thannhauser-Schneider. Following results were obtained: 1. Adrenal RNA and DNA contents and RNA/DNA ratio were all significantly higher in the ginseng group compared with the values obtained from the normal control and the saline groups. Generally administration of ACTH reduced nucleic acid contents of the viscera examined. However, in the ginseng group the rate of decrease [(value of ginseng-ACTH subgroup-value of ginseng subgroup) x100/value of ginseng subgroup)] in adrenal RNA and DNA contents and in RNA/DNA ratio were more conspicuous than they were in the normal control and the saline groups. 2. Hepatic RNA and DNA contents and RNA/DNA ratio were all significantly less in the ginseng group than in the normal control and the saline groups. After ACTH, the rate of decrease in hepatic RNA, DNA, and RNA/DNA ratio of the ginseng· group was less conspicuous than those of the other 2 groups. 3. With regard to the splenic nucleic acid contents, the RNA and the RNA/DNA values of the ginseng group were higher than those of the normal control group but lower than those of the saline group, while the DNA value of the ginseng group was lower than that of the normal control group but higher than that of the saline group. Following administration of ACTH, the rate of decrease in RNA and DNA contents and in RNA/DNA ratio of the ginseng group was more conspicuous than that of the normal control group but less remarkable than that of the saline group. 4. Pancreatic RNA and DNA contents were notably lower in the ginseng group than in the normal control and the saline groups. However, the RNA/DNA ratio of the ginseng group was higher than that of the normal control and the saline groups.'After ACTH, the rate of decrease in pancreatic RNA and RNA/DNA ratio of the ginseng group was less than that of the normal. control group but more than that of the saline group, while the DNA content was actually increased in the ginseng group though it decreased in the normal control and the saline groups. Although the results are not clear enough for an accurate interpretation, they seem to indicate that ginseng exerts notable influence upon the RNA and DNA contents and the RNA/DNA ratio of the viscera stodied. On the whole the drug tends to increase the RNA and DNA contents and RNA/DNA ratio of the adrenal gland but seems to diminish the values of the other 3 viscera. In the early period following ACTH, ginseng facilitates the fall in RNA and DNA contents and RNA/DNA ratio of the adrenal gland, while it tends to reduce the fall in the values of the other viscera studied. II. Autoradiographic and histochemical analysis It was planned autoradiographically and histochemically to affirm and extend the results obtained in part I with regard to the chemically assessed change in the adrenal, the pancreatic, the hepatic and the splenic DNA and RNA contents under the influence of ginseng and ACTH. Fourty male mice (body weight: $18{\sim}20gm$) and 20 male rats were used. Each animal species was divided into the saline, the ginseng, the saline-ACTH, and the ginseng-ACTH groups according to the administered drugs. In the mice, the adrenal, the pancreatic, the splenic and the hepatic DNA-synthetic activity was assessed autoradiographically after administration of $^3H$-thymidine. In the rats, the RNA content of the above 4 organs was assessed histochemically after staining them with methylgreen pyronine. Following results were obtained: 1. Labeled cells were significantly more numerous in the adrenal cortex, the spleen and the liver of the ginseng group than in those of the saline group, although they were less numerous in the pancreas of the ginseng group than in the pancreas of the saline group. The adrenocortical, the pancreatic, the splenic and the hepatic tissues were stained with methylgreen pyronine more deeply in the ginseng group than in the saline group. 2. The adrenocortical, the pancreatic, the splenic and the hepatic tissues contained labeled cells less numerously in the saline-ACTH and the ginseng-ACTH group than in the saline and the ginseng groups. All these tissues were also stained with methylgreen pyronine less deeply in the saline-ACTH and the ginseng-ACTH groups than in the saline and the ginseng groups. 3. However, the adrenal cortex, the spleen, the pancreas, and the liver contained labeled cells more numerously in the ginseng-ACTH group than in the saline-ACTH group. the 4 tissues were stained with methylgreen pyronine more deeply in the ginseng-ACTH group than in the saline-ACTH group. It is inferred from the above results that though with exception, the ginseng mostly facilitates cellular synthesis of nucleic acids and mitigates reduction in nucleic acid content of tissues after administration of ACTH.

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Evaluating the Impact of Attenuation Correction Difference According to the Lipiodol in PET/CT after TACE (간동맥 화학 색전술에 사용하는 Lipiodol에 의한 감쇠 오차가 PET/CT검사에서 영상에 미치는 영향 평가)

  • Cha, Eun Sun;Hong, Gun chul;Park, Hoon;Choi, Choon Ki;Seok, Jae Dong
    • The Korean Journal of Nuclear Medicine Technology
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    • v.17 no.1
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    • pp.67-70
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    • 2013
  • Purpose: Surge in patients with hepatocellular carcinoma, hepatic artery chemical embolization is one of the effective interventional procedures. The PET/CT examination plays an important role in determining the presence of residual cancer cells and metastasis, and prognosis after embolization. The other hand, the hepatic artery chemical embolization of embolic material used lipiodol produced artifacts in the PET/CT examination, and these artifacts results in quantitative evaluation influence. This study, the radioactivity density and the percentage error was evaluated by the extent of the impact of lipiodol in the image of PET/CT. Materials and Methods: 1994 NEMA Phantom was acquired for 2 minutes and 30 seconds per bed after the Teflon, water and lipiodol filled, and these three inserts into the enough to mix the rest behind radioactive injection with $20{\pm}10MBq$. Phantom reconfigure with the iterative reconstruction method the number of iterations for two times by law, a subset of 20 errors. We set up region of interest at each area of the Teflon, water, lipiodol, insert artifact occurs between regions, and background and it was calculated and compared by the radioactivity density(kBq/ml) and the% Difference. Results: Radioactivity density of the each region of interest area with the teflon, water, lipiodol, insert artifact occurs between regions, background activity was $0.09{\pm}0.04$, $0.40{\pm}0.17$, $1.55{\pm}0.75$, $2.5{\pm}1.09$, $2.65{\pm}1.16 kBq/ml$ (P <0.05) and it was statistically significant results. Percentage error of lipiodol in each area was 118%, compared to the water compared with the background activity 52%, compared with a teflon was 180% of the difference. Conclusion: We found that the error due to under the influence of the attenuation correction when PET/CT scans after lipiodol injection performed, and the radioactivity density is higher than compared to other implants, lower than background. Applying the nonattenuation correction images, and after hepatic artery chemical embolization who underwent PET/CT imaging so that the test should be take the consideration to the extent of the impact of lipiodol be.

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