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Poster Presentations

Abstract

Ultraviolet-A radiation UVA (320-400 nm) is scattered rapidly in water with biologically useful amounts to at least 100 m deep in clear aquatic environments. The impact of UVA on the aquatic organism was widely investigated, but little is known about the putative role of antioxidants in alleviating its negative impacts. The present study aimed to elucidate the toxicity of UVA on the African catfish by investigate the impact of UVA on the haematological parameters, biochemical variables, and micronuclei and nuclear lesions formation. Also, the putative role of Spirulina platensis administration in alleviating these negative effects was evaluated. Fish were divided into four groups in triplicates as follows: group I was not exposed to UVA, group II was exposed to UVA only, group III was exposed to UVA with 100 ml ∕ L of Spirulina platensis extract, and group IV was exposed to UVR with 200 ml ∕ L of Spirulina platensis extract. At the end of this period, blood samples were collected, and the selected biomarkers were analysed. In the present result, a significant reduction was recorded in the total White Blood Cell count, Red Blood Cell counts, Haemoglobin concentration and Haematocrit value in the blood of fish exposed to UVA compared to the control one. The biochemical parameters (Aspartic Amino Transferase, Alanine Amino Transferase blood glucose, total protein, total lipid, creatinine, uric acid, and urea exhibited significant increases in the blood of fish exposed to UVA. The groups of fish exposed to UVA subjected to the Micronuclei (MN) and Nuclear Lesion (NL) tests showed statistically significant increase in the frequencies of MN and NL compared to the control. Treatment with Spirulina platensis attenuated the UVA-induced changes, and this improvement was more pronounced in fish received the high Spirulina platensis dose (200mg/L water). All the altered parameters were restored to be near the normal levels. The selected biomarkers could be effectively used as potential biomarkers in the field of environmental biomonitoring. The obtained results evoked that Spirulina platensis administration alleviated the destructive effects of UVA and reduced its toxicity effect on African catfish

Biography

Alaa G. M. Osman is a Professor at Zoology Department, Faculty of Science, Al-Azhar University (Assiut Branch), Egypt having excellent publication record and expertise in Aquatic Toxicology. His principal research interests lie in the field of Ecotoxicology and Aquatic Toxicology which is done to assess the effects of pollution on the aquatic environment using biomarker responses in fishes. He earned his PhD at Humboldt University Berlin, Germany in 2007. He got the best grade possible for his thesis (magna cum laude). Prof. Osman have succeeded to get highly appreciated Alexander von Humboldt postdoctoral research fellowship. He did his postdoctoral stint (2010-2012) at Leibniz Institute of Freshwater Ecology and Inland Fisheries, Berlin. Afterward, he awarded IGB postdoctoral fellowship and return fellowship from Alexander von Humboldt foundation. He contributed during the last years (2010-2018), 30 peer reviewed papers being mostly the first author.

Speaker
Alaa G. M. Osman / Al-Azhar University, Egypt

Abstract

The enhanced expression of heat shock proteins (HSPs) and metallothionein (MT) can be detected in response to many environmental stressors, including exposure to heavy metals. We identified partial mRNA sequences for beta2-microglobulin (ß2m), heat shock cognate 70 kDa protein (HSP70), and MT in embryos of the African catfish Clarias gariepinus (Burchell, 1822). Levels of these transcripts were assessed using reverse-transcription quantitative polymerase chain reaction (RT-QPCR) after embryos of various stages were exposed to different concentrations of lead nitrate. ß2m gene expression exhibited a continuous increase over time. Neither HSP70 nor MT were upregulated, supporting the well-known sensitivity of these organisms to environmental pollutants. Interestingly, the partial MT and HSP70 mRNA sequences revealed an intimate phylogenetic relationship with these proteins in siluriforms. These partial sequences were more closely related to salmoniform proteins than to cypriniform proteins. The expression levels of HSP70 and MT were lower in embryonic tissues exposed to high concentrations of lead (500 µg/L), which impaired the fish's coping strategy via toxication at the cellular level. In conclusion, early developmental stages appear to be particularly vulnerable to lead and fail to activate the typical coping mechanisms. Therefore, these early life stages may not be suitable to characterize concentration-dependent toxicity.

Biography

Alaa G. M. Osman is a Professor at Zoology Department, Faculty of Science, Al-Azhar University (Assiut Branch), Egypt having excellent publication record and expertise in Aquatic Toxicology. His principal research interests lie in the field of Ecotoxicology and Aquatic Toxicology which is done to assess the effects of pollution on the aquatic environment using biomarker responses in fishes. He earned his PhD at Humboldt University Berlin, Germany in 2007. He got the best grade possible for his thesis (magna cum laude). Prof. Osman have succeeded to get highly appreciated Alexander von Humboldt postdoctoral research fellowship. He did his postdoctoral stint (2010-2012) at Leibniz Institute of Freshwater Ecology and Inland Fisheries, Berlin. Afterward, he awarded IGB postdoctoral fellowship and return fellowship from Alexander von Humboldt foundation. He contributed during the last years (2010-2018), 30 peer reviewed papers being mostly the first author.

Speaker
Alaa G. M. Osman / Al-Azhar University, Egypt

Abstract

Pulmonary fibrosis induced by silica particles is a chronic and irreversible lung disease with no effective treatment at present. Recent studies have revealed that epithelial-mesenchymal transition (EMT) is linked to fibrosis following exposure to silica particles. The scavenger receptor, macrophage receptor with collagenous structure (MARCO) plays an important role in silica-induced inflammation, however, the effect of MARCO on silica-induced fibrosis has not been identified. We hypothesized that MARCO would regulate EMT and be involved in the development of silicosis. In our study, silicosis model was constructed by a method of non-surgical intratracheal instillation and a MARCO inhibitor PolyG was administrated at the same time as silica exposure. Herein, we found that MARCO was highly expressed in lung tissue after exposure to silica and PolyG could alleviate pulmonary fibrosis in vivo. Our results confirmed that the expression of epithelial marker such as E-cadherin decreased, while the expression of mesenchymal markers, including vimentin and α-SMA increased after silica treatment. Furthermore, PolyG administration efficiently blocked the mRNA and protein expression of EMT markers and decreased the level of fibrosis-related transcription factors and proteins, such as Col1a1, Col3a1, Collagen I and Collagen III in the lungs of silica-exposed rats. The findings demonstrate that the macrophage membrane receptor MARCO controls the fibrotic response through regulating EMT in experimental silicosis and suggest a novel target for preventive intervention.

Biography

Meng Yang is a Ph.D student in Tongji Medical Collage, Huazhong University of Science and Technology, China. He majors in occupational and environmental health and devotes to the prevention and treatment of occupational lung disease, especially crystalline silica induced pulmonary fibrosis.

Speaker
Meng Yang / Huazhong University of Science and Technology,China

Abstract

Exposure to silica can cause silicosis, which is an irreversible lung disease characterized by pulmonary inflammation and fibrosis. Recently, it is reported that targeting of Gas6/Mer pathway alleviates the development of idopathic pulmonary fibrosis, which is similar to the pathological changes of silicosis. While the role of Gas6/Mer in silica-induced lung fibrosis is still poorly understood. Hence, we hypothesize that Gas6/Mer deficiency would inhibit silica-induced pulmonary inflammation and fibrosis. In the present study, we used quantative mRNA, protein, and pathology analyses to assess the pulmonary inflammation and fibrosis after silica suspension exposure by intratracheal administration. The anti-fibrotic and anti-inflammatory effects of Gas6/Mer pathway were exmined in the same exposure using Cas6- and Mer-deficient (Gas6-/- and Mer-/-) mice. We found that Gas6-/- and Mer-/- mice exhibited reduction of lung inflammation in histopathological section staining from day 7 to day 84 after silica exposure. Meanwhile, compared with wild-type mice, the levels of IL-1β, TNF-α and MCP-1 in the bronchoalveolar lavage fluid (BALF) decreased significantly in Gas6-/- and Mer-/- mice accompanied with limited F4/80-positive macrophage infiltration. Gas6 and Mer deficiency also reduced hydroxyproline and collgen content by limiting cytokine/chemokine release. Moreover, the loss of Gas6 and Mer expression induced the suppressor of cytokine signaling SOCS1 after silica exposure. In conclusion, our results suggest that Gas6/Mer deficiency ameliorates silica-induced pulmonary fibrosis, which is linked to an inhibition of the inflammatory response as the consequence of defective macrophage recruitment and overexpression of an inhibitory signal cytokine SOCS1.

Biography

Wei Li is a PhD student in Tongji Medical Collage, Huazhong University of Science and Technology,Chnia and she has have a bachelor degree in China Medical University. She majors in occupational and environmental health, and devotes to the toxicology and mechanism of crystalline silica on lung lesion. She also participated in the follow-up of the Wuhan-Zhuhai cohort.

Speaker
Wei Li / Huazhong University of Science and Technoloyg,china

Abstract

The photosafety assessment of new drugs is needed before large numbers of human subjects are exposed (phase 3). ICH Guideline S 10 describes the prerequisites of the evaluation during nonclinical and clinical studies. Advice how to manage identified risks is essential, e.g. sun protection. Phototoxicity, photoallergy, photogenotoxicity and photocarcinogencitiy will be discussed. Phototoxicity (photoirritation) is an acute light-induced tissue response to a photoreactive chemical. Photoallergy is an immunologically mediated reaction to a chemical inducing photoproducts (e.g., protein adducts). Typical characteristics for such diagnosis are: • absorbs light within the range of natural sunlight (290-700 nm); • generates a reactive species following absorption of UV-visible light; • distributes sufficiently to light-exposed tissues (e.g., skin, eye). The lack of any of these conditions indicate that there is no concern for direct phototoxicity. The assessment of phototoxicity requires good cooperations of nonclinical and clinical development: The nonclinical development uses tools like in vitro assay for phototoxicity ( 3T3 neutral red uptake phototoxicity test /3T3 NRU-PT/ OECD guideline) or reconstructed human skin models. Recommendations for in vivo studies, the selection of relevant animal model, the clarification of kinetic and tissue distribution data follow. The clinical expert illustrates clinical tools like MED or Photo Patch Test and provides photo documentations as support to facilitate the differential diagnostic activity. A list of phototoxic compounds will be delivered and the medical management of any lesions outlined. The objective of this paper is to increase the awareness of such unwanted toxicities in the public and medical world.

Biography

Gerd Bode has completed his PhD from the University of Duesseldorf and his habilitation at the University of Goettingen, Germany. He is board certified expert in Pathology, Neuropathology, Legal Medicine, Pharmacology and Toxicology. He was head of Drug Research Institutes in Germany and France. He has published more than 130 papers and has served as Topic Leader for Safety at the International Conferences on Harmonization for 16 years.

Speaker
Bode. Gerd / University of Goettingen, Germany

Abstract

Success of pharmaceutical development declines,but costshave increasedto ca.€ 2.5 billion. Theneed for better safety testing remains. Which optionscan overcome failure from early drug discovery into clinical research? Can alternative methodsimprove the value of standard preclinical development programs? Consider usefulness and practicability ofselected methods: 1. Identification of skin toxicity:OECD guidelines recommend replacement of animal studies for products other than drugs.Use in drug development is awaited. 2.Cell studies: 2-3 dimensional models for in-vitro metabolism studies deliver more reliable results than monolayers: better mimicking cell-to-cell adhesion and resistance to drug-induced apoptosis. 3. Three-dimensional tissue reconstruction and organ on-a-chip models of epidermis, epithelia and organs cells focus onkinetic and mechanistic reactions and conditions. 4. Systems toxicology integrates routine studies with quantitative analysis of various large datasets for clarifying pathophysiological reactions.Higher potential for improved toxicity assessment is expected. Discussion and Conclusion New paradigms are becoming available to support the search for the “most humanised /-like models“in the non-clinical and clinical development areas. They respect scientific rigor and patient needs, thus increasing the validity of predictive data. Registration of allexperiments, data sharing and systematic reviewswill further improve the “weight–of-evidence” analysis. Intensive cooperation of Agencies and Industry should facilitate the validation of such new translational tools, and build confidence in novel approaches to select best candidates for anticipating the safety and efficacy of drugs for patients.

Biography

R. Bass, MD, apl Prof Pharmacology and Toxicology, CharitéUniversitätsmedizin (Freie Universität). Research in prenatal toxicology. He served various positions at the BfArM, and was Head of “Human medicines” at the EMA, and visiting Prof for Pharmaceutical Medicine at the University of Basel. He was advisor to the Polish MoH – for Drug authorization and GMP inspections. He created the ICH Guideline on Reproductive Toxicity Testing. G. Bode, MD, PhD University of Duesseldorf, and habilitation at the University of Goettingen. He is board certified in Pathology, Neuropathology, Legal Medicine, and Pharmacology and Toxicology. He was head of Drug Research Institutes in Germany and France. He has published more than 130 papers and has served as Topic Leader for Safety at the International Conferences on Harmonization for 16 years.

Speaker
Rolf Bass / Germany

Abstract

Drugs must be subjected to toxicological testing to support clinical development and market authorisation. To that end, animal studies should be performed according to current regulatory provisions. Hereby, the European Agencies require from the industry to implement the 3Rs into their development programs. However, millions of animals are still used every year in biological and medical research as well as in pharmaceutical development. The present work provides an overview about the recent promising developments in the field of alternative testing approaches such as “multi-organ-chips”, “omics”, and “organoids” together with their status of regulatory acceptance by EU health authorities. To assess the status of industrial adoption and regulatory acceptance of the above-mentioned technologies, regulatory and scientific publications, including European Public Assessment Reports published between July 2016 and July 2018 by the European Medicines Agency, have been evaluated. To date, a broad adoption of alternative testing methods by the pharmaceutical industry is still missing. One of the reasons is that most of these innovative technologies have not yet reached full regulatory acceptance, except in-silico models. Therefore, the pharmaceutical companies mainly prefer to rely on long-established animal models and avoid introducing alternative testing methods. To accelerate the implementation process of alternative testing strategies into drug development, international programs fostering the 3Rs such as EU-ToxRisk must be expanded and continued. Scientific data should be shared and published by academia and the industry. Moreover, a close cooperation with regulatory authorities is needed to further accelerate the implementation process of the 3Rs in regulatory toxicity testing.

Biography

Dr. Sandra Mahr did her PhD and postdoctoral studies at the German Rheumatism research Center, Berlin, Germany and at the Institute of Immunology, University of Rostock, Germany. Afterwards she worked in pharmaceutical research and development at NOXXON Pharma AG, Berlin, Germany for several years. She is regulatory affairs consultant (clinical expert) and one of the managing directors of Riegler-Klar & Partner Pharma-Consulting GbR in Potsdam, Germany, providing consulting services in drug regulatory affairs. In 2018, she prepared her master thesis in drug regulatory affairs in the area of regulatory toxicity testing.

Speaker
Sandra Mahr / Riegler-Klar & Partner Pharma-Consulting GbR, Germany

Abstract

Indomethacin is considered a potent anti-inflammatory, but its undesirable side effects leading to discontinuation of drug treatment. One of the ways to reduce undesirable effects is the association of drugs with nanoparticles. Mesoporous silica structures are being studied by the ability of bioconjugation with different molecules, to be distinguished by the fact that it has the ability to penetrate the cell membrane and by the high efficiency in the incorporation of several therapeutic agents. In this sense, the present work aimed to evaluate the anti-inflammatory potential of indomethacin incorporated into nanoparticles of mesoporous silica (NP+IND). To do so, the nociceptive potential was evaluated by formalin test and NO dosage. In addition, cytotoxicity testing and assessment of locomotor potential were included. The incorporation of indomethacin to the nanoparticle significantly altered the cytotoxicity of indomethacin from 125 to 37.5 μg/mL in peritoneal macrophages. In the evaluation of acute toxicity was observed absence of acute toxicity and the locomotion test excluded a possible sedative effect or motor disorder. The indomethacin dose of 10 mg/kg and NP+IND 2.5 and 5 mg/kg, similarly, significantly reduced inflammation in the formalin test; on the other hand the dose of 10 mg/kg of NP+IND was significantly more effective than the same dose of indomethacin alone. In the evaluation of NO in vitro, NP+IND was not able to reduce NO release at non-cytotoxic concentrations. In sum, the incorporation increases the anti-inflammatory capacity of indomethacin, however it is not related to the reduction of NO release.

Biography

Ricardo A Furtado has completed his PhD from University of São Paulo, BR and postdoctoral studies from University of Franca, BR. Currently, he is professor at University of Franca. He published 29 papers in reputed journals and this work is supported by FAPESP 2017/10241-6 and University of Franca.

Speaker
Ricardo Andrade Furtado / University of Franca, Brazil

Abstract

Objective: To assess the toxic effects of sub lethal concentration pendimethalin (PM) (0.52 mg/l) onhaematological, and biochemical variables,liver lipid peroxidation (LPO) and antioxidant enzymes of Nile Tilapia, Oreochromis niloticus and the ability of Moringaoleifera (Mo) leaf extract to ameliorate the destructive effects of (PM). Methods: Tilapia fish were categorized into four groups in tri-replicates as follows: Group (1) was the control group, Group (2) was treated with Moringaoleifera (Mo) leaf extract (20 ml /30 L. H2O), Group (3) was exposed to pendimethalin(PM) (0.52 mg/l), Group (4) was exposed to (PM) (0.52 mg/l) and treated with (MO) leaf extract (20 ml /30 L. H2O), respectively for 28 days. Results: pendimethalin(PM) decreasednumber of red blood cells (RBCs),white blood cells (WBCs), haemoglobin (Hb) concentration, and haematocrit (Ht) level. Furthermore, PM exposure induced a significant (p < 0.05) increase in serum AST, ALT, creatinine, uric acid, as well as, the level of liver LPO, and percentage of hepatic DNA fragmentation. Marked(p<0.05) reductions in serum acetylcholinesterase (AchE), total protein, albumin and the activity of liver (CAT) and (SOD) enzymes were also recorded. On the other hand, the combined treatment of (PM)with (MO) leaf extract into group (4) restored the tested parameters close to the control values. Conclusion: It could be concluded that addition of Moringaoleifera leaf extract into the water was able to reinstate the haematological and biochemical alterations, antioxidant biomarkers, and hepatic DNA damage induced by pendimethalin.

Biography

Prof.HebaS.HamediscurrentlyworkingasanAssociateProfessorofFishPhysiologyin Zoology department, Faculty of Women for Arts, Science &Education, AinShams University,Cairo,Egypt.ShehadherdoctoralofPhilosophyofSciencein2012andMasterof Sciencedegreein2010 fromAinShamsUniversity,Cairo,Egypt.Prof.Hamedhaddiplomain biochemistryandphysiologyfromSuezCanalUniversity,facultyofScience,Ismailia,Egypt in2014-2015. She also had a Professional diploma in Quality & Accreditation management systems 2015-2016. Her major research interests include Fish Physiology, ReproductiveToxicology, and Aquatic Toxicology. She has been able to prove scientifically that extractionofsomemedicinalplantsusedlocallyinfishdietscontainspharmacologically activeprinciples,capableofamelioratingfishreproductivedysfunctionsandenhancing fecundity.Prof.HamedisaneditorialboardmemberofInternationalJournalofEcotoxicologyandExobiologyand Frontiers in physiologyJournal.She is also areviewerinEnvironmentalToxicologyandPharmacology, NaturalProductResearchAquaculture and Fisheries, andmanyotherInternationalJournals.

Speaker
Heba Salah Mohamed Hamed / Ain shams University, Egypt

Abstract

During the review of relevant literatures, the author found that different researchers gave inconsistent or even contradictory results on the genetic toxicity of nanogold (GNPs).On the one hand, gold is generally considered to be a bioinert metal element, and some researchers have not observed genetic toxicity of gold nanoparticles in eukaryotic cells. For example, Conde J et al. constructed an anti-transcriptional gold composite marker composed of double-labeled stem ring structure oligonucleotides and GNPs (3'-cy3 and 5'-thiol-c6) in their study, which not only effectively blocked gene expression of colorectal cancer cells in vitro, but also assessed gene toxicity in this system through micronucleus test and comet test. The results showed that the antitranscriptional gold nanocomposite marker showed no obvious genetic toxicity. On the other hand, some studies have shown that direct interaction between GNPs and DNA molecules can cause DNA breakage, degradation, gene mutation, etc., indicating that GNPs has genotoxic effects under certain conditions. For example, Huang C et al. believed that GNPs could induce biological molecular damage. In the molecular model he constructed, 80% ethanol aqueous solution was used to make the DNA molecule in A conformation, and when the ratio of GNPs and DNA was 2:1, the combination of GNPs and DNA resulted in the transformation of 50% of DNA superhelix structure into single strand structure (SSB). During transcription, the DNA-RNA hybrid is also A conformation. Therefore, it can be inferred that GNPs -DNA complex has cell division arrest in the late stage of eukaryotic mitosis, leading to failure of division and cell apoptosis. So GNPs is genotoxic. The above two studies analyzed the genotoxicity of GNPs with molecular and cellular reaction systems respectively, and came to different conclusions. The author believes that these two results are not contradictory, because the two reaction systems are different. Huang C et al. used a molecular model with a simple reaction system. GNPs can directly bind to DNA, leading to DNA damage. Its conclusion is based solely on the physical and chemical properties of DNA molecules. Conde J et al. used an in vitro model of colon cancer cells. DNA molecules exist as chromosomes, and there is a complete set of DNA damage repair system in the cell to deal with DNA damage that may occur at any time, so as to maintain the stability of genetic material in the nuclear, and the reaction system is relatively complex. If it is transformed into an in vivo system, it will be more complex, so it is wrong to simply draw the conclusion of genotoxicity of GNPs. Researchers must consider the genotoxicity of GNPs comprehensively in combination with molecular biology, cell biology, functional genomics and other aspects. The same is true in the study of genetic toxicity effects and toxicological mechanism of other metal nanomaterials.

Biography

Chen Lifen, master of biology, now works in the Pharmacology and Toxicology Research Laboratory of Shanghai Institute of Planned Parenthood Research. She is mainly engaged in the toxicology and pharmacology research of reproductive drugs, reproductive disease model, and is in charge of genetic toxicology projects and research interns

Speaker
LiFen. Chen / Shanghai Institute of Planned Parenthood Research, China

Abstract

BisphenolA (BPA) is a well-known endocrine disruptor compound reported to have prostate toxicity. This study aimed to assess the effect of BPA on the proliferation of dorsolateral prostate (DLP) and the expression of epithelial-mesenchymal transition (EMT)-related genes in aged rats. Male aged SD rats were treated with BPA (10.0, 30.0, and 90.0 µg/kg i.g., daily) or vehicle (i.g., daily) for 3 months. Treatment with BPA resulted in increased the expression of PCNA, DLP weight and DLP epithelial height compared with the control group (P < 0.01);such effects were more obvious at higher BPA doses. 90 µg/kg BPA signifcantly increased the estrogen to androgen ratio (P < 0.05). The EMT chip showed the BPA induced upregulation of vimentin,Snail,Twist1, and transforming growth factor beta 1, as well as the downregulation of E-cadherin in the DLP. Immunohistochemical data showed that the expression of vimentin, estrogen receptor subtypes, and androgen receptor increased and the expression of E-cadherin decreased in 30 and 90 µg/kg BPA groups. It was concluded that environmental exposure to low doses of BPA might promote the proliferation of DLP in aged rats by increasing the estrogen to androgen ratio and inducing EMT.

Biography

Dong-Yan Huang has completed his master's degree from Fudanuniversity, China and worked in Shanghai Institute of Planned Parenthood Research, China. Her research interests include the etiological mechanism of prostate hyperplasia and the preclinical safety evaluation of new drugs. She Participated in complete national natural fund project, Shanghai talent development fund projects and projects of Shanghai r&d public service platform,etc., published 14 papers, and applied for 2 national invention patents.

Speaker
Dongyan Huang / Shanghai Institute of Planned Parenthood Research, China

Abstract

Epigallocatechin-3-gallate (EGCG), the most abundant component of green tea, has been reported to possess cancer chemoprevention or anticancer effects in several human cancers. In this study, we examined the dose-response effects of EGCG on human urothelial carcinoma (UC) cells and the underlying mechanism. Our results showed EGCG in higher dose (>300μM) inhibited UC cell viability; whereas low-dose EGCG (<100μM) increased cell viability in T24 and BFTC-905 cells. High-dose EGCG (100 - 300 μM) suppressed the expression of phospho-AKT and phosphor-ERK1/2; in contrast, the level of phospho-AKT and phospho-ERK1/2 of proteins increased at 48 hours after EGCG treatment in lower dose (1, 10, and 50 μM). In vivo data of xenograft model also supported the finding. High-dose EGCG (200mg/kg/day administered intraperitoneally) for 4 weeks showed significant antitumor effect compared to control group (p < 0.05). Nevertheless, mice treated by high-dose EGCG presented with reduced activity and body weight loss and had 40% mortality rate within 10 days after treatment. Serum examinations revealed hepatotoxicity in high-dose EGCG-treated group. Low-dose EGCG did not change tumor size without concomitant side effects. In summary, our data imply that EGCG may exert biphasic effects on UC cells. High-dose EGCG elicit antitumor effects with concomitant hepatotoxicity.

Biography

Dr. Hsu has completed his M.A. Medical Sciencedegree at the age of 26 years from National Taiwan University. His main surgical interest are endoscopic prostatic surgery and minimal invasive surgery in onco-urology field. He has published more than 10 papers in reputed journals and is a PhD candidate in Graduate Institute of Clinical Medicine, National Taiwan University.

Speaker
Hsu, Fu-Shun / New Taipei City Hospital, Taiwan