Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer最新文献

{"title":"Detection of human papillomavirus DNA, serum p53, and p53 antibodies in patients with cervical cancer.","authors":"R. Sobti, K. Parashar, R. Kaur, N. Capalash","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I1.80","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I1.80","url":null,"abstract":"Human papillomavirus (HPV) was detected in 85% and 63.6% of patients with invasive cervical cancer and minor cervical abnormalities, respectively. HPV-16 was the dominant type in both groups of women. Because of the high oncogenic potential of HPV-16 and the greater chance of its persistence, a follow-up of cases with minor cervical abnormalities harboring HPV-16 is warranted in order to observe the progression of the lesion. As many as 61.5% of the cases with invasive cervical cancer were found to have higher levels of serum p53 protein than did healthy controls. None of the patients had antibodies against the overexpressed p53. This suggests that, even if mutated, the p53 protein may not be immunogenic in all cases. An inverse relationship between the presence of HPV and the alteration in p53 expression was observed in 71.43% of the cases. This could mean the loss of p53 function as a result of either HPV-E6-mediated degradation or mutation in the p53 gene.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85891729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arsenic-mediated cellular signal transduction, transcription factor activation, and aberrant gene expression: implications in carcinogenesis.","authors":"Chengfeng Yang, K. Frenkel","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I4.20","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I4.20","url":null,"abstract":"Arsenic is a common environmental and occupational pollutant and a well-known human carcinogen that causes cancers in many human organs. The exact molecular mechanisms of arsenic carcinogenesis, however, are not well understood. It is generally acknowledged that arsenic does not act via a classic genotoxic or mutagenic mechanism, because it is not a direct mutagen. On the other hand, a growing amount of evidence has shown that arsenic shares many properties with tumor promoters by inducing intracellular signal transduction, activating transcription factors, and changing the expression of genes that are involved in promoting cell growth, proliferation, and malignant transformation. It is postulated that arsenic-induced mitogen-activated protein kinases (MAPKs) signal transduction, which leads to activation of transcription factors such as activator protein-1 (AP-1) and nuclear factor-kappa B (NF-kappaB) (which in turn alter gene expression), is associated with the carcinogenicity of arsenic. In this article, we review the recent findings in arsenic-induced MAPKs, AP-1 and NF-kappaB activation, and aberrant gene expression; their implications in arsenic carcinogenesis are discussed. The elucidation of arsenic-induced signal transduction pathways that lead to aberrant gene expression involved in the arsenic-triggered malignant transformation could help to identify novel molecular targets for the treatment of human cancers resulting from arsenic exposure.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89149756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of MMP1 in surgical and radiation-impaired wound healing and its effects on the healing process.","authors":"Q. Gu, De-wen Wang, Ya-bin Gao, Jie Zhou, R. Peng, Yufang Cui, G. Xia, Quanhong Qing, Hong Yang, Jie Liu, Mei-lan Zhao","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I1.70","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I1.70","url":null,"abstract":"Radiation-impaired wound is characterized by delayed healing, nonhealing, and carcinogenesis. The mechanism remains unclear. Matrix metalloproteinases (MMPs) are one family of key regulators of the process of wound healing. Their abnormal expression plays important roles in the formation of some chronic skin ulcers. The objective of this project was to study the expression of MMP1 in surgical and radiation-impaired wound healing and its effects on the healing process and tissue remodeling. A rat model of radiation-impaired wound healing was used. Routine light microscopy, electron microscopy, immunohistochemistry, and in situ hybridization, all of which enabled the detection of MMP1 expression during the healing process, were performed. The wound healing process was impaired and delayed. In rats receiving 25Gy gamma-ray locally, the irradiated wounds healed 6 days later than the nonirradiated controls. The following changes in MMP1 expression were found: (1) In the early inflammatory phase and in the period of granulation tissue formation, MMP1 expression was only slightly if at all affected in the newly formed epidermis of irradiated wounds compared with controls. Later, the epidermal expression of MMP1 in radiation wounds was comparatively increased following the delay of the healing process. (2) MMP1 expression in irradiated wounds was markedly decreased in fibroblasts, endothelial cells, and macrophages compared with controls. The expression phase was prolonged because of the delay of the healing process. The reduced expression of MMP1 in granulation tissue retards such important processes as cell migration, angiogenesis, and tissue remodeling, thus slowing the healing process. The expression ofMMP1 in the proliferating keratinocytes may help re-epithelialization. However, in the late healing period, overexpression of MMP1 in the epidermis may hinder the establishment of basal membrane and the formation of granulation tissue, and affect the tissue remodeling process.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82539670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidant-sensitive transcription factor and cyclooxygenase-2 by Helicobacter pylori stimulation in human gastric cancer cells.","authors":"Hyeyoung Kim, J. Lim, J. Seo, K. Kim","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.50","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.50","url":null,"abstract":"Helicobacter pylori (H. pylori) infection might activate nuclear factor-kappaB (NF-kappaB), an oxidant-sensitive transcription regulator of inducible expression of inflammatory genes such as cyclooxygenase-2 (COX-2). We studied the role of NF-kappaB on expression of COX-2 in H. pylori-stimulated gastric cancer cell lines by using antioxidants, glutathione (GSH), and N-acetylcysteine (NAC) as well as an NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC). Gastric adenocarcinoma cell lines derived from Caucasian (AGS) cells and Korean (SNU-484) cells were used to study the role of NF-kappaB on COX-2 expression by H. pylori. They were treated with GSH, NAC, or PDTC in the presence of H. pylori. mRNA expression and protein level for COX-2 were determined by Northern blot and RT-PCR analysis as well as Western blot analysis. NF-kappaB activation was examined by electrophoretic mobility shift assay. As a result, H. pylori induced a time-dependent expression of mRNA and protein for COX-2 via activation of NF-kappaB, which was inhibited by GSH, NAC, and PDTC in the cells. In conclusion, oxidant-sensitive transcription factor NF-kappaB may play a novel role in expression of COX-2 by H. pylori stimulation in gastric cancer cells.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85089214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro evidence of the role of COX-2 in attenuating gastric inflammation and promoting gastric carcinogenesis.","authors":"K. Hahm, Ho Yeong Lim, S. Sohn, Hyuk Jae Kwon, K-Myung Lee, Jeong‐Sang Lee, Y. Surh, Young‐Bae Kim, H. Joo, Won-Seok Kim, Seung-Won Cho","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.100","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.100","url":null,"abstract":"Although gastric adenocarcinoma is one of the most common malignancies in the world, little is known about its exact molecular processes in development and progression. Recent studies suggest that COX-2 is important in carcinogenesis of gastrointestinal cancers, and is especially involved in carcinogenesis in a mouse model of familial adenomatosis polyposis. To understand the role of COX-2 in gastric carcinogenesis and Helicobacter pylori-associated gastritis, we measured COX-2 expression in 170 human gastric carcinoma tissues byimmunohistochemical analysis and compared the expression of COX-2 in paired tissues obtained from normal-looking and cancer-bearing mucosa. Further evidence of the involvement of COX-2 in gastritis and gastric carcinogenesis was obtained by establishing stable cell lines overexpressing COX-2. After subcloning of COX-2 into pCB7 mammalian expression vector, two stable cell lines named MKN-28-COX-2 and MKN-45-COX-2 were generated by transfection of COX-2 cDNA. To understand the effect of COX-2 on gastritis, we performed an electrophoretic mobility shift assay of NF-kappaB (inflammation-associated transcription factor), and measured malondialdehyde levels and chemiluminescence activities in both mock-transfected MKN and MKN-COX-2 cells after stimulation of H. pylori (1 x 10(6) CFU/mL) and neutrophils (10(2) cells/mL). A marked attenuation of NF-kappaB bindings and generation of free radicals was observed in COX-2 overexpressed cells. Another set of experiments, including the growth inhibition by TGF-beta treatment, Matrigel invasion assay, and apoptosis assay, was done. COX-2 showed the advantage of the escape from the growth inhibition by TGF-beta through decreasing TGF-beta RII expression and increased cell invasiveness. In conclusion, COX-2 expression seems to be induced to attenuate the degree of atrophic gastritis, the initial event in gastric carcinogenesis, and promote gastric carcinogenesis.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84842311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spermatogonial cytogenetic toxicity of vincristine and its transmission in the germline cells of Swiss mice.","authors":"R. C. Choudhury, B. Das, S. Misra, M. Jagdale","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I3.60","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I3.60","url":null,"abstract":"We tested the anticancer drug vincristine sulfate (VCR) and cyclophosphamide for their cytogenetic toxic effects on spermatogonia in Swiss mice, and we assessed the possible transmission of such effects in the germline cells. Spermatogonial metaphase chromosome aberration study, primary spermatocytic chromosome analysis, and sperm morphology assay were examined after a single intraperitoneal exposure of VCR 0.25, 0.5, and 1.0 mg/kg and CTX 40 mg/kg body weight at 24 hours, 4 weeks, and 8 weeks posttreatment, respectively. The induction of statistically significant percentages of aberrant spermatogonial metaphases and chromosomal aberrations (excluding gaps) in the VCR-treated mice indicated its clastogenicity. The occurrence of significant percentages of aberrant primary spermatocytes with atypical bivalents and higher percentages of abnormal spermatozoa (sperm), although not statistically significant, indicated the transmission of the induced cytogenetic effects of VCR from spermatogonia to sperm. We conclude that VCR is genotoxic to the male germline cells of Swiss mice, and has the potential of transmitting the cytogenetic toxic effects to the next generation.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86602462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is cyclooxygenase-2 important in skin carcinogenesis?","authors":"S. Fischer","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.120","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.120","url":null,"abstract":"Our studies have focused on the role of arachidonic acid and its products in chemically and UV light-induced murine models of skin carcinogenesis, with an emphasis on determining the importance of prostaglandins (PGs), which are synthesized by the two isoforms of cyclooxygenase (COX). Different types of tumor promoters elevate COX-2 expression in keratinocytes, with little change in COX-1, suggesting that there are multiple signaling pathways by which COX-2 expression can be regulated. We found that the expression of both COX isoforms is increased by treatment with PGs and that this autoregulation occurs via PG receptors linked to a cAMP signaling pathway. We also observed that COX-2 is constitutively upregulated in papillomas and carcinomas from either chemical initiation-promotion or UV-irradiation carcinogenesis experiments. We next investigated cis- and transacting factors required for COX-2 expression. Two regions of the COX-2 promoter, an E box and a nuclear factor-IL6 (NF-IL6) site, were identified as positive regulatory elements through transient transfection with luciferase reporter vectors containing various 5'-flanking regions of the promoter. We found that overexpression of COX-2 in tumors maybe caused by a dysregulation in the expression pattern of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors. To demonstrate the importance of PG synthesis in the carcinogenesis process, several nonsteroidal anti-inflammatory (NSAIDs) drugs were administered either orally or topically during UV carcinogenesis. Dietary administration of indomethacin, piroxicam, or the selective COX-2 inhibitor celecoxib prevented the development of UV-induced skin cancers by up to 85%. In addition, celecoxib had therapeutic efficacy in that it caused regression of preexisting tumors. Topical administration of indomethacin after each UV exposure was also effective, suggesting that a postexposure approach to skin cancer prevention maybe effective. Collectively, these studies suggest that prostaglandins play a critical role in skin cancer development.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84275466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of recombinant human tumor necrosis factor-alpha on Ehrlich ascites tumor growth.","authors":"S. Terlikowski, M. Sułkowska, H. Nowak","doi":"10.1615/JEnvironPatholToxicolOncol.v21.i1.90","DOIUrl":"https://doi.org/10.1615/JEnvironPatholToxicolOncol.v21.i1.90","url":null,"abstract":"We studied the antitumor effect of recombinant human tumor necrosis factor-alpha (rhTNF-alpha) on the intraperitoneal (i.p.) growth of Ehrlich ascites tumor (EAT) in Swiss albino male mice. The animals were treated with i.p. injection of rhTNF-alpha in doses of 5, 7.5, or 10 microg three times a week for 2 weeks, respectively, starting on the 4th day after the EAT inoculation. The effect of the cytokine was evaluated based on the following parameters: total ascites volume, packed cell volume, total packed cell volume, inhibitory growth rate, cellular population of EAT, morphological EAT cell changes, and mean survival time (MST). RhTNF-alpha in a dose of 5 microg had only a slight effect on MST and inhibitory growth rate (IGR). After a dose of 7.5 microg, an increased IGR (p < 0.01) was observed, but the animals did not live longer than the controls. After 7.5- and 10-microg doses (p < 0.001), the number of cells in EAT decreased significantly and enhanced cellular damage to EAT cells was found. In mice treated with 10 microg, a significant IGR (p < 0.001) was accompanied by enhancement of MST (p < 0.01). Although the 10 microg dose exerted a greater effect compared with the remaining doses, no complete regression was attained.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89542557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro protective effects of Terminalia arjuna bark extracts against the 4-nitroquinoline-N-oxide genotoxicity.","authors":"R. Pasquini, G. Scassellati-Sforzolini, M. Villarini, M. Moretti, M. Marcarelli, C. Fatigoni, S. Kaur, Subodh Kumar, I. S. Grover","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I1.20","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I1.20","url":null,"abstract":"We determined the antimutagenic potential of chloroform, acetone, methanol, methanol+HCl, diethyl ether, and ethyl acetate extracts of Terminalia arjuna bark against the model mutagen 4-nitroquinoline-N-oxide (4-NQO) using the Salmonella/microsome, comet, and micronucleus (MN) tests. Salmonella typhimurium TA100 strain and human peripheral white blood cells were coincubated with various concentrations (from 5 to 500 microg) of the six extracts and 4-NQO (from 0.05 to 2 microg). We found that the 4-NQO mutagenicity was inhibited by more than 70% in the Salmonella/microsome test at the highest nontoxic extract dose of ethyl acetate (50 microg/plate), chloroform (100 microg/plate), acetone, (100 microg/plate), and methanol (500 microg/plate). A less marked antimutagenicity activity (inhibition of about 40-45%) was observed for the acidic methanol and diethyl ether extracts. The comet assay showed that acetone extract (100 microg/mL) was more effective in reducing the DNA damage caused by 4-NQO (ca. 90%), whereas the chloroform, ethyl acetate, and diethyl ether extracts were cytotoxic. In the MN test, the decrease in 4-NQO clastogenicity was observed by testing the mutagen especially with chloroform and ethyl acetate extracts (inhibition about 40-45%). The acetone and methanol extracts showed a less marked activity (33% and 37%, respectively). The results of the present study suggest that T. arjuna bark contains some nonpolar as well as polar compounds with antimutagenic activity against 4-NQO. Several explanations can be suggested, but further investigations are necessary to definitely identify the active compounds.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76451879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer incidence rates and environmental factors: an ecological study.","authors":"G. Steiner","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I3.10","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I3.10","url":null,"abstract":"The environmental factors latitude, temperature, and water consumption have been correlatedwithcancerincidencerates. To date, there is noconsensus of opinion that explains how these environmental factors alter the incidence of cancer. A fluoride belt stretches across the north and east of Africa, through the Middle East, across Pakistan and India, into Southeast Asia, and the south of China. There appears to be an association between areas with low cancer incidence rates and high fluoride concentrations in the water supply. This ecologic study attempts to determine if fluoride is correlated with cancer incidence rates. If so, this study also attempts to determine whether fluoride is a factor in the correlation between latitude, temperature, and cancer incidence rates. Population groups with very high cancer incidence rates and population groups with very low cancer incidence rates are compared to identify environmental factors that might explain the correlation between cancer incidence rates and the environmental factors of latitude, temperature, and fluoride. There is a positive correlation between cancer incidence rates and latitude (r = 0.71). There is an inverse correlation between cancer incidence rates and temperature (r = -0.87). There is also an inverse correlation between cancer incidence rates and fluoride concentration in the drinking water (r = -0.75). Very low cancer incidence was found in areas with high fluoride concentrations in the drinking water.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82619673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}