Pub Date : 2015-01-01DOI: 10.1615/JENVIRONPATHOLTOXICOLONCOL.2015013049
B. Gopu, R. Dileep, Matukumalli Usha Rani, C.S.V. Satish Kumar, Matham Vijay Kumar, A. Gopala Reddy
Ulcerative colitis is a chronically recurrent inflammatory bowel disease of unknown origin. The present study is to evaluate the effect of flunixin and curcumin in experimentally induced ulcerative colitis in rats. Animals were randomly divided into four groups, each consisting of 12 animals: normal control group, acetic acid group, curcumin-treated group, and flunixin-treated group. Induction of colitis by intracolonic administration of 4% acetic acid produced severe macroscopic inflammation in the colon, 14 days after acetic acid administration as assessed by the colonic damage score. Microscopically, colonic tissues showed ulceration, edema, and inflammatory cells infiltration. Biochemical studies revealed increased serum levels of lactate dehydrogenase (LDH), colonic alkaline phosphatase (ALP), and myeloperoxidase (MPO). Oxidative stress was indicated by elevated lipid peroxide formation and depleted reduced glutathione concentrations in colonic tissues. After induction of colitis, treatment with curcumin (50 mg/kg daily, p.o.) and flunixin (2.5 mg/kg daily, s.c.) decreased serum LDH, ALP, interleukin (IL)-1β, and tumor necrosis factor-α levels, as well as colonic MPO and lipid peroxide levels, whereas increased colonic prostaglandin E2 and IL-10 concentrations were observed. Moreover, effective doses of curcumin and flunixin were effective in restoring the histopathological changes induced by acetic acid administration. The findings of the present study provide evidence that flunixin may be beneficial in patients with inflammatory bowel disease.
{"title":"Protective Role of Curcumin and Flunixin Against Acetic Acid-Induced Inflammatory Bowel Disease via Modulating Inflammatory Mediators and Cytokine Profile in Rats.","authors":"B. Gopu, R. Dileep, Matukumalli Usha Rani, C.S.V. Satish Kumar, Matham Vijay Kumar, A. Gopala Reddy","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.2015013049","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.2015013049","url":null,"abstract":"Ulcerative colitis is a chronically recurrent inflammatory bowel disease of unknown origin. The present study is to evaluate the effect of flunixin and curcumin in experimentally induced ulcerative colitis in rats. Animals were randomly divided into four groups, each consisting of 12 animals: normal control group, acetic acid group, curcumin-treated group, and flunixin-treated group. Induction of colitis by intracolonic administration of 4% acetic acid produced severe macroscopic inflammation in the colon, 14 days after acetic acid administration as assessed by the colonic damage score. Microscopically, colonic tissues showed ulceration, edema, and inflammatory cells infiltration. Biochemical studies revealed increased serum levels of lactate dehydrogenase (LDH), colonic alkaline phosphatase (ALP), and myeloperoxidase (MPO). Oxidative stress was indicated by elevated lipid peroxide formation and depleted reduced glutathione concentrations in colonic tissues. After induction of colitis, treatment with curcumin (50 mg/kg daily, p.o.) and flunixin (2.5 mg/kg daily, s.c.) decreased serum LDH, ALP, interleukin (IL)-1β, and tumor necrosis factor-α levels, as well as colonic MPO and lipid peroxide levels, whereas increased colonic prostaglandin E2 and IL-10 concentrations were observed. Moreover, effective doses of curcumin and flunixin were effective in restoring the histopathological changes induced by acetic acid administration. The findings of the present study provide evidence that flunixin may be beneficial in patients with inflammatory bowel disease.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"92 1","pages":"309-20"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86030740","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}
Pub Date : 2008-07-01DOI: 10.1016/S1359-6349(08)71376-4
F. Saleh, W. Reno, G. Ibrahim, A. Behbehani, H. Dashti, S. Asfar
{"title":"The first pilot study on characteristics and practice patterns of Kuwaiti breast cancer patients.","authors":"F. Saleh, W. Reno, G. Ibrahim, A. Behbehani, H. Dashti, S. Asfar","doi":"10.1016/S1359-6349(08)71376-4","DOIUrl":"https://doi.org/10.1016/S1359-6349(08)71376-4","url":null,"abstract":"","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"24 1","pages":"61-75"},"PeriodicalIF":0.0,"publicationDate":"2008-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90309824","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}
Pub Date : 2003-07-03DOI: 10.1615/JENVIRONPATHOLTOXICOLONCOL.V22.I2.80
P. Herring, J. Ingels, L. Carbone, K. D. Barrow, D. Osborn, D. Dietzen, L. Pifer
{"title":"Lack of efficacy of the combination of pamidronate and vitamin D on regression of prostate cancer in the Dunning rat model.","authors":"P. Herring, J. Ingels, L. Carbone, K. D. Barrow, D. Osborn, D. Dietzen, L. Pifer","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V22.I2.80","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V22.I2.80","url":null,"abstract":"","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"34 1","pages":"vii-viii"},"PeriodicalIF":0.0,"publicationDate":"2003-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82974969","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}
Pub Date : 2003-01-01DOI: 10.1615/JENVPATHTOXONCOL.V22.I1.50
S. Ray, N. Chattopadhyay, A. Mitra, M. Siddiqi, A. Chatterjee
Curcumin (diferuloyl methane), the major pigment from the rhizome of Curcuma longa L., has been widely studied for its tumor-inhibiting properties. Recent studies indicate that curcumin can modify cell receptor binding, it also affects intracellular signalling reactions. Curcumin-treated B16F10 melanoma cells formed eight-fold fewer lung metastases in C57BL6 mice. In the cell adhesion assays, curcumin-treated cells showed a dose-dependent reduction in their binding to four extracellular matrix (ECM) proteins. The binding to fibronectin, vitronectin, and collagen IV decreased by over 50% in 24 hours, and by 100% after 48 hours of curcumin treatment, it persisted at this level even after 15 days of cultivating cells in curcumin-free medium. Curcumin-treated cells showed a marked reduction in the expression of alpha5beta1 and alpha(v)beta3 integrin receptors. In addition, curcumin treatment inhibited pp125 focal adhesion kinase (FAK), tyrosine phosphorylation of a 120 kD protein, and collagenase activity. Curcumin enhances the expression of antimetastatic proteins, tissue inhibitor metalloproteinase (TIMP)-2, nonmetastatic gene 23 (Nm23), and E-cadherin. In this article we report on the effect of curcumin on the expression of integrin, TIMP-2, Nm23, E-cadherin, adhesion, and metalloproteinase activity.
{"title":"Curcumin exhibits antimetastatic properties by modulating integrin receptors, collagenase activity, and expression of Nm23 and E-cadherin.","authors":"S. Ray, N. Chattopadhyay, A. Mitra, M. Siddiqi, A. Chatterjee","doi":"10.1615/JENVPATHTOXONCOL.V22.I1.50","DOIUrl":"https://doi.org/10.1615/JENVPATHTOXONCOL.V22.I1.50","url":null,"abstract":"Curcumin (diferuloyl methane), the major pigment from the rhizome of Curcuma longa L., has been widely studied for its tumor-inhibiting properties. Recent studies indicate that curcumin can modify cell receptor binding, it also affects intracellular signalling reactions. Curcumin-treated B16F10 melanoma cells formed eight-fold fewer lung metastases in C57BL6 mice. In the cell adhesion assays, curcumin-treated cells showed a dose-dependent reduction in their binding to four extracellular matrix (ECM) proteins. The binding to fibronectin, vitronectin, and collagen IV decreased by over 50% in 24 hours, and by 100% after 48 hours of curcumin treatment, it persisted at this level even after 15 days of cultivating cells in curcumin-free medium. Curcumin-treated cells showed a marked reduction in the expression of alpha5beta1 and alpha(v)beta3 integrin receptors. In addition, curcumin treatment inhibited pp125 focal adhesion kinase (FAK), tyrosine phosphorylation of a 120 kD protein, and collagenase activity. Curcumin enhances the expression of antimetastatic proteins, tissue inhibitor metalloproteinase (TIMP)-2, nonmetastatic gene 23 (Nm23), and E-cadherin. In this article we report on the effect of curcumin on the expression of integrin, TIMP-2, Nm23, E-cadherin, adhesion, and metalloproteinase activity.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"1 1","pages":"49-58"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86499897","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}
Pub Date : 2003-01-01DOI: 10.1615/JENVPATHTOXONCOL.V22.I1.70
S. Kaur, Saroj Arora, S. Kaur, Subodh Kumar
In the course of our search for novel polyphenolic antimutagenic agents from medicinal plants, we examined water, acetone, and chloroform extracts of Terminalia bellerica for their antimutagenic potency using the Ames Salmonella/microsome assay. Acetone extract exhibited variable inhibitory activity of 65.6%, and 69.7% with 4-O-nitrophenylenediamine (NPD) and sodium azide, respectively (as direct-acting mutagens), and 81.4% with 2-aminofluorene (2AF) (an S9-dependent mutagen), in the preincubation mode of experimentation. Inhibition with chloroform and water extracts was rather insignificant. Studies are well underway to isolate and identify the active polyphenolic compounds from acetone extract, which could be used as effective chemopreventive agents in the future.
在我们从药用植物中寻找新的多酚类抗诱变剂的过程中，我们使用Ames沙门氏菌/微粒体试验检测了Terminalia bellerica的水、丙酮和氯仿提取物的抗诱变效力。在实验的预孵育模式下，丙酮提取物对4- o -硝基苯二胺(NPD)和叠氮化钠的抑制活性分别为65.6%和69.7%，对2-氨基芴(2AF) (s9依赖性诱变剂)的抑制活性为81.4%。氯仿和水提取物的抑制作用不明显。从丙酮提取物中分离和鉴定活性多酚类化合物的研究正在进行中，这些活性多酚类化合物有望在未来成为有效的化学预防剂。
{"title":"Bioassay-guided isolation of antimutagenic factors from fruits of Terminalia bellerica.","authors":"S. Kaur, Saroj Arora, S. Kaur, Subodh Kumar","doi":"10.1615/JENVPATHTOXONCOL.V22.I1.70","DOIUrl":"https://doi.org/10.1615/JENVPATHTOXONCOL.V22.I1.70","url":null,"abstract":"In the course of our search for novel polyphenolic antimutagenic agents from medicinal plants, we examined water, acetone, and chloroform extracts of Terminalia bellerica for their antimutagenic potency using the Ames Salmonella/microsome assay. Acetone extract exhibited variable inhibitory activity of 65.6%, and 69.7% with 4-O-nitrophenylenediamine (NPD) and sodium azide, respectively (as direct-acting mutagens), and 81.4% with 2-aminofluorene (2AF) (an S9-dependent mutagen), in the preincubation mode of experimentation. Inhibition with chloroform and water extracts was rather insignificant. Studies are well underway to isolate and identify the active polyphenolic compounds from acetone extract, which could be used as effective chemopreventive agents in the future.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"32 1","pages":"69-76"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88873023","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}
Pub Date : 2003-01-01DOI: 10.1615/JENVPATHTOXONCOL.V22.I1.60
K. Kaur, Husheem Michael, Saroj Arora, P. Härkönen, Subodh Kumar
We investigated the effect of water and acetone extract of Juglans regia L. to evaluate its antimutagenic and antiproliferative activities. The antimutagenic study using TA98 and TA100 tester strains of Salmonella revealed the water and acetone extracts to be more effective than the benzene and chloroform extracts in inhibiting the revertants induced by 2-aminoflourene (2AF) in TA100 tester strains. The most effective extracts in the Ames assay were further evaluated using the Lucifer luciferase assay and in time course studies for antiproliferative activities using the Hoechst staining to observe apoptotic cell deaths. The acetone extract showed a correlation of antimutagenic activities in the Ames assay with its antiproliferative effect in different cell lines, while the water extract exerted its effect distinctly in each cell line. Further studies are still needed to evaluate the cytotoxicity in experiments carried out in vivo.
{"title":"Studies on correlation of antimutagenic and antiproliferative activities of Juglans regia L.","authors":"K. Kaur, Husheem Michael, Saroj Arora, P. Härkönen, Subodh Kumar","doi":"10.1615/JENVPATHTOXONCOL.V22.I1.60","DOIUrl":"https://doi.org/10.1615/JENVPATHTOXONCOL.V22.I1.60","url":null,"abstract":"We investigated the effect of water and acetone extract of Juglans regia L. to evaluate its antimutagenic and antiproliferative activities. The antimutagenic study using TA98 and TA100 tester strains of Salmonella revealed the water and acetone extracts to be more effective than the benzene and chloroform extracts in inhibiting the revertants induced by 2-aminoflourene (2AF) in TA100 tester strains. The most effective extracts in the Ames assay were further evaluated using the Lucifer luciferase assay and in time course studies for antiproliferative activities using the Hoechst staining to observe apoptotic cell deaths. The acetone extract showed a correlation of antimutagenic activities in the Ames assay with its antiproliferative effect in different cell lines, while the water extract exerted its effect distinctly in each cell line. Further studies are still needed to evaluate the cytotoxicity in experiments carried out in vivo.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"96 1","pages":"59-67"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85646801","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}
Pub Date : 2002-10-15DOI: 10.1615/JENVIRONPATHOLTOXICOLONCOL.V20.I4.50
A. Natarajan
Structural and numerical chromosomal aberrations have been considered important biological end points in genotoxic studies. Conventional solid staining (such as Giemsa) has been employed to evaluate the frequencies ofinduced chromosomal aberrations following exposure to chemical or physical agents. Recently, molecular cytogenetic techniques that have become available, such as fluorescence in situ hybridization (FISH) using chromosome-specific or chromosomal regions-specific DNA libraries, have increased the resolution of detection of aberrations. The present paper reviews briefly the results obtained from basic and applied studies using the FISH technique.
{"title":"Fluorescence in situ hybridization (FISH) in genetic toxicology.","authors":"A. Natarajan","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V20.I4.50","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V20.I4.50","url":null,"abstract":"Structural and numerical chromosomal aberrations have been considered important biological end points in genotoxic studies. Conventional solid staining (such as Giemsa) has been employed to evaluate the frequencies ofinduced chromosomal aberrations following exposure to chemical or physical agents. Recently, molecular cytogenetic techniques that have become available, such as fluorescence in situ hybridization (FISH) using chromosome-specific or chromosomal regions-specific DNA libraries, have increased the resolution of detection of aberrations. The present paper reviews briefly the results obtained from basic and applied studies using the FISH technique.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"68 1","pages":"293-8"},"PeriodicalIF":0.0,"publicationDate":"2002-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85506668","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}
Pub Date : 2002-06-29DOI: 10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.90
Bandaru S. Reddy, C. Rao
During recent years, multidisciplinary studies in epidemiology and molecular biology, as well as preclinical studies, have contributed much to our understanding of the etiology of colorectal cancer; more importantly they have enabled us to approach its prevention. An impressive body of epidemiological data suggests an inverse relationship between colorectal cancer risk and regular use of nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin. Clinical trials with NSAIDs have demonstrated that NSAID treatment caused regression of preexisting colon adenomas in patients with familial adenomatous polyposis. Preclinical efficacy studies have provided compelling evidence that several phytochemicals with antiinflammatory properties and NSAIDs act to retard, block, or reverse colon carcinogenesis. Equally exciting are opportunities for effective chemoprevention with selective cyclooxygenase-2 (COX-2) inhibitors including celecoxib and rofecoxib in a variety of preclinical models of colon cancer. Naturally occurring COX-2 inhibitors such as curcumin and certain phytosterols have been proven to be effective as chemopreventive agents against colon carcinogenesis with minimal gastrointestinal toxicity. Multistep process of carcinogenesis has provided substantial insights into the mechanisms by which naturally occurring and synthetic antiinflammatory agents modulate these events leading to suppression of tumorigenesis. Growing knowledge in this area has brought about innovative approaches using a combination of agents with different modes of action as a means of increasing efficacy and minimizing toxicity. The natural history of colorectal cancer, from dysplastic aberrant crypts to adenomas and adenocarcinomas, offers multiple opportunities for assessment and intervention. Of further importance would be to identify molecular targets that are critical in the growth and survival of the malignant colorectal cell and are modulated by NSAIDs and COX-2 inhibitors.
{"title":"Novel approaches for colon cancer prevention by cyclooxygenase-2 inhibitors.","authors":"Bandaru S. Reddy, C. Rao","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.90","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.90","url":null,"abstract":"During recent years, multidisciplinary studies in epidemiology and molecular biology, as well as preclinical studies, have contributed much to our understanding of the etiology of colorectal cancer; more importantly they have enabled us to approach its prevention. An impressive body of epidemiological data suggests an inverse relationship between colorectal cancer risk and regular use of nonsteroidal antiinflammatory drugs (NSAIDs), including aspirin. Clinical trials with NSAIDs have demonstrated that NSAID treatment caused regression of preexisting colon adenomas in patients with familial adenomatous polyposis. Preclinical efficacy studies have provided compelling evidence that several phytochemicals with antiinflammatory properties and NSAIDs act to retard, block, or reverse colon carcinogenesis. Equally exciting are opportunities for effective chemoprevention with selective cyclooxygenase-2 (COX-2) inhibitors including celecoxib and rofecoxib in a variety of preclinical models of colon cancer. Naturally occurring COX-2 inhibitors such as curcumin and certain phytosterols have been proven to be effective as chemopreventive agents against colon carcinogenesis with minimal gastrointestinal toxicity. Multistep process of carcinogenesis has provided substantial insights into the mechanisms by which naturally occurring and synthetic antiinflammatory agents modulate these events leading to suppression of tumorigenesis. Growing knowledge in this area has brought about innovative approaches using a combination of agents with different modes of action as a means of increasing efficacy and minimizing toxicity. The natural history of colorectal cancer, from dysplastic aberrant crypts to adenomas and adenocarcinomas, offers multiple opportunities for assessment and intervention. Of further importance would be to identify molecular targets that are critical in the growth and survival of the malignant colorectal cell and are modulated by NSAIDs and COX-2 inhibitors.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"5 1","pages":"155-64"},"PeriodicalIF":0.0,"publicationDate":"2002-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74651781","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}
Pub Date : 2002-01-01DOI: 10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I4.30
Liying Wang, D. Medan, R. Mercer, Xianglin Shi, Chuanshu Huang, V. Castranova, M. Ding, Y. Rojanasakul
Pulmonary exposure to airborne vanadium and vanadium-containing compounds is associated with acute pulmonary inflammation, characterized by a rapid influx of neutrophilic polymorphonuclear leukocytes with a peak response at 6 hours and resolution by 3 days. We hypothesized that neutrophil apoptosis is involved in the resolution of vanadium-induced lung inflammation. To test this hypothesis, mice were exposed to inspired vanadium or saline control and the bronchoalveolar lavage (BAL) cells were examined at various times for apoptosis using terminal deoxyribonucleotidyl transferase-mediated nick end labeling (TUNEL). Control mice showed only resident alveolar macrophages in the BAL with no evidence of apoptosis. In contrast, vanadium-treated mice showed clear apoptosis of BAL cells, which were predominantly neutrophils. The number of apoptotic cells gradually increased and reached a maximal level by 24 hours with subsequent decline. After 24 hours, when the vanadium-induced lung inflammation was in the resolution phase, we observed an increased number of alveolar macrophages in BAL and the engulfment of apoptotic bodies by these macrophages. At 72 hours, the total number of neutrophils in BAL fell to the baseline level, and the number of apoptotic cells was reduced. Clearance of the apoptotic product was demonstrated by the presence of apoptotic bodies in the cytoplasm of alveolar macrophages. We conclude that apoptosis of neutrophils and clearance by alveolar macrophages are important mechanisms in the resolution of vanadium-induced lung inflammation.
{"title":"Role of neutrophil apoptosis in vanadium-induced pulmonary inflammation in mice.","authors":"Liying Wang, D. Medan, R. Mercer, Xianglin Shi, Chuanshu Huang, V. Castranova, M. Ding, Y. Rojanasakul","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I4.30","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I4.30","url":null,"abstract":"Pulmonary exposure to airborne vanadium and vanadium-containing compounds is associated with acute pulmonary inflammation, characterized by a rapid influx of neutrophilic polymorphonuclear leukocytes with a peak response at 6 hours and resolution by 3 days. We hypothesized that neutrophil apoptosis is involved in the resolution of vanadium-induced lung inflammation. To test this hypothesis, mice were exposed to inspired vanadium or saline control and the bronchoalveolar lavage (BAL) cells were examined at various times for apoptosis using terminal deoxyribonucleotidyl transferase-mediated nick end labeling (TUNEL). Control mice showed only resident alveolar macrophages in the BAL with no evidence of apoptosis. In contrast, vanadium-treated mice showed clear apoptosis of BAL cells, which were predominantly neutrophils. The number of apoptotic cells gradually increased and reached a maximal level by 24 hours with subsequent decline. After 24 hours, when the vanadium-induced lung inflammation was in the resolution phase, we observed an increased number of alveolar macrophages in BAL and the engulfment of apoptotic bodies by these macrophages. At 72 hours, the total number of neutrophils in BAL fell to the baseline level, and the number of apoptotic cells was reduced. Clearance of the apoptotic product was demonstrated by the presence of apoptotic bodies in the cytoplasm of alveolar macrophages. We conclude that apoptosis of neutrophils and clearance by alveolar macrophages are important mechanisms in the resolution of vanadium-induced lung inflammation.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"28 1","pages":"343-50"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80412907","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}
Pub Date : 2002-01-01DOI: 10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.40
Yong Soo Lee, E. Kwon, Da-qing Jin, S. Park, Y. Kang, K. Huh, Jung-Ae Kim
Cyclooxygenases (COX) appear to be involved in the mechanism of apoptosis in various cancer cells. In this study we investigated the role of COX in the capsaicin (Cap)-induced apoptosis in SK-N-SH human neuroblastoma cells. Cap induced decreased cell viability and apoptosis in a dose-dependent manner. Cap also significantly reduced the basal generation of reactive oxygen species (ROS) and lipid peroxidation in a time-dependent fashion. Cap markedly suppressed the expression of COX-1 and COX-2. Pretreatment with NS-398, a selective COX-2 inhibitor, or indomethacin, a nonselective COX inhibitor, significantly enhanced the Cap-induced decreased cell viability and apoptosis. Exogenous application of an oxidant, H2O2, significantly prevented the Cap-induced apoptosis and suppressed the expression of COX isoforms. These results suggest that redox status-dependent regulation of COX expression may mediate apoptosis induced by Cap in human neuroblastoma cells.
{"title":"Redox status-dependent regulation of cyclooxygenases mediates the capsaicin-induced apoptosis in human neuroblastoma cells.","authors":"Yong Soo Lee, E. Kwon, Da-qing Jin, S. Park, Y. Kang, K. Huh, Jung-Ae Kim","doi":"10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.40","DOIUrl":"https://doi.org/10.1615/JENVIRONPATHOLTOXICOLONCOL.V21.I2.40","url":null,"abstract":"Cyclooxygenases (COX) appear to be involved in the mechanism of apoptosis in various cancer cells. In this study we investigated the role of COX in the capsaicin (Cap)-induced apoptosis in SK-N-SH human neuroblastoma cells. Cap induced decreased cell viability and apoptosis in a dose-dependent manner. Cap also significantly reduced the basal generation of reactive oxygen species (ROS) and lipid peroxidation in a time-dependent fashion. Cap markedly suppressed the expression of COX-1 and COX-2. Pretreatment with NS-398, a selective COX-2 inhibitor, or indomethacin, a nonselective COX inhibitor, significantly enhanced the Cap-induced decreased cell viability and apoptosis. Exogenous application of an oxidant, H2O2, significantly prevented the Cap-induced apoptosis and suppressed the expression of COX isoforms. These results suggest that redox status-dependent regulation of COX expression may mediate apoptosis induced by Cap in human neuroblastoma cells.","PeriodicalId":94332,"journal":{"name":"Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer","volume":"52 1","pages":"113-20"},"PeriodicalIF":0.0,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86163782","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}
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