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Chie Furihata - One of the best experts on this subject based on the ideXlab platform.
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cause and effect between concentration dependent tissue damage and temporary cell proliferation in rat Stomach Mucosa by nacl a Stomach tumor promoter
Carcinogenesis, 1996Co-Authors: Chie Furihata, H Ohta, T KatsuyamaAbstract:: This study was designed to test whether concentration or dose of NaCl was responsible for the initial tissue damage (after 1 min) and resulting temporary cell proliferation at 17 h in Stomach Mucosa of male F344 rats after gastric intubation of 0.65, 1.3, 2.6 and 3.7 M NaCl. Histological damage was studied by dual staining combining horseradish peroxidase-labeled Griffonia simplicifolia agglutinin-II staining (HRP-GSA-II) and periodic acid cold thionin-Schiff reaction (PATS). Cell proliferation was studied by measuring replicative DNA synthesis with liquid scintillation counting and by BrdU staining. NaCl at the same overall dose of 0.8 g/kg body weight induced different degrees of response depending on the concentration. For 4 ml of 0.65 M NaCl, there was no tissue damage after 1 min nor any increase in replicative DNA synthesis after 17 h in the pyloric Mucosa. Administration of 1.3 M NaCl (2 ml), 2.6 M NaCl (1 ml) and 3.7 M NaCl (0.7 ml) induced concentration-dependent damage of the surface mucous cell layer after 1 min and increased replicative DNA synthesis after 17 h (P<0.05). Concentration-dependent increase in replicative DNA synthesis at 17 h was also induced with the same volume (1 ml) of 1.3, 2.6, and 3.7 M NaCl, while a volume-dependent increase in replicative DNA synthesis at 17 h was induced with 0.4, 0.7 and 1 ml of 3.7 M NaCl. However, a greater increase in replicative DNA synthesis was always observed when using higher NaCl concentrations at the same dose. Liquid scintillation counting was well-correlated with BrdU staining. These results suggest that a high concentration of NaCl is responsible for the initial tissue damage and resulting temporary cell proliferation during Stomach tumor promotion.
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cytotoxicity of nacl a Stomach tumor promoter and prevention by rice extract in Stomach Mucosa of f344 rats
Cancer Detection and Prevention, 1996Co-Authors: Chie Furihata, S Ishida, H Ohta, T Tokuyama, T Katsuyama, Z I OgitaAbstract:Cytotoxicity of NaCl and its prevention by rice extract were studied in the pyloric Mucosa of male F344 rat Stomach after oral administration of rice extract and 2.6 M NaCl. Effect were observed histologically by hematoxylin and eosin staining and the bromodeoxyuridine method. Replicative DNA synthesis (RDS) was assayed by liquid scintillation counter with [3H]thymidine. NaCl (2.6 M) induced destruction of the surface mucous cells within 1 min. RDS and S-phase cells increased significantly (p < 0.01) and to a maximum at 17 h, and returned to control levels 48 h after exposure. Administration of aqueous rice extract 3 h before NaCl exposure reduced the morphological damage to the Mucosa and prevented the increase in RDS dose dependently by up to 65% (p < 0.01). These results showed that NaCl induced rapid Mucosal damage and cell proliferation in rat Stomach Mucosa and that rice extract prevented the damage and reduced the increase in RDS.
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dna damaging and cell proliferative activity of 1 methyl 1 nitrosourea in rat glandular Stomach Mucosa
Mutation Research Letters, 1995Co-Authors: Chie Furihata, Emi Ikui, Taijiro MatsushimaAbstract:The DNA damaging and cell proliferative activity of 1-methyl-1-nitrosourea (MNU), a glandular Stomach carcinogen, was studied in the pyloric Mucosa of male F344 rats after administration by gastric tube. DNA damage was measured with unscheduled DNA synthesis (UDS) and DNA single strand scission as markers, while cell proliferation was measured with replicative DNA synthesis (RDS) and ornithine decarboxylase (ODC) as markers. MNU at doses of 30 and 60 mg/kg body wt and 80 min after administration dose-dependently induced UDS (49 and 79 (0 dose, 19) dpm/micrograms DNA) measured by liquid scintillation counting in the presence of hydroxyurea (an inhibitor of RDS). RDS (DNA synthesis in the absence of hydroxyurea; 239 dpm/micrograms DNA at 0 dose) did not increase at that time. MNU at doses of 10 and 60 mg/kg body wt and 2 h after administration dose-dependently induced DNA single strand scission of 8.2 and 43.5 (0 dose, 1.4) elution rate constant (x 10(-3)/ml). MNU at doses of 30 and 60 mg/kg body wt and 24 h after administration dose-dependently induced an increase in RDS (1362 and 2393 (0 dose, 682) dpm/micrograms DNA). MNU at doses of 60, 90 and 120 mg/kg body wt and 24 h after administration dose-dependently induced an increase in ODC activity (22.0, 29.4 and 38.4 (0 dose, 6.3) p mol CO2/30 min/mg protein). These results suggest that MNU has possible tumor initiating activity (UDS and DNA single stand scission) and tumor promoting activity (RDS and ODC) in rat Stomach Mucosa.
Susan J Hagen - One of the best experts on this subject based on the ideXlab platform.
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claudin 18 loss alters transcellular chloride flux but not tight junction ion selectivity in gastric epithelial cells
Cellular and molecular gastroenterology and hepatology, 2021Co-Authors: Tyler J Caron, Kathleen E Scott, Nishita Sinha, Sureshkumar Muthupalani, Mahnoor Baqai, Layhong Ang, Jerrold R Turner, James G Fox, Susan J HagenAbstract:Background & Aims Tight junctions form a barrier to the paracellular passage of luminal antigens. Although most tight junction proteins reside within the apical tight junction complex, claudin-18 localizes mainly to the basolateral membrane where its contribution to paracellular ion transport is undefined. Claudin-18 loss in mice results in gastric neoplasia development and tumorigenesis that may or may not be due to tight junction dysfunction. The aim here was to investigate paracellular permeability defects in Stomach Mucosa from claudin-18 knockout (Cldn18-KO) mice. Methods Stomach tissue from wild-type, heterozygous, or Cldn18-KO mice were stripped of the external muscle layer and mounted in Ussing chambers. Transepithelial resistance, dextran 4 kDa flux, and potential difference (PD) were calculated from the chambered tissues after identifying differences in tissue histopathology that were used to normalize these measurements. Marker expression for claudins and ion transporters were investigated by transcriptomic and immunostaining analysis. Results No paracellular permeability defects were evident in Stomach Mucosa from Cldn18-KO mice. RNAseq identified changes in 4 claudins from Cldn18–KO mice, particularly the up-regulation of claudin-2. Although claudin-2 localized to tight junctions in cells at the base of gastric glands, its presence did not contribute overall to Mucosal permeability. Stomach tissue from Cldn18–KO mice also had no PD versus a lumen-negative PD in tissues from wild-type mice. This difference resulted from changes in transcellular Cl– permeability with the down-regulation of Cl– loading and Cl– secreting anion transporters. Conclusions Our findings suggest that Cldn18-KO has no effect on tight junction permeability in the Stomach from adult mice but rather affects anion permeability. The phenotype in these mice may thus be secondary to transcellular anion transporter expression/function in the absence of claudin-18.
T Katsuyama - One of the best experts on this subject based on the ideXlab platform.
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cause and effect between concentration dependent tissue damage and temporary cell proliferation in rat Stomach Mucosa by nacl a Stomach tumor promoter
Carcinogenesis, 1996Co-Authors: Chie Furihata, H Ohta, T KatsuyamaAbstract:: This study was designed to test whether concentration or dose of NaCl was responsible for the initial tissue damage (after 1 min) and resulting temporary cell proliferation at 17 h in Stomach Mucosa of male F344 rats after gastric intubation of 0.65, 1.3, 2.6 and 3.7 M NaCl. Histological damage was studied by dual staining combining horseradish peroxidase-labeled Griffonia simplicifolia agglutinin-II staining (HRP-GSA-II) and periodic acid cold thionin-Schiff reaction (PATS). Cell proliferation was studied by measuring replicative DNA synthesis with liquid scintillation counting and by BrdU staining. NaCl at the same overall dose of 0.8 g/kg body weight induced different degrees of response depending on the concentration. For 4 ml of 0.65 M NaCl, there was no tissue damage after 1 min nor any increase in replicative DNA synthesis after 17 h in the pyloric Mucosa. Administration of 1.3 M NaCl (2 ml), 2.6 M NaCl (1 ml) and 3.7 M NaCl (0.7 ml) induced concentration-dependent damage of the surface mucous cell layer after 1 min and increased replicative DNA synthesis after 17 h (P<0.05). Concentration-dependent increase in replicative DNA synthesis at 17 h was also induced with the same volume (1 ml) of 1.3, 2.6, and 3.7 M NaCl, while a volume-dependent increase in replicative DNA synthesis at 17 h was induced with 0.4, 0.7 and 1 ml of 3.7 M NaCl. However, a greater increase in replicative DNA synthesis was always observed when using higher NaCl concentrations at the same dose. Liquid scintillation counting was well-correlated with BrdU staining. These results suggest that a high concentration of NaCl is responsible for the initial tissue damage and resulting temporary cell proliferation during Stomach tumor promotion.
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cytotoxicity of nacl a Stomach tumor promoter and prevention by rice extract in Stomach Mucosa of f344 rats
Cancer Detection and Prevention, 1996Co-Authors: Chie Furihata, S Ishida, H Ohta, T Tokuyama, T Katsuyama, Z I OgitaAbstract:Cytotoxicity of NaCl and its prevention by rice extract were studied in the pyloric Mucosa of male F344 rat Stomach after oral administration of rice extract and 2.6 M NaCl. Effect were observed histologically by hematoxylin and eosin staining and the bromodeoxyuridine method. Replicative DNA synthesis (RDS) was assayed by liquid scintillation counter with [3H]thymidine. NaCl (2.6 M) induced destruction of the surface mucous cells within 1 min. RDS and S-phase cells increased significantly (p < 0.01) and to a maximum at 17 h, and returned to control levels 48 h after exposure. Administration of aqueous rice extract 3 h before NaCl exposure reduced the morphological damage to the Mucosa and prevented the increase in RDS dose dependently by up to 65% (p < 0.01). These results showed that NaCl induced rapid Mucosal damage and cell proliferation in rat Stomach Mucosa and that rice extract prevented the damage and reduced the increase in RDS.
Delir Correa Gomes - One of the best experts on this subject based on the ideXlab platform.
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larvae of hysterothylacium sp nematoda anisakidae in the sole fish paralichthys isosceles jordan 1890 pisces teleostei from the littoral of the state of rio de janeiro brazil
Veterinary Parasitology, 2009Co-Authors: Nilza Nunes Felizardo, Rodrigo Caldas Menezes, Rogerio Tortelly, Marcelo Knoff, Roberto Magalhaes Pinto, Delir Correa GomesAbstract:Sixty specimens of Paralichthys isosceles captured in the southeastern Brazilian coast were investigated for helminths from October 2006 to March 2008. One thousand eight hundred and twenty larvae (third and fourth stages) of Hysterothylacium sp. were recovered from the abdominal cavity, free or inserted in the mesentery, intestine, Stomach, Stomach wall, liver, spleen, ovaries, and serosas of heart, kidneys, ovaries and abdominal musculature. Gross lesions appeared as nodules in the Stomach Mucosa and intestinal serosa. Histological examination of these nodules revealed sections of Hysterothylacium sp. larvae inserted in the abdominal musculature, in the subMucosa, muscular and serosa layers of the Stomach and intestine. Associated granulomas consisted of fibrous connective tissue, macrophages and lymphocytes that surrounded, besides the larvae, necrotic material and tunnels with acidophilic lining, sometimes devoid of inflammatory reaction. The pathological alterations as well as the occurrence of Hysterothylacium sp. are reported for the first time in this host. The parasitic indexes refer to a prevalence of 100%, mean intensity of 30.3, mean abundance of 32 and range of intensity variation from 1 to 596.
Norman E Sladek - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of human class 3 aldehyde dehydrogenase, and sensitization of tumor cells that express significant amounts of this enzyme to oxazaphosphorines, by chlorpropamide analogues☆
Biochemical pharmacology, 1998Co-Authors: Ganaganur K. Rekha, Lakshmaiah Sreerama, Varadahalli R. Devaraj, Melinda J. C. Lee, Herbert T. Nagasawa, Norman E SladekAbstract:Abstract In some cases, acquired as well as constitutive tumor cell resistance to a group of otherwise clinically useful antineoplastic agents collectively referred to as oxazaphosphorines, e.g. cyclophosphamide and mafosfamide, can be accounted for by relatively elevated cellular levels of an enzyme, viz. cytosolic class 3 aldehyde dehydrogenase (ALDH-3), that catalyzes their detoxification. Ergo, inhibitors of ALDH-3 could be of clinical value since their inclusion in the therapeutic protocl would be expected to sensitize such cell to these agents. Identified in the present investigation were two chlorpropamide analogues showing promise in that regard, viz. (acetyloxy)[(4-chlorophenyl)sulfonyl]carbamic acid 1,1-dimethylethyl ester (NPI-2) and 4-chloro-N-methoxy-N-[(propylamino) carbonyl]benzenesulfonamide (API-2). Each inhibited NAD-linked benzaldehyde oxidation catalyzed by ALDH-3s purified from human breast adenocarcinoma MCF-7/0/CAT cells ( ic 50 values we were 16 and 0.75 μM, respectively) and human normal Stomach Mucosa ( ic 50 values were 202 and 5 μM, respectively). The differential sensitivities of Stomach Mucosa ALDH-3 and breast tumor ALDH-3 to each of the two inhibitors can be viewed as further evidence that the latter is a subtle variant of the former. Human class 1 (ALDH-1) and class 2 (ALDH-2) aldehyde dehydrogenases were much less sensitive to NPI-2; ic 50 values were >300 μM in each case. API-2, however, did not exhibit a similar degree of specificity; ic 50 values for ALDH-1 and ALDH-2 were 7.5 and 0.08 μM, respectively. Each sensitized MCF-7/0/CAT cells to mafosfamide; the lc 90 value decreased from >2 mM to 175 and 200 μM, respectively. Thus, the therapeutic potential of combining NPI-2 or API-2 with oxazaphosphorines is established.
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identification of a methylcholanthrene induced aldehyde dehydrogenase in a human breast adenocarcinoma cell line exhibiting oxazaphosphorine specific acquired resistance
Cancer Research, 1994Co-Authors: Lakshmaiah Sreerama, Norman E SladekAbstract:The class-3 aldehyde dehydrogenase that is overexpressed (>100-fold) in human breast adenocarcinoma MCF-7/0 cells made resistant (>30-fold as judged by LC90s) to oxazaphosphorines, such as mafosfamide, by growing them in the presence of polycyclic aromatic hydrocarbons, e.g. , methylcholanthrene (3 µm for 5 days), was isolated and characterized. Its physical and catalytic properties were identical to those of the prototypical human Stomach Mucosa cytosolic class-3 aldehyde dehydrogenase, type-1 ALDH-3, except that it catalyzed, though not very rapidly, the oxidation of aldophosphamide, whereas the Stomach Mucosa enzyme essentially did not; hence, it was judged to be a slight variant of the prototypical enzyme. Carcinogens that are not ligands for the Ah receptor, barbiturates known to induce hepatic cytochrome P450s, steroid hormones, an antiestrogen, and oxazaphosphorines did not induce the enzyme or the largely oxazaphosphorine-specific acquired resistance. Whereas methylcholanthrene induced ( a ) resistance to mafosfamide and ( b ) class-3 aldehyde dehydrogenase activity, as well as glutathione S -transferase and DT-diaphorase activities, in the estrogen receptor-positive MCF-7/0 cells, it did not do so in two other human breast adenocarcinoma cell lines, MDA-MB-231 and SK-BR-3, each of which is estrogen receptor negative. Expression of the class-3 aldehyde dehydrogenase and the loss of sensitivity to mafosfamide by polycyclic aromatic hydrocarbon-treated MCF-7/0 cells were transient; each returned to essentially basal levels within 15 days when the polycyclic aromatic hydrocarbon was removed from the culture medium. Insensitivity to the oxazaphosphorines on the part of polycyclic aromatic hydrocarbon-treated MCF-7/0 cells was not observed when exposure to mafosfamide (30 min) was in the presence of benzaldehyde or octanal, each a relatively good substrate for cytosolic class-3 aldehyde dehydrogenases, whereas it was retained when exposure to mafosfamide was in the presence of acetaldehyde, a relatively poor substrate for these enzymes. These observations demonstrate that ligands for the Ah receptor can induce a transient, largely oxazaphosphorine-specific, acquired cellular resistance, and they are consistent with the notion that elevated levels of a cytosolic class-3 aldehyde dehydrogenase nearly identical to the prototypical type-1 class-3 aldehyde dehydrogenase expressed by human Stomach Mucosa account for the Ah receptor ligand-induced oxazaphosphorine-specific acquired resistance, most probably by catalyzing the detoxification of aldophosphamide.