The Experts below are selected from a list of 633 Experts worldwide ranked by ideXlab platform
Takuji Tanaka - One of the best experts on this subject based on the ideXlab platform.
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no involvement of ki ras or p53 gene mutations in colitis associated rat colon tumors induced by 1 hydroxyanthraquinone and Methylazoxymethanol acetate
Molecular Carcinogenesis, 1995Co-Authors: Masumi Suzui, Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki Mori, T Ushijima, Yoshinobu Hirose, Hiroki Makita, Tshihiko Kawamori, Minako NagaoAbstract:1-Hydroxyanthraquinone (1-HA), which is present in some herbs, and Methylazoxymethanol (MAM) acetate, a metabolite of azoxymethane, show synergistic carcinogenicity in rat colon, and 1-HA induces ulcerative changes with simultaneous severe inflammation of the entire colon. In this study, mutations in Ki-ras (exons 1 and 2) and p53 (exons 4–7) were studied by polymerase chain reaction (PCR)–single-strand conformation polymorphism (SSCP) analysis. Of 18 adenomas and 38 adenocarcinomas induced in male F344 rats (52 tumors induced by 1-HA plus MAM acetate, three by 1-HA alone, and one by MAM acetate alone), no mutations in Ki-ras of p53 were detected under two conditions of PCR-SSCP analysis. Because human colon carcinomas from patients with ulcerative colitis have a very low incidence of Ki-ras mutation, this experimental system would be a good animal model of human colon carcinomas with ulcerative colitis and of human colon carcinomas without Ki-ras of p53 mutations. © 1995 Wiley-Liss Inc.
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inhibitory effects of magnesium hydroxide on c myc expression and cell proliferation induced by Methylazoxymethanol acetate in rat colon
Cancer Letters, 1993Co-Authors: Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki MoriAbstract:Abstract The effects of magnesium hydroxide were examined on Methylazoxymethanol (MAM) acetate-induced c- myc expression and cell proliferation of colonic mucosal epithelium in rats. Rats were divided into four groups and treated as follows: MAM acetate alone (25 mg/kg i.p.injection, five times, once a week for 5 weeks), MAM acetate and feeding of 0.2% magnesium hydroxide in diet, magnesium hydroxide alone and non-treatment. At 4, 8 and 16 weeks after the start of experiment, 10 rats in each group were sacrificed. Magnesium hydroxide inhibited the MAM-induced expression of c- myc proto-oncogene, and also suppressed the increased bromodeoxyuridine (BrdU) and proliferating cell nuclear antigen (PCNA) labelling indexes induced by MAM acetate in colon mucosa in initiation and post-initiation phase. These results suggest that the anti-carcinogenic effect of magnesium hydroxide on rat colon carcinogenesis induced by MAM acetate may be related to the inhibition of the carcinogen-induced expression of c- myc protooncogene and cell proliferation.
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synergistic effect of radiation on colon carcinogenesis induced by Methylazoxymethanol acetate in aci n rats
Japanese Journal of Cancer Research, 1993Co-Authors: Takuji Tanaka, Shigeyuki Sugie, Yukio Morishita, Toshihiko Kawamori, Masumi Suzui, Toshihiro Kojima, Hideki MoriAbstract:The effect on colon and liver carcinogenicity in rats of a single X-irradiation exposure given either before or after Methylazoxymethanol (MAM) acetate was studied in ACI/N rats of both sexes. A single dose of X-irradiation (3 Gy) was administered either 3 months before or after three weekly s.c. injections of MAM acetate (25 mg/kg body weight). At 365 days after the start, the incidence and multiplicity of MAM acetate-induced intestinal tumors were enhanced by X-irradiation either prior to or after the MAM acetate treatment. In addition, X-irradiation before MAM acetate increased the incidence of hepatocellular foci in either sex. In females, X-irradiation either before or after MAM acetate exposure decreased intestinal tumorigenesis. These findings suggest an apparent synergism of these agents in intestinal carcinogenesis of male rats.
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effect of magnesium hydroxide on Methylazoxymethanol acetate induced epithelial proliferation in the large bowels of rats
Cancer Letters, 1992Co-Authors: Hideki Mori, Naoki Yoshimi, Shigeyuki Sugie, Yukio Morishita, Yoshio Mori, Takuji TanakaAbstract:The effect of magnesium hydroxide on the epithelial proliferation of the large bowel was examined using rats given Methylazoxymethanol (MAM) acetate. Dietary administration of magnesium hydroxide at 250, 500, 1000 or 2000 ppm. for 1, 3 or 5 weeks did not influence the cell cycle of the cryptal cells of the large bowel. However, the exposure to magnesium hydroxide under these conditions lowered the bromodeoxyuridine labeling index of the cells of the large bowel of the rats which had been initiated by MAM acetate (25 mg/kg, 3 times). The decrease in labeling index was more apparent in the proximal segment than in the distal segment. Such an inhibitory effect on the DNA synthesis of the epithelial cells by magnesium hydroxide may be related to the suppressive action of the trace element on the carcinogen-induced large bowel carcinogenesis.
Hideki Mori - One of the best experts on this subject based on the ideXlab platform.
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no involvement of ki ras or p53 gene mutations in colitis associated rat colon tumors induced by 1 hydroxyanthraquinone and Methylazoxymethanol acetate
Molecular Carcinogenesis, 1995Co-Authors: Masumi Suzui, Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki Mori, T Ushijima, Yoshinobu Hirose, Hiroki Makita, Tshihiko Kawamori, Minako NagaoAbstract:1-Hydroxyanthraquinone (1-HA), which is present in some herbs, and Methylazoxymethanol (MAM) acetate, a metabolite of azoxymethane, show synergistic carcinogenicity in rat colon, and 1-HA induces ulcerative changes with simultaneous severe inflammation of the entire colon. In this study, mutations in Ki-ras (exons 1 and 2) and p53 (exons 4–7) were studied by polymerase chain reaction (PCR)–single-strand conformation polymorphism (SSCP) analysis. Of 18 adenomas and 38 adenocarcinomas induced in male F344 rats (52 tumors induced by 1-HA plus MAM acetate, three by 1-HA alone, and one by MAM acetate alone), no mutations in Ki-ras of p53 were detected under two conditions of PCR-SSCP analysis. Because human colon carcinomas from patients with ulcerative colitis have a very low incidence of Ki-ras mutation, this experimental system would be a good animal model of human colon carcinomas with ulcerative colitis and of human colon carcinomas without Ki-ras of p53 mutations. © 1995 Wiley-Liss Inc.
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inhibitory effects of magnesium hydroxide on c myc expression and cell proliferation induced by Methylazoxymethanol acetate in rat colon
Cancer Letters, 1993Co-Authors: Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki MoriAbstract:Abstract The effects of magnesium hydroxide were examined on Methylazoxymethanol (MAM) acetate-induced c- myc expression and cell proliferation of colonic mucosal epithelium in rats. Rats were divided into four groups and treated as follows: MAM acetate alone (25 mg/kg i.p.injection, five times, once a week for 5 weeks), MAM acetate and feeding of 0.2% magnesium hydroxide in diet, magnesium hydroxide alone and non-treatment. At 4, 8 and 16 weeks after the start of experiment, 10 rats in each group were sacrificed. Magnesium hydroxide inhibited the MAM-induced expression of c- myc proto-oncogene, and also suppressed the increased bromodeoxyuridine (BrdU) and proliferating cell nuclear antigen (PCNA) labelling indexes induced by MAM acetate in colon mucosa in initiation and post-initiation phase. These results suggest that the anti-carcinogenic effect of magnesium hydroxide on rat colon carcinogenesis induced by MAM acetate may be related to the inhibition of the carcinogen-induced expression of c- myc protooncogene and cell proliferation.
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synergistic effect of radiation on colon carcinogenesis induced by Methylazoxymethanol acetate in aci n rats
Japanese Journal of Cancer Research, 1993Co-Authors: Takuji Tanaka, Shigeyuki Sugie, Yukio Morishita, Toshihiko Kawamori, Masumi Suzui, Toshihiro Kojima, Hideki MoriAbstract:The effect on colon and liver carcinogenicity in rats of a single X-irradiation exposure given either before or after Methylazoxymethanol (MAM) acetate was studied in ACI/N rats of both sexes. A single dose of X-irradiation (3 Gy) was administered either 3 months before or after three weekly s.c. injections of MAM acetate (25 mg/kg body weight). At 365 days after the start, the incidence and multiplicity of MAM acetate-induced intestinal tumors were enhanced by X-irradiation either prior to or after the MAM acetate treatment. In addition, X-irradiation before MAM acetate increased the incidence of hepatocellular foci in either sex. In females, X-irradiation either before or after MAM acetate exposure decreased intestinal tumorigenesis. These findings suggest an apparent synergism of these agents in intestinal carcinogenesis of male rats.
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effect of magnesium hydroxide on Methylazoxymethanol acetate induced epithelial proliferation in the large bowels of rats
Cancer Letters, 1992Co-Authors: Hideki Mori, Naoki Yoshimi, Shigeyuki Sugie, Yukio Morishita, Yoshio Mori, Takuji TanakaAbstract:The effect of magnesium hydroxide on the epithelial proliferation of the large bowel was examined using rats given Methylazoxymethanol (MAM) acetate. Dietary administration of magnesium hydroxide at 250, 500, 1000 or 2000 ppm. for 1, 3 or 5 weeks did not influence the cell cycle of the cryptal cells of the large bowel. However, the exposure to magnesium hydroxide under these conditions lowered the bromodeoxyuridine labeling index of the cells of the large bowel of the rats which had been initiated by MAM acetate (25 mg/kg, 3 times). The decrease in labeling index was more apparent in the proximal segment than in the distal segment. Such an inhibitory effect on the DNA synthesis of the epithelial cells by magnesium hydroxide may be related to the suppressive action of the trace element on the carcinogen-induced large bowel carcinogenesis.
Naoki Yoshimi - One of the best experts on this subject based on the ideXlab platform.
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no involvement of ki ras or p53 gene mutations in colitis associated rat colon tumors induced by 1 hydroxyanthraquinone and Methylazoxymethanol acetate
Molecular Carcinogenesis, 1995Co-Authors: Masumi Suzui, Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki Mori, T Ushijima, Yoshinobu Hirose, Hiroki Makita, Tshihiko Kawamori, Minako NagaoAbstract:1-Hydroxyanthraquinone (1-HA), which is present in some herbs, and Methylazoxymethanol (MAM) acetate, a metabolite of azoxymethane, show synergistic carcinogenicity in rat colon, and 1-HA induces ulcerative changes with simultaneous severe inflammation of the entire colon. In this study, mutations in Ki-ras (exons 1 and 2) and p53 (exons 4–7) were studied by polymerase chain reaction (PCR)–single-strand conformation polymorphism (SSCP) analysis. Of 18 adenomas and 38 adenocarcinomas induced in male F344 rats (52 tumors induced by 1-HA plus MAM acetate, three by 1-HA alone, and one by MAM acetate alone), no mutations in Ki-ras of p53 were detected under two conditions of PCR-SSCP analysis. Because human colon carcinomas from patients with ulcerative colitis have a very low incidence of Ki-ras mutation, this experimental system would be a good animal model of human colon carcinomas with ulcerative colitis and of human colon carcinomas without Ki-ras of p53 mutations. © 1995 Wiley-Liss Inc.
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inhibitory effects of magnesium hydroxide on c myc expression and cell proliferation induced by Methylazoxymethanol acetate in rat colon
Cancer Letters, 1993Co-Authors: Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki MoriAbstract:Abstract The effects of magnesium hydroxide were examined on Methylazoxymethanol (MAM) acetate-induced c- myc expression and cell proliferation of colonic mucosal epithelium in rats. Rats were divided into four groups and treated as follows: MAM acetate alone (25 mg/kg i.p.injection, five times, once a week for 5 weeks), MAM acetate and feeding of 0.2% magnesium hydroxide in diet, magnesium hydroxide alone and non-treatment. At 4, 8 and 16 weeks after the start of experiment, 10 rats in each group were sacrificed. Magnesium hydroxide inhibited the MAM-induced expression of c- myc proto-oncogene, and also suppressed the increased bromodeoxyuridine (BrdU) and proliferating cell nuclear antigen (PCNA) labelling indexes induced by MAM acetate in colon mucosa in initiation and post-initiation phase. These results suggest that the anti-carcinogenic effect of magnesium hydroxide on rat colon carcinogenesis induced by MAM acetate may be related to the inhibition of the carcinogen-induced expression of c- myc protooncogene and cell proliferation.
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effect of magnesium hydroxide on Methylazoxymethanol acetate induced epithelial proliferation in the large bowels of rats
Cancer Letters, 1992Co-Authors: Hideki Mori, Naoki Yoshimi, Shigeyuki Sugie, Yukio Morishita, Yoshio Mori, Takuji TanakaAbstract:The effect of magnesium hydroxide on the epithelial proliferation of the large bowel was examined using rats given Methylazoxymethanol (MAM) acetate. Dietary administration of magnesium hydroxide at 250, 500, 1000 or 2000 ppm. for 1, 3 or 5 weeks did not influence the cell cycle of the cryptal cells of the large bowel. However, the exposure to magnesium hydroxide under these conditions lowered the bromodeoxyuridine labeling index of the cells of the large bowel of the rats which had been initiated by MAM acetate (25 mg/kg, 3 times). The decrease in labeling index was more apparent in the proximal segment than in the distal segment. Such an inhibitory effect on the DNA synthesis of the epithelial cells by magnesium hydroxide may be related to the suppressive action of the trace element on the carcinogen-induced large bowel carcinogenesis.
Glen E Kisby - One of the best experts on this subject based on the ideXlab platform.
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Cycad β-N-methylamino-L-alanine (BMAA), Methylazoxymethanol, genotoxicity, and neurodegeneration
Toxicon, 2018Co-Authors: Peter S. Spencer, Valerie S. Palmer, Glen E KisbyAbstract:Abstract Cycad-associated neurodegenerative disease is more strongly correlated with the gymnosperm's major neurotoxin cycasin (Methylazoxymethanol glucoside) than with the minor neurotoxin β-N-methylamino-L-alanine (L-BMAA).
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Is Neurodegenerative Disease a Long-Latency Response to Early-Life Genotoxin Exposure?
International Journal of Environmental Research and Public Health, 2011Co-Authors: Glen E Kisby, Peter S. SpencerAbstract:Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer’s disease. Cycads contain neurotoxic and genotoxic principles, notably cycasin and Methylazoxymethanol, the latter sharing chemical relations with nitrosamines, which are derived from nitrates and nitrites in preserved meats and fertilizers, and also used in the rubber and leather industries. This review includes new data that influence understanding of the neurobiological actions of cycad and related genotoxins and the putative mechanisms by which they might trigger neurodegenerative disease.
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www.mdpi.com/journal/ijerph Review Is Neurodegenerative Disease a Long-Latency Response to
2011Co-Authors: Early-life Genotoxin Exposure, Glen E Kisby, Peter S. SpencerAbstract:Abstract: Western Pacific amyotrophic lateral sclerosis and parkinsonism-dementia complex, a disappearing neurodegenerative disease linked to use of the neurotoxic cycad plant for food and/or medicine, is intensively studied because the neuropathology (tauopathy) is similar to that of Alzheimer’s disease. Cycads contain neurotoxic and genotoxic principles, notably cycasin and Methylazoxymethanol, the latter sharing chemical relations with nitrosamines, which are derived from nitrates and nitrites in preserved meats and fertilizers, and also used in the rubber and leather industries. This review includes new data that influence understanding of the neurobiological actions of cycad and related genotoxins and the putative mechanisms by which they might trigger neurodegenerative disease
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transport of cycasin by the intestinal na glucose cotransporter
Biochimica et Biophysica Acta, 1994Co-Authors: Bruce A Hirayama, Ernest M Wright, Akihiro Hazama, Glen E KisbyAbstract:Abstract The medicinal and food use of seed from the cycad plant ( Cycas spp. ), which contains the neurotoxin cycasin, is a proposed etiological factor for amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC), a prototypical neurodegenerative disease found in the western Pacific. Cycasin, the β- d -glucoside of Methylazoxymethanol might enter neurons and other cells via a glucose transporter. Since the intestinal brush-border Na + /glucose cotransporter plays a major role in the absorption of monosaccharides, the following studies were conducted to determine if cycasin, the β- d -glucoside of Methylazoxymethanol, is a substrate for the transporter. We measured the ability of cycasin to (i) inhibit Na + /glucose uptake into rabbit intestinal brush-border membrane vesicles, and (ii) to generate current by the cloned Na + /glucose cotransporter (SGLT1) expressed in Xenopus laevis oocytes. The results show that cycasin inhibits Na + -dependent sugar transport in the vesicles, and cycasin generates phlorizin-sensitive currents in oocytes. We conclude that cycasin is a substrate for the intestinal brush-border Na + /glucose cotransporter, albeit with a lower affinity than d -glucose. This suggests that cycasin may be absorbed from the gut lumen by the cotransporter, and as a result either cycasin or the aglycone is presented to the blood-brain barrier for uptake into the brain.
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content of the neurotoxins cycasin Methylazoxymethanol β d glucoside and bnlaa β n methylamino l alanine in cycad flour prepared by guam chamorros
Neurology, 1992Co-Authors: Glen E Kisby, Mike Ellison, Peter S. SpencerAbstract:Exposure to cycad seed kernel is an etiologic factor for the western Pacific amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia complex (PDC). Traditionally processed cycad flours ( n = 17) obtained from Chamorro residents of Guam and the adjacent island of Rota at risk for neurodegenerative disease were extracted and analyzed by high-performance liquid chromatography for content of β- N -methylamino-L-alanine (BMAA) and Methylazoxymethanol β-D-glucoside (cycasin). Cycasin (detection limit: picomole) was present in concentrations of 0.004 to 75.93 μg/g (mean, 12.45 ± 5.0 μg/g), and levels of BMAA (detection limit: subpicomole) ranged from 0.00 to 18.39 μg/g (mean, 5.44 ± 1.56 μg/g). On average, cycasin content was approximately 10 times higher than that of BMAA. The largest concentrations of cycasin were found in samples from villages with a high reported prevalence of ALS/PDC. Ingestion of cycad-derived food would result in estimated human exposure to milligram amounts of cycasin per day. The cytotoxic properties of cycasin merit consideration in relation to the etiology of western Pacific ALS/PDC.
Aijin Wang - One of the best experts on this subject based on the ideXlab platform.
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no involvement of ki ras or p53 gene mutations in colitis associated rat colon tumors induced by 1 hydroxyanthraquinone and Methylazoxymethanol acetate
Molecular Carcinogenesis, 1995Co-Authors: Masumi Suzui, Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki Mori, T Ushijima, Yoshinobu Hirose, Hiroki Makita, Tshihiko Kawamori, Minako NagaoAbstract:1-Hydroxyanthraquinone (1-HA), which is present in some herbs, and Methylazoxymethanol (MAM) acetate, a metabolite of azoxymethane, show synergistic carcinogenicity in rat colon, and 1-HA induces ulcerative changes with simultaneous severe inflammation of the entire colon. In this study, mutations in Ki-ras (exons 1 and 2) and p53 (exons 4–7) were studied by polymerase chain reaction (PCR)–single-strand conformation polymorphism (SSCP) analysis. Of 18 adenomas and 38 adenocarcinomas induced in male F344 rats (52 tumors induced by 1-HA plus MAM acetate, three by 1-HA alone, and one by MAM acetate alone), no mutations in Ki-ras of p53 were detected under two conditions of PCR-SSCP analysis. Because human colon carcinomas from patients with ulcerative colitis have a very low incidence of Ki-ras mutation, this experimental system would be a good animal model of human colon carcinomas with ulcerative colitis and of human colon carcinomas without Ki-ras of p53 mutations. © 1995 Wiley-Liss Inc.
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inhibitory effects of magnesium hydroxide on c myc expression and cell proliferation induced by Methylazoxymethanol acetate in rat colon
Cancer Letters, 1993Co-Authors: Aijin Wang, Naoki Yoshimi, Takuji Tanaka, Hideki MoriAbstract:Abstract The effects of magnesium hydroxide were examined on Methylazoxymethanol (MAM) acetate-induced c- myc expression and cell proliferation of colonic mucosal epithelium in rats. Rats were divided into four groups and treated as follows: MAM acetate alone (25 mg/kg i.p.injection, five times, once a week for 5 weeks), MAM acetate and feeding of 0.2% magnesium hydroxide in diet, magnesium hydroxide alone and non-treatment. At 4, 8 and 16 weeks after the start of experiment, 10 rats in each group were sacrificed. Magnesium hydroxide inhibited the MAM-induced expression of c- myc proto-oncogene, and also suppressed the increased bromodeoxyuridine (BrdU) and proliferating cell nuclear antigen (PCNA) labelling indexes induced by MAM acetate in colon mucosa in initiation and post-initiation phase. These results suggest that the anti-carcinogenic effect of magnesium hydroxide on rat colon carcinogenesis induced by MAM acetate may be related to the inhibition of the carcinogen-induced expression of c- myc protooncogene and cell proliferation.