The Experts below are selected from a list of 165 Experts worldwide ranked by ideXlab platform
Akihiko Nakaizumi - One of the best experts on this subject based on the ideXlab platform.
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inhibition by galanin of Experimental Carcinogenesis induced by azaserine in rat pancreas
International Journal of Cancer, 1998Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of galanin on pancreatic Carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 μg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic Carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas. Int. J. Cancer 75:396–399, 1998. © 1998 Wiley-Liss, Inc.
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inhibition by amiloride of Experimental Carcinogenesis induced by azaserine in rat pancreas
Cancer Letters, 1996Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of prolonged administration of the diuretic amiloride on pancreatic Carcinogenesis induced by azaserine and on the labeling index of carcinogen-induced pancreatic lesions were investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight azaserine and also 5 mg/kg body weight amiloride every other day until the end of the experiment at week 62. Carcinogen-induced pancreatic lesions were examined by histochemical techniques and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histologic analysis showed that prolonged administration of amiloride significantly reduced the number and size (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the subsequent development of pancreatic cancer. Amiloride also significantly decreased the labeling index of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. In contrast, amiloride has no significant influence on the number and size of ATPase-negative pancreatic lesions. These findings indicate that amiloride inhibits pancreatic Carcinogenesis, and that this effect may be related to the reduction of ATPase-positive lesions and to amiloride's inhibition of cell proliferation in neoplastic lesions of the pancreas.
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Chemoprevention by amiloride of Experimental Carcinogenesis in rat colon induced by azoxymethane
Carcinogenesis, 1995Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko NakaizumiAbstract:The effects of amiloride on the incidence and histology of colon tumors induced by azoxymethane, on the labeling index of the colon mucosa and on the activity of ornithine decarboxylase in the colon wall were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body wt azoxymethane and s.c. injections of 5 or 7.5 mg/kg body wt amiloride in depot form every other day for 35 weeks. Prolonged administration of amiloride at a dose of 7.5 mg/kg, but not 5 mg/kg, significantly reduced the incidence of colon tumors at week 35. However, administration of amiloride had little or no significant influence on the histological types of colon tumors and cancers. Administration of amiloride at 7.5 mg/kg significantly decreased the labeling index of the colon mucosa and ornithine decarboxylase activity in the colon wall during and after administration of azoxymethane. These findings suggest that amiloride inhibits development of colon tumors. A possible mechanism of inhibition of colon Carcinogenesis by amiloride is its suppression of proliferation of colon tumor cells.
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Inhibition by putrescine of Experimental Carcinogenesis in rat colon induced by azoxymethane.
International journal of cancer, 1991Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko Nakaizumi, Makoto Ichii, Haruo TaniguchiAbstract:The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.
Masaharu Tatsuta - One of the best experts on this subject based on the ideXlab platform.
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inhibition by galanin of Experimental Carcinogenesis induced by azaserine in rat pancreas
International Journal of Cancer, 1998Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of galanin on pancreatic Carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 μg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic Carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas. Int. J. Cancer 75:396–399, 1998. © 1998 Wiley-Liss, Inc.
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inhibition by amiloride of Experimental Carcinogenesis induced by azaserine in rat pancreas
Cancer Letters, 1996Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of prolonged administration of the diuretic amiloride on pancreatic Carcinogenesis induced by azaserine and on the labeling index of carcinogen-induced pancreatic lesions were investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight azaserine and also 5 mg/kg body weight amiloride every other day until the end of the experiment at week 62. Carcinogen-induced pancreatic lesions were examined by histochemical techniques and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histologic analysis showed that prolonged administration of amiloride significantly reduced the number and size (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the subsequent development of pancreatic cancer. Amiloride also significantly decreased the labeling index of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. In contrast, amiloride has no significant influence on the number and size of ATPase-negative pancreatic lesions. These findings indicate that amiloride inhibits pancreatic Carcinogenesis, and that this effect may be related to the reduction of ATPase-positive lesions and to amiloride's inhibition of cell proliferation in neoplastic lesions of the pancreas.
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Chemoprevention by amiloride of Experimental Carcinogenesis in rat colon induced by azoxymethane
Carcinogenesis, 1995Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko NakaizumiAbstract:The effects of amiloride on the incidence and histology of colon tumors induced by azoxymethane, on the labeling index of the colon mucosa and on the activity of ornithine decarboxylase in the colon wall were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body wt azoxymethane and s.c. injections of 5 or 7.5 mg/kg body wt amiloride in depot form every other day for 35 weeks. Prolonged administration of amiloride at a dose of 7.5 mg/kg, but not 5 mg/kg, significantly reduced the incidence of colon tumors at week 35. However, administration of amiloride had little or no significant influence on the histological types of colon tumors and cancers. Administration of amiloride at 7.5 mg/kg significantly decreased the labeling index of the colon mucosa and ornithine decarboxylase activity in the colon wall during and after administration of azoxymethane. These findings suggest that amiloride inhibits development of colon tumors. A possible mechanism of inhibition of colon Carcinogenesis by amiloride is its suppression of proliferation of colon tumor cells.
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Enhancement by thyroxine of Experimental Carcinogenesis induced in rat colon by azoxymethane.
International journal of cancer, 1992Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Shigeru Okuda, Haruo TaniguchiAbstract:The effect of thyroxine (T4) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the labeling index of colon mucosa were investigated in Wistar rats. Rats were given AOM by injection once a week for 10 weeks, together with T4 in depot form until the end of the experiment. Administration of T4 resulted in a significant increase in the incidence of colon tumors in week 35. However, it did not influence the histological appearance of the colon tumors or the histological types and depths of involvement of colon adenocarcinomas. Furthermore, it caused a significant increase in the labeling index of the colon during, but not after, AOM treatment. Our findings indicate that T4 enhances the development of colon tumors, which may be related to its effect in increasing proliferation of epithelial cells in the colon mucosa during administration of the carcinogen.
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Inhibition by putrescine of Experimental Carcinogenesis in rat colon induced by azoxymethane.
International journal of cancer, 1991Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko Nakaizumi, Makoto Ichii, Haruo TaniguchiAbstract:The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.
Hiroyasu Iishi - One of the best experts on this subject based on the ideXlab platform.
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inhibition by galanin of Experimental Carcinogenesis induced by azaserine in rat pancreas
International Journal of Cancer, 1998Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of galanin on pancreatic Carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 μg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic Carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas. Int. J. Cancer 75:396–399, 1998. © 1998 Wiley-Liss, Inc.
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inhibition by amiloride of Experimental Carcinogenesis induced by azaserine in rat pancreas
Cancer Letters, 1996Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of prolonged administration of the diuretic amiloride on pancreatic Carcinogenesis induced by azaserine and on the labeling index of carcinogen-induced pancreatic lesions were investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight azaserine and also 5 mg/kg body weight amiloride every other day until the end of the experiment at week 62. Carcinogen-induced pancreatic lesions were examined by histochemical techniques and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histologic analysis showed that prolonged administration of amiloride significantly reduced the number and size (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the subsequent development of pancreatic cancer. Amiloride also significantly decreased the labeling index of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. In contrast, amiloride has no significant influence on the number and size of ATPase-negative pancreatic lesions. These findings indicate that amiloride inhibits pancreatic Carcinogenesis, and that this effect may be related to the reduction of ATPase-positive lesions and to amiloride's inhibition of cell proliferation in neoplastic lesions of the pancreas.
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Chemoprevention by amiloride of Experimental Carcinogenesis in rat colon induced by azoxymethane
Carcinogenesis, 1995Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko NakaizumiAbstract:The effects of amiloride on the incidence and histology of colon tumors induced by azoxymethane, on the labeling index of the colon mucosa and on the activity of ornithine decarboxylase in the colon wall were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body wt azoxymethane and s.c. injections of 5 or 7.5 mg/kg body wt amiloride in depot form every other day for 35 weeks. Prolonged administration of amiloride at a dose of 7.5 mg/kg, but not 5 mg/kg, significantly reduced the incidence of colon tumors at week 35. However, administration of amiloride had little or no significant influence on the histological types of colon tumors and cancers. Administration of amiloride at 7.5 mg/kg significantly decreased the labeling index of the colon mucosa and ornithine decarboxylase activity in the colon wall during and after administration of azoxymethane. These findings suggest that amiloride inhibits development of colon tumors. A possible mechanism of inhibition of colon Carcinogenesis by amiloride is its suppression of proliferation of colon tumor cells.
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Enhancement by thyroxine of Experimental Carcinogenesis induced in rat colon by azoxymethane.
International journal of cancer, 1992Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Shigeru Okuda, Haruo TaniguchiAbstract:The effect of thyroxine (T4) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the labeling index of colon mucosa were investigated in Wistar rats. Rats were given AOM by injection once a week for 10 weeks, together with T4 in depot form until the end of the experiment. Administration of T4 resulted in a significant increase in the incidence of colon tumors in week 35. However, it did not influence the histological appearance of the colon tumors or the histological types and depths of involvement of colon adenocarcinomas. Furthermore, it caused a significant increase in the labeling index of the colon during, but not after, AOM treatment. Our findings indicate that T4 enhances the development of colon tumors, which may be related to its effect in increasing proliferation of epithelial cells in the colon mucosa during administration of the carcinogen.
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Inhibition by putrescine of Experimental Carcinogenesis in rat colon induced by azoxymethane.
International journal of cancer, 1991Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko Nakaizumi, Makoto Ichii, Haruo TaniguchiAbstract:The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.
Miyako Baba - One of the best experts on this subject based on the ideXlab platform.
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inhibition by galanin of Experimental Carcinogenesis induced by azaserine in rat pancreas
International Journal of Cancer, 1998Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of galanin on pancreatic Carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 μg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine-induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase-positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine-labeling index of azaserine-induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic Carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas. Int. J. Cancer 75:396–399, 1998. © 1998 Wiley-Liss, Inc.
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inhibition by amiloride of Experimental Carcinogenesis induced by azaserine in rat pancreas
Cancer Letters, 1996Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Kazushige Iseki, Hiroyuki Uehara, Hiroyuki Yano, Akihiko NakaizumiAbstract:The effects of prolonged administration of the diuretic amiloride on pancreatic Carcinogenesis induced by azaserine and on the labeling index of carcinogen-induced pancreatic lesions were investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight azaserine and also 5 mg/kg body weight amiloride every other day until the end of the experiment at week 62. Carcinogen-induced pancreatic lesions were examined by histochemical techniques and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histologic analysis showed that prolonged administration of amiloride significantly reduced the number and size (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the subsequent development of pancreatic cancer. Amiloride also significantly decreased the labeling index of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. In contrast, amiloride has no significant influence on the number and size of ATPase-negative pancreatic lesions. These findings indicate that amiloride inhibits pancreatic Carcinogenesis, and that this effect may be related to the reduction of ATPase-positive lesions and to amiloride's inhibition of cell proliferation in neoplastic lesions of the pancreas.
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Chemoprevention by amiloride of Experimental Carcinogenesis in rat colon induced by azoxymethane
Carcinogenesis, 1995Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko NakaizumiAbstract:The effects of amiloride on the incidence and histology of colon tumors induced by azoxymethane, on the labeling index of the colon mucosa and on the activity of ornithine decarboxylase in the colon wall were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body wt azoxymethane and s.c. injections of 5 or 7.5 mg/kg body wt amiloride in depot form every other day for 35 weeks. Prolonged administration of amiloride at a dose of 7.5 mg/kg, but not 5 mg/kg, significantly reduced the incidence of colon tumors at week 35. However, administration of amiloride had little or no significant influence on the histological types of colon tumors and cancers. Administration of amiloride at 7.5 mg/kg significantly decreased the labeling index of the colon mucosa and ornithine decarboxylase activity in the colon wall during and after administration of azoxymethane. These findings suggest that amiloride inhibits development of colon tumors. A possible mechanism of inhibition of colon Carcinogenesis by amiloride is its suppression of proliferation of colon tumor cells.
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Enhancement by thyroxine of Experimental Carcinogenesis induced in rat colon by azoxymethane.
International journal of cancer, 1992Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Shigeru Okuda, Haruo TaniguchiAbstract:The effect of thyroxine (T4) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the labeling index of colon mucosa were investigated in Wistar rats. Rats were given AOM by injection once a week for 10 weeks, together with T4 in depot form until the end of the experiment. Administration of T4 resulted in a significant increase in the incidence of colon tumors in week 35. However, it did not influence the histological appearance of the colon tumors or the histological types and depths of involvement of colon adenocarcinomas. Furthermore, it caused a significant increase in the labeling index of the colon during, but not after, AOM treatment. Our findings indicate that T4 enhances the development of colon tumors, which may be related to its effect in increasing proliferation of epithelial cells in the colon mucosa during administration of the carcinogen.
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Inhibition by putrescine of Experimental Carcinogenesis in rat colon induced by azoxymethane.
International journal of cancer, 1991Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko Nakaizumi, Makoto Ichii, Haruo TaniguchiAbstract:The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.
Haruo Taniguchi - One of the best experts on this subject based on the ideXlab platform.
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Enhancement by thyroxine of Experimental Carcinogenesis induced in rat colon by azoxymethane.
International journal of cancer, 1992Co-Authors: Hiroyasu Iishi, Masaharu Tatsuta, Miyako Baba, Shigeru Okuda, Haruo TaniguchiAbstract:The effect of thyroxine (T4) on the incidence, number and histology of colon tumors induced by azoxymethane (AOM), and on the labeling index of colon mucosa were investigated in Wistar rats. Rats were given AOM by injection once a week for 10 weeks, together with T4 in depot form until the end of the experiment. Administration of T4 resulted in a significant increase in the incidence of colon tumors in week 35. However, it did not influence the histological appearance of the colon tumors or the histological types and depths of involvement of colon adenocarcinomas. Furthermore, it caused a significant increase in the labeling index of the colon during, but not after, AOM treatment. Our findings indicate that T4 enhances the development of colon tumors, which may be related to its effect in increasing proliferation of epithelial cells in the colon mucosa during administration of the carcinogen.
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Inhibition by putrescine of Experimental Carcinogenesis in rat colon induced by azoxymethane.
International journal of cancer, 1991Co-Authors: Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Uehara, Akihiko Nakaizumi, Makoto Ichii, Haruo TaniguchiAbstract:The effects of putrescine on the incidence and number of colon tumors induced by azoxymethane, and on the labelling index and the activity of ornithine decarboxylase (ODC) in the colon mucosa were investigated in Wistar rats. Rats received 10 weekly injections of 7.4 mg/kg body weight of azoxymethane and i.p. injections of 300 mumol/kg body weight of putrescine every 2 days until the end of the experiment at week 40. This prolonged treatment with putrescine significantly reduced the incidence and number of colon tumors. Administration of putrescine also significantly decreased the labelling index and the ODC activity in the colon mucosa during, but not after, treatment with the carcinogen. These last effects may be related to the action of putrescine in inhibiting the development of colonic tumors.
