Expressão de superóxido dismutase em focos de criptas aberrantes induzidas pelo azoximetano em ratos Wistar e inibição pelo inositol hexafosfato
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Date
2006
Authors
Amaral, Eva Glória Abrão Siufi do [UNIFESP]
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Fagundes, Djalma José [UNIFESP]
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Dissertação de mestrado
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Abstract
Objetivo: desenvolver um modelo experimental de carcinogênese em colo de rato
induzido pelo azoximetano e estabelecer um padrão de ação protetora do hexafosfato de
inositol, pela expressão da enzima superóxido dismutase em foco de cripta aberrante.
Métodos: 48 ratos Wistar, adultos, machos, foram mantidos em observação por seis
semanas. GI (n=12) recebeu injeções de solução salina subcutânea durante a terceira e
quarta semanas, enquanto que o GII (n=12), no mesmo período, recebeu azoximetano
(AOM) na dose 20mg.Kg-1 subcutânea. O GIII (n=12) recebeu inositol hexafosfato 1%
(IP6) na água de beber durante as seis semanas, enquanto que o GIV, além do IP6 na
água de beber, recebeu também as injeções subcutâneas de AOM durante a terceira e
quarta semanas. Ao término da sexta semana os animais sofreram a eutanásia e foram
coletados segmentos de intestino grosso à cerca de um centímetro da transição íleocólica.
Fragmentos foram preparados e submetidos à coloração imunoistoquímica para
de anticorpo primário anti-SOD1 (superóxido dismutase1) e anticorpo secundário antirato,
revelador de cor DAB (diamino-benzidina) com obtenção de expressão SOD1 na
coloração marrom. A porcentagem da expressão de SOD em FCA (foco de cripta
aberrante) foi quantificada por meio de processamento de imagem assistida por
computador (ImageLab). Os resultados foram submetidos aos testes de análise de
variância (ANOVA) e estabelecido o nível de 5% (p≤0,05) para rejeição da hipótese de
nulidade. Resultados: a porcentagem média da expressão da SOD no GI (16,0 ± 3,7)
foi semelhante ao GIII (16,9 ± 3,1) mostrando que a solução salina (controle) e o IP6
não provocaram alterações em FCA; o grupo II (26,7 ± 3,5) mostrou uma significante
porcentagem de expressão da SOD em FCA, demonstrando sua capacidade de provocar
lesões pré-malignas em cólon de roedores; por outro lado este estímulo de indução
carcinogênica foi protegido pela administração de IP6 representada pelos resultados do
GIV (20,9 ± 3,3). Conclusões: O estímulo carcinogênico do AOM proporcionou um
modelo de carcinogênese em colo de rato Wistar que foi protegido pela administração
do IP6, sendo que a expressão da SOD em FCA mostrou-se um parâmetro
imunoistoquímico confiável para representar as lesões pré-neoplásicas em FCA.
Objective: to develop an experimental model of carcinogenesis in Wistar rats induced by the azoximethane and to establish a pattern of protecting action of the inositol hexafosfate, for the expression of the enzyme superoxide dismutase in foci of aberrant crypts. Methods: 48 Wistar male rats, adults, were maintained in observation by six weeks. GI (n=12) received injections of subcutaneous saline solution during the third and fourth weeks, while GII (n=12), in the same period, received 20mg.Kg-1 of subcutaneous azoximetano (AOM). GIII (n=12) received inositol hexafosfato 1% (IP6) in the drinking water during the six weeks, while GIV, besides IP6 in the drinking water, also received the subcutaneous injections of AOM during the third and fourth weeks. At the end of the sixth week large intestine segments were collected to the about a centimeter of the ileo-colic transition. Fragments were prepared and submitted to the imunohistochemical process to antibody primary anti-SOD1 (superoxide dismutase1) and antibody secondary anti-rat, color discloser DAB (diamino-benzidina) with expression obtaining SOD1 in the brown coloration. The percentage of the expression of SOD in FCA (focus of aberrant crypt) was quantified through image processing attended by computer (ImageLab). The results were submitted to the tests of variance analysis (ANOVA) and established the level of 5% (p≤0.05) for rejection of the nullity hypothesis. Results: the medium percentage of the expression of SOD in GI (16.0 ± 3.7) was similar to GIII (16.9 ± 3.1) showing that the saline solution (controls) and IP6 didn't provoke alterations in FCA; the group II (26.7 ± 3.5) showed a significant percentage of expression of SOD in FCA, demonstrating the capacity to provoke preneoplasic lesions in colon of rodents; on the other hand this promotion of carcinogenic induction was protected by the administration of IP6 showed by the results of GIV (20.9 ± 3.3). Conclusions: The carcinogenic action of AOM provided a carcinogênese model in colon of Wistar rat that was protected by the administration of IP6, and the expression of SOD in FCA was a histochemical parameter reliable to represent the preneoplasic lesions in FCA.
Objective: to develop an experimental model of carcinogenesis in Wistar rats induced by the azoximethane and to establish a pattern of protecting action of the inositol hexafosfate, for the expression of the enzyme superoxide dismutase in foci of aberrant crypts. Methods: 48 Wistar male rats, adults, were maintained in observation by six weeks. GI (n=12) received injections of subcutaneous saline solution during the third and fourth weeks, while GII (n=12), in the same period, received 20mg.Kg-1 of subcutaneous azoximetano (AOM). GIII (n=12) received inositol hexafosfato 1% (IP6) in the drinking water during the six weeks, while GIV, besides IP6 in the drinking water, also received the subcutaneous injections of AOM during the third and fourth weeks. At the end of the sixth week large intestine segments were collected to the about a centimeter of the ileo-colic transition. Fragments were prepared and submitted to the imunohistochemical process to antibody primary anti-SOD1 (superoxide dismutase1) and antibody secondary anti-rat, color discloser DAB (diamino-benzidina) with expression obtaining SOD1 in the brown coloration. The percentage of the expression of SOD in FCA (focus of aberrant crypt) was quantified through image processing attended by computer (ImageLab). The results were submitted to the tests of variance analysis (ANOVA) and established the level of 5% (p≤0.05) for rejection of the nullity hypothesis. Results: the medium percentage of the expression of SOD in GI (16.0 ± 3.7) was similar to GIII (16.9 ± 3.1) showing that the saline solution (controls) and IP6 didn't provoke alterations in FCA; the group II (26.7 ± 3.5) showed a significant percentage of expression of SOD in FCA, demonstrating the capacity to provoke preneoplasic lesions in colon of rodents; on the other hand this promotion of carcinogenic induction was protected by the administration of IP6 showed by the results of GIV (20.9 ± 3.3). Conclusions: The carcinogenic action of AOM provided a carcinogênese model in colon of Wistar rat that was protected by the administration of IP6, and the expression of SOD in FCA was a histochemical parameter reliable to represent the preneoplasic lesions in FCA.
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Citation
São Paulo: [s.n.], 2006. 44 p.