Keywords
carcinogenesis
stadiums
protocols
survival
in vivo models
BALB/c mice
azoxymethane
sodium dextran sulfate
lipid oxidation
protein oxidation
inflammation
tumors
chemoprevention
oncology
intestinal dysbiosis
carcinoma
intestinal microbiota
intestinal inflammatory diseases cáncer de colon
carcinogénesis
estadíos
protocolos
supervivencia
modelos in vivo
ratones BALB/c
azoximetano
dextran sulfato de sodio
oxidación de lípidos
oxidación de proteínas
inflamación
tumores
quimioprevención
oncología
disbiosis intestinal
carcinoma
microbiota intestinal
enfermedades inflamatorias intestinales
How to Cite
Abstract
Introduction: Colon cancer diagnosis is usually performed late; so, it is necessary to search for prevention options. In vivo models are an option for the evaluation of chemopreventive agents, which are based mainly on the induction and promotion of carcinogenesis; however, they take a long time. This work aimed to evaluate and propose a carcinogenesis model, with tumor manifestation in a short time to prove the efficacy of chemopreventive compounds.
Method: Colon carcinogenesis was induced in three groups (n = 7) male BALB/c mice with azoxymethane (AOM) and dextran sodium sulfate (DSS). The damage was assessed 14 weeks after the induction. Protocols were: 1) P1: two AOM injections and two DSS cycles at 1.5 % for five days, with three resting days between cycles; 2) P2: one AOM injection and two DSS cycles at 2 % for seven days with five rest days, and 3) P3: one AOM injection and two DSS cycles at 2 % for four days, with four resting days. Negative control was used in parallel, P0: with one injection of saline solution and water ad libitum. Weight, disease activity index (DAI), survival, tumor incidence, lipids, and protein oxidation were determined.
Results: P2 showed greater severity in the assessed signs (100 % tumor incidence, colon weight/length ratio 101.68 ± 2.99 mg/cm), with low survival (43 %). P1 depicted lower mortality (14 %) and 83 % tumor incidence, without a significant difference to P2. P3 developed the disease but to a lesser degree (33 % tumor incidence). Furthermore, the three protocols showed lipid oxidation (0.4-0.58 ng/μg of protein) and proteins oxidation (0.6-1 ng/μg of protein). The P1 and P3 induction protocols presented less mortality, weight loss, and acceptable DAI, a weight/length ratio higher than the negative control and presence of tumors.
Discussion: The use of AOM (10mg/kg) combined with DSS (1.5-2 %) are suitable models to evaluate the carcinogenic effect of compounds of interest, inflammation signs, lipids and proteins oxidation and a survival number adequate to perform the statistical analysis leading to accurate conclusions. Therefore, P1 and P3 are protocols that can be used in chemoprevention assays with satisfactory results.
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