Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A diet enriched with biologically active substances as a protecting factor against carcinogenesis process induced by 1,2-dimethylhydrazine in rat liver

ABSTRACT: The aim of this study was to evaluate the ability of a diet enriched with biologically active compounds to protect against 1,2-dimethylhydrazine - induced carcinogenesis in 14-month old rats liver. Rats from control and experimental groups after 14 months of experiment were given 5 times 1,2-dimethylhydrazine (DMH) by intraperitoneal treatment at a dose of 30mg/kg of body weight once a week to induce the process of carcinogenesis. RNA from their livers were hybridized to Agilent two color microarrays with a common reference. Then, the transcriptomic profile of these livers were compared to the transcriptomic profile of 14-month rats received the same control diet and diet enriched with biologically active substances, but without 1,2-dimethylhydrazine - induction (data from GEO Submission - GSE51657).

ORGANISM(S): Rattus norvegicus

SUBMITTER: Hanna Oszkiel

PROVIDER: E-GEOD-55378 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Post-menopausal obesity is an established risk factor for breast cancer. Consumption of diets high in fat is known to be highly correlated with obesity. In this, we sought to evaluate the interaction(s) between high fat diet, weight gain and mammary carcinogenesis using an obese-resistant and obese-prone rat model with direct correlates to human disease. Methods: Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly. Results: The DMBA-treated OR rats on the 39% safflower diet had significantly greater incidence of ductal carcinoma-in-situ (DCIS) lesions and significantly greater DCIS multiplicity than DMBA-treated OR rats on the 10% safflower diet. These differences were not seen in the OP strain. Gene expression analysis of mammary ductal epithelium from OR rats on the high fat diet showed significant upregulation of proliferation-related genes compared to those consuming the low fat safflower diet. Again, these differences were not seen in the OP strain. Conclusion: Our findings indicate that consumption of high fat safflower diet enhances mammary carcinogenesis in an OR rat strain through increased proliferation of mammary epithelium at the time of exposure, but not in the OP rat strain. Thus, the diet-induced increase in sensitivity was strain-specific and independent of weight gain or obesity level. Female obese-prone (OP) and obese-resistant (OR) weanling rats were placed on either a low fat (10% kcal) or a high fat (39% kcal) n-6 polyunsaturated (PUFA) safflower diet for 30 days. At post natal day (PND) 50, global gene expression profiling was performed on microdissected mammary epithlelium from one cohort of rats and another cohort of rats were given a single oral gavage of either 7,12-dimethylbenz[a]anthracene (DMBA at 14 mg/kg) or vehicle. Rats were then maintained on the diets and body weights, food consumption and development of mammary lesions were monitored weekly.

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A diet enriched with biologically active substances as a protecting factor against carcinogenesis process induced by 1,2-dimethylhydrazine in rat liver

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