Alimentary triggers of hormone dependent breast cancers
AbstractBreast cancer (BC) consistently holds the leading positions in the structure of morbidity and mortality of the female population. Food containing veterinary hormones is extremely dangerous to human health: estrogens are female sex hormones. Excessive level of estrogen in the body gives rise to diseases of varying severity: in women (especially of older age) it may cause breast cancer. The paper investigates the processes of lipid peroxidation and the status of antioxidant protection system in rats of different ages exposed to exogenous estrogens. The purpose of the work is to study lipid peroxidation and antioxidative protection status in rats of different ages exposed to exogenous estrogens for determining the trigger mechanisms for tumor development. Experiments were conducted on female Wistar rats exposed to exogenous estrogen for 45 days. At the beginning of the experiment, age of experimental animals was 3 months in pubertal period and 6 months as mature ones. The control groups consisted of intact animals of appropriate age. To simulate the influence of exogenous estrogen, rats’ food was treated with the Sinestron drug at the rate of 2 mg per kg. The research materials were serum and liver of rats. Objects of the research were indicators of lipid peroxidation activity (content of TBA-active products) and antioxidant protection system (reduced glutathione (RG) level), glutathione transferase (GT), glutathione reductase (GR), glutathione peroxidase (GP), superoxide dismutase (SOD) activity, and total antioxidative activity (AOA). Data obtained was treated with standard methods of estimation of variation series. Various degrees of peroxidation intensification depending on the age and organs were determined. Maximum excess of control indexes in the serum was observed and it indicated synthetic estrogen effect of on all major body systems. In prepubertal period females’ liver the reaction of prooxidant system and tension in the antioxidant protection system exceeded the strength of response in the body of mature animals. The organ discreteness of changes in the activity of antioxidant protection enzymes depending on the age of the animals was recorded. Given the involvement of glutathione system in the deactivation of estrogens through their conjugation in reactions catalyzed by glutathione transferase, decreased enzyme activity may lead to accumulation of highly active intermediate metabolites with subsequent damage to intracellular structures. Later on, these phenomena may become a trigger of reduction of the compensatory mechanisms’ potential, which together with the genotoxic effect of exogenous estrogens is an important pathogenetic element in carcinogenesis: they initiate the development of proliferative processes and occurrence of cancer conditions, in particular, hormone dependent breast tumors, in future.
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