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Growth and development in utero is a complex and dynamic process that requires interaction between the mother organism and the fetus. The delivery of macro--and micronutrients, oxygen and endocrine signals has crucial importance for providing a high level of proliferation, growth and differentiation of cells, and a disruption in food intake not only has an influence on the growth of the fetus, but also has negative consequences for the offspring’s health in the future. Diseases that traditionally are linked to inappropriate life style of adults, such as type 2 diabetes, obesity, and arterial hypertension, can be "programmed" in the early stage of life and the disturbed growth of the fetus leads to the symptoms of the metabolic syndrome. The structural changes of some organs, such as the brain, pancreas and kidney, modifications of the signaling and metabolic pathways in skeletal muscles and in fatty tissue, epigenetic mechanisms and mitochondrial dysfunction are the basis of the metabolic disruptions. The programming of the metabolic disturbances is connected with the disruption in the intrauterine environment experienced in the early and late gestation period. It causes the changes in deposition of triglycerides, activation of the hormonal "stress axis" and disturbances in the offspring’s glucose tolerance. The present review summarizes experimental results that led to the identification of the above-mentioned links and it underlines the role of animal models in the studies of this important concept.

Aim: The aim of the study was to determine the content of cadmium and lead in different parts of the placenta and fetal membranes of women who were exposed to cigarette smoke. The correlation between the two chemical elements and the impact of the Cd and Pb accumulation on newborn parameters were established., Materials and Methods: The study material was collected immediately after delivery from 40 patients of the Department of Obstetrics and Gynecology Katowice. The marginal and central parts of the placenta and fetal membranes (amnion) were taken. The women were divided into two groups: smokers and non-smokers. Metal concentration in placenta was determined by flame atomic absorption spectrometry (FAAS). Bioethical Commission approved of the study, Results: In both studied groups, smokers and non-smokers, the presence of cadmium and lead was detected. Smokers turned out to have accumulated more of the investigated heavy metals in the placenta and fetal membranes. In the analyzed groups of women of smokers and non-smokers, differences in the content of the studied metals were found, but they were not statistically significant. Differences in newborn parameters in the two groups of women occurred, but again they lacked statistical significance. The level of lead increases along with the increase in the amount of cadmium, which proves the existence of a statistically significant correlation between them (p = 0.000)., Conclusions: The number of smoked cigarettes increases cadmium content in maternal placenta and fetal membranes. No significant differences in newborn parameters of either smoker or non-smokers were observed, which may indicate women's adaptation to the environment containing cigarette smoke. The placenta and fetal membranes are biomarkers of the level of toxic exposure for the developing baby.

Fetal germ cells transform neoplastically probably at the fetal period of life. The best place for their maintenance is a testis with the disturbed organogenesis (differentiation). These testes are called dysgenetic gonads. Besides the classical form of gonadal dysgenesis, appearing by the reversed sex features (female in genetic males), there are probably hidden forms without the disturbances in the sex differentiation. The overt and hidden disturbances of the testes' organogenesis are called testicular dysgenesis syndrome (TDS). Gonadal dysgenesis is more frequent in normal male karyotype than in numerical and structural aberrations of sex chromosomes. The cause of TDS is an inappropriate expression of genes of Y chromosome or autosomes, taking part in testicular differentiation, and/or exposition to the influence of environmental factors, mainly with estrogen-like action. It is supposed that TDS determines a cascade of events leading to germ cell tumours (GCT). This mechanism may appear as follows: 1) the inhibited organogenesis of seminal tubules (sometimes at the level of sex cords) causes 2) the delay in differentiation and development of germ and somatic Sertoli/granulosa cells; 3) disturbed somatic cells contribute to the death of most germ cells, but germ cells which retain fetal antigens have the possibility to survive and proliferate; 4) if the survived germ cells are in the undifferentiated tissue of fetal gonad (retardation of testicular development at the level of gonadal anlage) their clonal expansion leads to the creation of neoplastic lesion termed gonadoblastoma. With time gonadoblastoma undergoes atrophy and/or calcification or may transform into GCT; 5) if the survived germ cells are placed inside the seminal tubules, they have better conditions to persist in the unchanged, but developmentally delayed, form for many years as preinvasive carcinoma in situ (CIS). CIS cells can disappear but with the advancing puberty they may give rise to GCT under the influence of gonadotropins and androgens.