Affection of developing organism by endocrine disruptors is an actively studied topic of scientific research in medicine, caused by a progressive increase in the number of diseases and disorders in the development of the reproductive and endocrine systems. Dichlorodiphenyltrichloroethane (DDT) is the most wide-spread endocrine disruptor. Low-dose exposure to DDT disrupts production of sex steroids by poorly known mechanisms. The research was focused on assessment of morphology of adrenal zona reticularis and fine structure of reticularis endocrine cells and changes in their secretory machinery in rats exposed to low doses of DDT during prenatal and postnatal development. The experimental group consisted of the male offspring of dams, who daily consumed solution of o, p-DDT at a concentration of 20 µg/l, from mating until the end of the suckling period in offspring, which then consumed a similar solution of DDT. Daily consumption of DDT by the offspring was 2,90±0,12 µg/kg body weight. These doses corresponds to levels of exposure of humans to DDT with food products taking to account the differences in metabolism of DDT in rats and humans. The control and experimental rats were sacrificed on the 42nd day of postnatal development (pubertal period). Light microscopy of adrenal sections found hypoplasia of zona reticularis in rats after developmental exposure to endocrine disruptor. Electron microscopy revealed prevalence of cells with low lipid content in cytoplasm, less developed endoplasmatic reticulum and Golgi complex and signs of lowered functional activity of mitochondria indicated decreased steroidogenic activity of zona reticularis. These findings explain previously found impaired production of sex steroids in DDT-exposed rats. Electron microscopy also found that disruption of steroid secretion in reticularis cells by DDT led to compensatory enlargement of cells and increase in number of mitochondria per m2 of cytoplasm indicating development of structural support for long-term enhancement of steroidogenic activity.
Asthma Pregnancy Alters Postnatal Development of Chromaffin Cells in the Rat Adrenal Medulla
