Developmental Exposure to Endocrine Disrupting Chemicals Alters the Epigenome: Identification of Reprogrammed Targets
Endocrine disruptions induced by environmental toxicants have placed an immense burden on
society to properly diagnose, treat and attempt to alleviate symptoms and disease.
Environmental exposures during critical periods of development can permanently reprogram normal physiological responses, thereby increasing susceptibility to disease later in life – a process known
as developmental reprogramming.
During development, organogenesis and tissue differentiation occur through a continuous series of tightly regulated and precisely-timed molecular, biochemical and cellular events.
Humans may encounter Endocrine Disrupting Chemicals (EDCs)
daily and during all stages of life, from conception and fetal development through adulthood
and senescence.
Though puberty and perimenopausal periods may be affected by endocrine
disruption due to hormonal effects, prenatal and early postnatal windows are most critical for
proper development due to rapid changes in system growth.
Developmental reprogramming is shown to be caused by alterations in the epigenome. Development is the time when epigenetic programs are ‘installed’ on the genome by ‘writers’, such as histone methyltransferases
(HMTs) and DNA methyltransferases (DNMTs), which add methyl groups to lysine and arginine residues on histone tails and to CpG sites in DNA, respectively.
A number of environmental compounds, referred to as Estrogenic Endocrine Disruptors (EEDs),
are able to bind to Estrogen Receptors (ERs) and interfere with the normal cellular development in target tissues
including the prostate and uterus. These EEDs, including diethylstilbestrol (DES), bisphenol
A (BPA), and genistein (a phytoestrogen derived from soybeans), have been implicated in the
malformation of reproductive organs and later development of disease.
Gynecol Obstet Res Open J. 2016; 3(1): 1-6. doi: 10.17140/GOROJ-3-127
