Environmental epigenetics
[1] The way that genes are expressed may be passed down from parent to offspring through epigenetic modifications, although environmental influences do not alter the genome itself.
These triggers can cause low birth weight, neurological disorders, cancers, autoimmune diseases, and many other malformations.
If the maternal figure experiences high levels of depression or stress it can lead to small litter sizes with lower birth rates.
Temperature can be considered a stressor in environmental epigenetics since it has the potential to change how offspring respond and react to their environment.
Exposure to environmental pollutants, psychological stress, dietary choices or restrictions, working habits, and consumption of drugs or alcohol all influence the epigenetics of an individual and what may be passed down to future offspring.
[9] Such exposures can affect important processes of epigenetics such as DNA methylation and histone acetylation, influencing the risk for noncommunicable diseases such as obesity.
[12] For example, research has shown that exposure to pollutants like biphenol A (BPA) and polycyclic acromatic hydrocarbons (PAHs) can lead to DNA methylation changes and histone modifications in plants, animals, and humans.
[14] Studies have shown that organisms can exhibit phenotypic plasticity through epigenetic modifications in response to environmental stressors such as temperature fluctuation, drought, and habitat loss.
[16] Studies in various organisms, including plants, insects, and mammals, have shown transgenerational epigenetic effects resulting from parental exposure to stressors such as toxins, dietary changes, and environmental contaminants.
[17] Epigenetic modifications can influence gene expression and phenotypic traits in oragamisms across different trophic levels, with implications for ecosystem stability.
Direct toxic effects that occur due to high levels of metal are inhibition of cytoplasmic and damage to the structure of the cell because of oxidative stress.
Studies have shown that lead acetate reduces protease and amylase activity in rice endosperm considerably.
This interferes with early seeding growth across plant species such as soybean, rice, tomato, barley, maize, and some legumes.
[20] Soil levels that have high levels of lead can also cause irregular root thickening, cell wall modifications in peas, growth reduction in sugar beets, oxidative stress due to increased reactive oxygen species (ROS) production, biomass, and protein content in maize, along with diminished lead count and area, plant height in Portia trees, and enzyme activity affecting CO2 fixation in oats.
In some species, toxicity can begin with chlorosis in older leaves, advancing to younger ones, and can inhibit chlorophyll synthesis by interfering with iron-related processes.
[27][28] Humans have displayed evidence of epigenetic changes such as DNA methylation, differentiation in expression, and histone modification due to environmental exposures.
Carcinogen development in humans has been studied in correlation to environmental inducements such as chemical and physical exposures and their transformative abilities on epigenetics.
[29] This area in China was historically known for its dangerously high levels of arsenic, therefore, there was opportunity to examine the timeline As exposures across the three generations.
The concluding argument based on the results of this study is that the DNA methylation changes were more prevalent in those that developed arsenic-induced diseases.
[29] Exposures to environmental factors during human lifetimes and their potential effect on phenotypes is a highly question topic involving epigenetics and disease development.
Driving evidence for adverse effects implemented by extrinsic factors from the environment, comes from studies done on nutrition and exposures to toxins.
Concentrations of Cd, Cr, Cu, Pb and Zn metals were identified in fishermen's blood and resulted in an increase in the expression of the IGF2 gene.
[33] Such disorders include breast and lung cancers and Silver–Russell and Beckwith–Wiedemann syndromes [33][34] The significance of IGF2 gene expression is found in its relationships to human health.
For example, in rats, mothers that lick and groom their pups pass down a specific behavior to their offspring causing them to do the same to the subsequent generation.
[36] DNA replication is a highly conserved process involving the copying of genetic information from parent one generation to the next.
[37] These epigenetic marks play a critical role in determining chromatin structure and thus gene expression in the newly synthesized DNA.
