Environmental Epigenetics - Exposure

Environmental Epigenetic example of triggers: Exposure

Exposure to certain materials or chemicals can cause an epigenetic reaction. The epigenetic causing substances cause issues like altered DNA methylation, CpG islands, chromatin, along with other transcription factors. Environmental epigenetics aims to relate such environmental triggers or substances to phenotypic variation.

Example 1

An example of exposure causing environmental epigenetic can be seen in lemon sharks, Negaprion brevirostris. Due to a dredging event, lemon sharks in the Bahamas experienced an epigenetic change. Dredging is done with a machine that clears out all mud and debris found at the bottom of a body of water. Dredging is extremely harmful to the physical environment and the organisms living there. This dredging caused exposure to different toxic metals like Manganese along with other trace amount of heavy metals, which then affected DNA methylation in juvenile lemon sharks. This exposure caused the lemon sharks’ DNA to methylate at abnormal rates which caused gene expression to be altered. Scientists hypothesized that this aberrant DNA methylation could be caused by the stress that the dredging caused. Exposure to a stressful event is also an example of an environmental epigenetic factor.

Example 2

Plants need some types of metals to help with their development, but when exposed to high amounts, the metals can become toxic to plants. Since plants can process metals that are important for their growth, they also process metals that are not needed to help them grow and develop. Once the levels of the metals get too high, they start to affect plants directly and indirectly because metals cannot be broken down. 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. Oxidative stress is like a bad storm that messes up the plant by damaging it so it cannot get the nutrients it needs to be healthy because things that are not supposed to be there are taking up space where the essential nutrients should go. Indirect toxic effects are the proxy nutrients at the plant's cation exchange. The cation exchange site is where the plant picks up the nutrients it needs, though if something comes in and starts taking all the valuable nutrients, such as heavy metal, there is nothing there to help the plant grow. An example of a heavy metal that is not required for plant growth is mercury. The relationship between Hg in the soil and how much plants take in is complex. It relies on many other factors, such as the pH of the soil, the type of plant species, etc.

Many types of heavy metals are toxic to plants, and here are just a few that the article talks about, such as lead. Typically, land plants absorb lead(Pb) from the soil, most retaining it in their roots with some evidence of foliage uptakes and potential distribution to other plant parts. Calcium and phosphorus can reduce the uptake of lead, a common and toxic soil element that impacts the plant, growth structure, and photosynthesis of the plant. Lead, in particular, inhibits the process by which a plant grows from a seed into a seedling, known as seed germination in various species, by interfering with crucial enzymes. 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.

Furthermore, lead delays root and steam elongation and leaf expansion, with the extent of root elongation inhibition varying based on the lead concentration, the medium's ionic composition, and pH. 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.

Manganese (Mn), is crucial for plants and involves in photosynthesis and other physiological processes. Deficiency commonly affects sandy, organic, or tropical soils with a high pH above six and heavily weathered tropical soils. Mn can move easily from roots to shoots, though it's not efficiently redistributed from leaves to other parts of the plant. The signs of Mn toxicity are necrotic brown spots on leaves, petioles, and steams that start on the lower leaves and move upward, leading to death. When damage to young leaves and stems, coupled with chlorosis and browning, called a "crinkle leaf." 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. Mn toxicity is more present in soils with a pH level lower than six. In the broad bean plant, Mn affects shoot and root length The spearmint plant, lowers chlorophyll and carotenoid levels and increases root Mn accumulation. Pea plant, lowers chlorophyll a and b, growth rate, and photosynthesis. In the tomato plant, it slows growth and decreases chlorophyll concentration.

https://www.researchgate.net/profile/Mohnish-Pichhode/publication/336148391_Effect_of_Heavy_Metals_on_Plants_An_Overview/links/5d92ef25299bf10cff1cd4af/Effect-of-Heavy-Metals-on-Plants-An-Overview.pdf

Example 3 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. Chemical and physical environmental factors are contributors to epigenetic statuses amongst humans.

Firstly, a study was performed on drinking water populations in China involving three generations: the F1 generation comprising of grandparents exposed to arsenic in adulthood, the F2 generation including the parents exposed to arsenic in utero and early childhood, and the F3 generation which were the grandchildren exposed to arsenic from germ cells. This area in China was historically known for it's dangerously high levels of arsenic, therefore, there was opportunity to examine the timeline As exposures across the three generations. The study was conducted to discover the linkage between the timeline effects of As exposure and DNA methylations. The population and environment for which the study was conducted were reportedly not exposed to other environmental exposures besides arsenic.

The results concluded from this experiment were that 744 CpG sites had been differentially methylated. The 744 sites were found across all three generations in the group exposed to arsenic. 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.

Exposures to environmental factors during human lifetimes and their potential effect on phenotypes is a highly question topic involving epigenetics and disease development. In the case of humans, "unhealthy" phenotypes have been identified to carry such evidence that environmental epigenetics could be a leading cause in gene regulation, disease development, cell development and differentiation, aging, and carcinogenic effect. Although the way that environmental factors and the human genome work together is not completely understood, their influence has been identified and is continuing to drive explanations for human genome modifications and their outcomes. Driving evidence for adverse effects implemented by extrinsic factors from the environment, comes from studies done on nutrition and exposures to toxins.

Besides arsenic exposures, other metals have been identified to cause such hypermethylations. 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. The IGF2 gene is responsible for making the insulin-like growth factor 2. The insulin-like growth factor is involved in growth and can result in disorders where cell growth and overgrowth are abnormal. Such disorders include breast and lung cancers and Silver–Russell and Beckwith–Wiedemann syndromes The significance of IGF2 gene expression is found in its relationships to human health. There is remaining uncertainty between the long-term environmental exposures and epigenetic changes, but conducted research has provided that heavy metal exposures cause DNA methylation changes.

Example 4: how environmental epigenetic exposure affects the planet