The Atlantic tomcod, a species of fish that evolved resistance to industrial toxins in just 50 years, could be the first documented case of pollution-driven vertebrate evolution.
Recent studies showed that the tomcod resists toxins in the Hudson River by storing the normally harmful compounds in fat.
According to Isaac Wirgin, associate professor of environmental medicine at New York University School of Medicine, this adaptation is not necessarily beneficial for the animals feeding on the tomcod.
Toxins in the tomcod can move up the food chain as the fish are consumed by predators, a process known as biomagnification.
Because the substances cannot be broken down naturally, tissue concentrations of the toxin will increase every time it moves up a tropic level. If a human happens to eat a contaminated organism, they could potentially ingest a potent dose of toxins.
Decades of exposure to industrial toxins that were dumped into the Hudson River have resulted in tomcods acquiring one of the highest liver PCB and dioxin levels known in nature.
As tomcods cannot detoxify PCB, Wirgin was surprised that the fish could store large amounts of contamination without being poisoned. The team later found that a single gene mutation was responsible for this phenomenon.
All vertebrates have proteins that facilitate binding to dioxins and other related compounds. These aryl hydrocarbon receptors, or AHRs, will bind with poisons diffusing into the cell.
After the poison molecules and receptors pick up a third molecule, they will dock with DNA segments in the cell nucleus to turn on genes that can poison the animal.
Unlike other vertebrates, the tomcod has two types of AHRs: an AHR-2 that effectively binds to pollutants and an AHR-2 variant that requires five times the normal amount of pollutants to trigger binding.
In rivers with low dioxins and PCB levels, 95 percent of tomcods only possessed the standard form of AHR-2. However, in the significantly more polluted Hudson River, Wirgin’s group found that 99 percent of tomcods had the poorly binding AHR-2.
While this is the first known case of vertebrate poison resistance, adaptations to poison have evolved many times in nature, sometimes as a response to human activities.
Some well-known examples of this include increasing bacterial resistance to antibiotics and DDT resistance in malaria-transmitting mosquitoes. Understanding the genetic and evolutionary causes of chemical resistance allows scientists to better exploit the system and more effectively address potential threats to human health.
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