For the first time, scientists at the University of Manchester and the University of North Texas have shown that an embryonic living heart can be programmed to survive the effects of a low-oxygen environment in later life.
Conducted on juvenile snapping turtles, the study explains the heart’s biological mechanisms, which help turtles to survive up to six months without oxygen uniquely. Moreover, the study is expected to be translated into treatments that alleviate damage to the heart caused by hypoxia.
Scientists think that it’s the exposure to low levels of oxygen during embryonic development which programs the animal’s hearts to be more resilient to what is known as hypoxia for the rest of their lives.
Hypoxia is a condition or state in which the supply of oxygen is insufficient for normal life functions. Exposure to hypoxia during development causes epigenetic changes to the genome that can turn genes on or off, which are vital to the astounding ability of the turtle heart cells to tolerate zero oxygen.
Ilan Ruhr, who is a postdoctoral researcher at The University of Manchester, said, “Turtles are incredible creatures that can uniquely survive for long periods under ice or at depths where there is little oxygen.”
“We’re excited to be the first to show that it is possible to change the degree of tolerance that turtles have for low oxygen environments by early exposure to hypoxia during development.”
“Now we hope to isolate those epigenetic signatures which help turtles to survive for so long without oxygen with a hope to developing epigenetic drugs that can switch on tolerance to low oxygen environments in human hearts.”
Scientists are studying the heart instead of other organs, as it is one of the organs most at risk of damage from hypoxia.
They isolated heart muscle cells from juvenile turtles, which lived as embryos in either average levels of oxygen at 21 percent O2—or half the levels of oxygen, 10 percent.
The procedure mimicked what happens in nature: eggs at the bottom of turtles’ nests are more exposed to hypoxia.
Moreover, they subjected the juvenile turtles to lower levels of oxygen while measuring intracellular calcium (which binds to the contractile proteins of the heart, known as the myofilaments), pH, and reactive oxygen species—a molecule we all have which can become toxic when tissue reoxygenates too quickly.
Dr. Gina Galli from The University of Manchester said: “Heart cells in turtles and humans are anatomically quite similar, so if we can learn to understand what factors allow them to survive in an oxygen-free environment, we’d hope to be able to apply that to a medical scenario.
“Our study showed that early exposure to hypoxia in these animals both reduces the number of reactive oxygen species that could protect their myofilaments from damage and allows them to contract generally in the complete absence of O2.
“A drug which is able to switch on mechanisms to protect the human heart from oxygen deprivation would be of enormous benefit
“It could, for example, protect individuals at risk of heart attack or protect organs for transplantation.”
The study is published in Proceedings of the Royal Society B.