The vast majority of vertebrates, from fish to humans, possess red blood due to the oxygen-carrying protein hemoglobin. This crimson hue reflects the presence of iron atoms within the blood cells. A striking exception exists in the tropical rainforests of Papua New Guinea and the Solomon Islands, where certain lizards circulate a vibrant green fluid instead. This unusual trait has long puzzled scientists, who seek to understand how these reptiles survive with a blood chemistry that would be acutely toxic to almost any other animal.
Identifying the Emerald-Blooded Lizards
The reptiles displaying this remarkable coloration belong to the genus Prasinohaema, a name that literally translates from Greek to “green blood.” These are small, arboreal skinks, characterized by their sleek bodies and short limbs. Although their outer skin appears typical, the intense green pigment saturates all their internal tissues.
The green color is not confined to the circulatory system; it is visible in their muscles, bones, mucosal membranes, and tongues. Species like Prasinohaema virens inhabit tropical forests, often found at lower altitudes. The discovery that this green blood has evolved independently multiple times among different lineages highlights its profound significance.
The Physiological Cause of Green Blood
The green blood results from a massive accumulation of the bile pigment biliverdin within the lizard’s plasma. In all vertebrates, biliverdin is a natural byproduct of old red blood cell breakdown. Hemoglobin, the red, iron-containing molecule that transports oxygen, is dismantled when a blood cell reaches the end of its life cycle. The heme group from the hemoglobin is metabolized into biliverdin, which is a naturally green compound.
In most animals, including humans, this biliverdin is quickly processed by the liver. It is converted into the yellow-brown pigment bilirubin and then excreted as waste. These green-blooded lizards, however, have evolved a mechanism that prevents this final step of excretion. Instead of being processed and eliminated, the biliverdin remains in the bloodstream and tissues at exceptionally high concentrations.
The resulting intense green color completely overwhelms the red hue of the remaining hemoglobin, masking it entirely. This accumulation of pigment gives the lizards their unique emerald coloration.
Surviving Toxic Levels of Biliverdin
The sheer quantity of biliverdin circulating in these skinks is the most remarkable aspect of the phenomenon. Researchers have measured concentrations in some Prasinohaema species ranging between 714 to over 1,000 micromoles per liter of blood plasma. For perspective, levels reaching just 50 micromoles per liter are considered potentially fatal in humans, resulting in a condition known as green jaundice. The lizards are thus thriving with a biliverdin load approximately 40 times higher than what would cause severe neurotoxicity and death in people.
This suggests a unique physiological adaptation that allows them to tolerate and neutralize the pigment’s toxic effects. Scientists hypothesize that the biliverdin is tightly bound to a specialized carrier protein within the lizard’s plasma, potentially serum albumin.
This binding mechanism would safely sequester the biliverdin, preventing it from crossing the blood-brain barrier and causing neurological damage. Recent genetic studies have pointed toward a possible evolutionary change in a protein, perhaps a form of alpha-fetoprotein, that aids in the tolerance. Unraveling this tolerance mechanism could offer insights into treating human bile pigment disorders like jaundice.
Evolutionary Hypotheses for the Trait
The fact that green blood evolved independently in at least four different Prasinohaema lineages suggests the trait provides a significant selective advantage. The leading scientific theory centers on biliverdin’s potential to fight infection from blood-borne parasites. The tropical environments these skinks inhabit are rife with parasites, including various species of Plasmodium. These parasites are related to the organisms that cause malaria in humans.
Studies have shown that bile pigments, including biliverdin, can interfere with the lifecycle and proliferation of Plasmodium parasites. Maintaining high concentrations of biliverdin in the blood may act as a constant defense against infection. This evolutionary arms race between host and parasite appears to have resulted in the extreme accumulation of this otherwise toxic compound.
Early hypotheses, such as the idea that the green coloration served as camouflage or deterred predators, have largely been dismissed. The consistent, repeated evolution of the hyper-biliverdin trait in a malaria-prone environment points to parasite resistance as the most probable explanation.