HEAT AND CADMIUM: A DAMAGING COCKTAIL

Abstract

Permanently glued to the rocks of their estuary home, eastern oysters(Crassostrea virginica) can cope with most of the extremes of their environment: daily and seasonal variations in temperature, from 5°C to 35°C, plus the coming and going of the tides. Add environmental stressors like pollution into the mix, however, and the oysters suffer from oxidative stress, where their cells' mitochondria produce more molecule-damaging reactive oxygen species (ROS) than the cells can clean up. It is important to understand how temperature and pollution interact with each other to affect the survival of marine invertebrates, such as oysters, given the predicted rise in global temperatures, explains Inna Sokolova of the University of North Carolina, Charlotte. Sokolova and her colleagues show that as the temperature rises, oysters suffer more from oxidative stress when they are exposed to cadmium, a toxic heavy metal (p. 46).Cadmium is similar in structure to zinc and calcium and it messes up many cellular processes, such as calcium dependent cell signalling, by blocking enzyme active sites. The metal also increases ROS production, and therefore oxidative stress, in mitochondria. Directly measuring ROS production in a cell is tricky, so to measure the level of oxidative stress the team focussed on a Krebs cycle enzyme called aconitase. This enzyme has an iron atom in the middle, which is a bit loose. `If the iron becomes oxidised by ROS, it falls off, and the enzyme doesn't work properly', says Sokolova. So if a cell is producing larger quantities of ROS, the activity of the aconitase enzyme goes down.To investigate the effects of cadmium and temperature on the aconitase enzyme, the team carefully isolated mitochondria from oyster gill tissue and transferred them to culture for experiments. They exposed the mitochondria to cadmium and higher temperatures and measured aconitase enzyme activity. At 20°C, cadmium slightly reduced aconitase activity, but mitochondria could mop up most of the excess ROS before they caused too much damage. However,when they exposed mitochondria to cadmium and raised the temperature to 30°C, the team found that aconitase activity decreased by up to 52%. This was probably because cadmium induces the mitochondria to produce more ROS at higher temperatures, which inhibits aconitase.Having shown that cadmium increases oxidative stress at higher temperatures, the team wondered if a group of mitochondrial membrane proteins called uncoupling proteins, which are known to diminish the effects of ROS,would reduce oxidative stress and the effects of ROS on aconitase. They suggested that stimulating uncoupling protein activity with fatty acids would reduce oxidative stress caused by cadmium and high temperature, while inhibiting uncoupling protein activity with ATP would increase it. They found no evidence that uncoupling proteins help protect aconitase from ROS, and Sokolova explains that the team also found a result that they weren't expecting: ATP directly inhibits the aconitase enzyme. This suggests ATP might play an important role in regulating the activity of the Krebs cycle, and scientists will need to look at the phenomenon more closely to see if it is unique to oysters or not.While the team's unexpected result will give researchers plenty of food for thought, their study also suggests that rising global temperatures could have a serious effect on oyster survival: `moderately polluted areas could become graveyards', says Sokolova. In the future, researchers might have to adjust their criteria for water quality, to take into account the effects of rising temperatures.