CO2-driven acidification and emerging contaminants, such as pharmaceuticals, pose
new threats for the maintenance of natural populations of marine organisms by interfering
with their normal biochemical pathways and defences. The combined effects of seawater
acidification, as predicted in climate change scenarios, and an emerging contaminant
(the non-steroidal anti-inflammatory drug, NSAID, diclofenac) on oxidative stress-related
parameters were investigated in the Mediterranean mussel Mytilus galloprovincialis
and the Manila clam Ruditapes philippinarum. A flow-through system was used to carry
out a three-week exposure experiment with the bivalves. First, the animals were exposed
to only three pH values for 7 days. The pH was manipulated by dissolving CO2 in the
seawater to obtain two reduced pH treatments (pH -0.4 units and pH -0.7 units), which
were compared with seawater at the natural pH level (8.1). Thereafter, the bivalves
were concomitantly exposed to the three experimental pH values and environmentally
relevant concentrations of diclofenac (0.00, 0.05 and 0.50 μg/L) for an additional
14 days. The activities of superoxide dismutase, catalase and cyclooxygenase, and
lipid peroxidation and DNA strand-break formation were measured in both the gills
and digestive gland after 7, 14 and 21 days of exposure to each experimental condition.
The results show that the biochemical parameters measured in both the mussels and
clams were more influenced by the reduced pH than by the contaminant or the pH*contaminant
interaction, although the biomarker variation patterns differed depending on the species
and tissues analysed. Generally, due to increases in its antioxidant defence, M. galloprovincialis
was more resistant than R. philippinarum to both diclofenac exposure and reduced pH.
Conversely, reduced pH induced a significant decrease in COX activity in both the
gills and digestive gland of clams, possibly resulting in the increased DNA damage
observed in the digestive gland tissue.