Climate Change and Ocean Acidification: Are We Just Treating The Symptoms?

The human caused rise in atmospheric greenhouse gases has been seen as the driver of both climate change and ocean acidification. However recent peer reviewed papers show that, while GHG emissions are part of the problem, the primary driver of both climate change and ocean acidification is human caused ecological degradation. Curbing greenhouse gas emissions, to date, has been an abject failure but addressing ecological degradation within the remaining time frame is safe and achievable.

Modeling Carbon Budgets and Acidification in the Mediterranean Sea Ecosystem Under Contemporary and Future Climate

We simulate and analyze the effects of a high CO2 emission scenario on the Mediterranean Sea biogeochemical state at the end of the XXI century, with a focus on carbon cycling, budgets and fluxes, within and between the Mediterranean sub-basins, and on ocean acidification. As a result of the overall warming of surface water and exchanges at the boundaries, the model results project an increment in both the plankton primary production and the system total respiration. However, productivity increases less than respiration, so these changes yield to a decreament in the concentrations of total living carbon, chlorophyll, particulate organic carbon and oxygen in the epipelagic layer, and to an increment in the DIC pool all over the basin. In terms of mass budgets, the large increment in the dissolution of atmospheric CO2 results in an increment of most carbon fluxes, including the horizontal exchanges between eastern and western sub-basins, in a reduction of the organic carbon component, and in an increament of the inorganic one. The eastern sub-basin accumulates more than 85% of the absorbed atmospheric CO2. A clear ocean acidification signal is observed all over the basin, quantitatively similar to those projected in most oceans, and well detectable also down to the mesopelagic and bathypelagic layers.

Mussels repair shell damage despite limitations imposed by ocean acidification

Bivalves frequently withstand shell boring attempts by predatory gastropods that result in shell damage that must be quickly repaired to ensure survival. While the processes that underlie larval shell development have been extensively studied within the context of ocean acidification (OA), it remains unclear whether shell repair is impaired by elevated pCO2. To better understand the stereotypical shell repair process, we monitored mussels (Mytilus edulis) with sublethal shell damage within both field and laboratory conditions to characterize the deposition rate, mineral composition, and structural integrity of repaired shell. These results were then compared with a laboratory experiment wherein mussels (Mytilus trossulus) repaired shell damage in one of seven pCO2 treatments (400–2500 µatm). Shell repair proceeded through four distinct stages; shell damage was first covered with an organic film, then mineralized over the course of weeks, acquiring the appearance of nacre after 8 weeks. OA did not impact the ability of mussels to close drill holes, nor the strength or density of the repaired shell after 10-weeks, as measured through mechanical testing and µCT analysis. However, as mussels progressed through each repair stage, significant interactions between pCO2, the length of exposure to treatment conditions, and the strength, inorganic content, and physiological condition of mussels within OA treatments were observed. These results suggest that, while OA may not prevent mussels from repairing shell damage, sustained exposure to elevated pCO2 may induce physiological stress responses that impose energetic constraints on the shell repair process.

Effects of Ocean Acidification on Molting, Oxidative Stress, and Gut Microbiota in Juvenile Horseshoe Crab Tachypleus tridentatus

Anthropogenic elevation of atmospheric carbon dioxide (CO2) drives global-scale ocean acidification (OA), which has aroused widespread concern for marine ecosystem health. The tri-spine horseshoe crab (HSC) Tachypleus tridentatus has been facing the threat of population depletion for decades, and the effects of OA on the physiology and microbiology of its early life stage are unclear. In this study, the 1st instar HSC larvae were exposed to acidified seawater (pH 7.3, pH 8.1 as control) for 28 days to determine the effects of OA on their growth, molting, oxidative stress, and gut microbiota. Results showed that there were no significant differences in growth index and molting rate between OA group and control group, but the chitinase activity, β-NAGase activity, and ecdysone content in OA group were significantly lower than those of the control group. Compared to the control group, reactive oxygen species (ROS) and malondialdehyde (MDA) contents in OA group were significantly increased at the end of the experiment. Superoxide dismutase (SOD), catalase (CAT), and alkaline phosphatase (AKP) activities increased first and then decreased, glutathione peroxidase (GPX) decreased first and then increased, and GST activity changed little during the experiment. According to the result of 16S rRNA sequencing of gut microbiota, microbial-mediated functions predicted by PICRUSt showed that “Hematopoietic cell lineage,” “Endocytosis,” “Staphylococcus aureus infection,” and “Shigellosis” pathways significantly increased in OA group. The above results indicate that OA had no significant effect on growth index and molting rate but interfered with the activity of chitinolytic enzymes and ecdysone expression of juvenile horseshoe crabs, and caused oxidative stress. In addition, OA had adverse effects on the immune defense function and intestinal health. The present study reveals the potential threat of OA to T. tridentatus population and lays a foundation for the further study of the physiological adaptation mechanism of juvenile horseshoe crabs to environmental change.