To the best of my knowledge, this is the first study to quantify the effect of ocean acidification and warming on skeletal mineralization of a breathing vertebrate waterfall. Overall, simulated ocean acidification increased the density of hydroxyapatite in major components of the elasmobranch skeleton. This result is in stark contrast to most previous studies in which the calcium carbonate exoskeleton of marine invertebrates showed decreased mineralization with ocean acidification. Although some invertebrate species are able to maintain a high pH at the site of calcification to maintain constant calcification rates, this comes at a cost. In a review of more than 40 studies on the effects of ocean acidification on molluscs, the emerging pattern is that shell acidification is reduced at low pH levels. When the shell or skeleton of calcifying invertebrates is thinner and therefore more susceptible to fractures, the predatory pressure for these animals increases. While in marine invertebrates the reduction of CaCO3 as a consequence of low pH is due to a relatively simple chemical reaction (i.e. H+ precipitates Ca2+ in the skeleton), the possible mechanism underlying the increase in HA in the vertebrate skeleton requires further investigation. Here, I outline some likely mechanisms responsible for increased mineralization in the skeleton of elasmobranch fishes. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay First, CO2 is a poison, known to affect the neurotransmitter responsible for regulating Ca2+ deposition. In particular, otolith growth and calcification have been shown to be regulated at the neural level. A study of the neuronal control of calcium supply in the inner ear of cichlids showed significant precipitation of accumulated calcium in the macular tight junctions. In fact, it is hypothesized that neuronal activity is responsible for the release of calcium into the endolymph of the otolith, altering the permeability of these junctions. Although cartilage tissue is not deeply innervated, sensory nerve fibers are shown to be in contact with the outer layer of cartilage. Neuronal activity, therefore, can influence the mineralization of the cartilaginous matrix. Another likely mechanism responsible for increased cartilage mineralization with ocean acidification may be linked to the physiological response of fish when affected by fluid acidosis. Fish are able to compensate for changes in the acid-base state in their extracellular body fluids by reducing acidosis with bicarbonate and non-bicarbonate buffers. In fact, fish gills respond quite quickly to acidification by increasing phosphate in body fluids. In skates, the increase in buffer capacity is proportional to the decrease in pH in the water, and skates can achieve acidity compensation within 24 hours. Perhaps this exceptional buffering capacity may have the side effect of accumulating phosphate in the blood and tissues, including cartilage. Therefore, CO2-induced acidosis may indirectly contribute to the increase in HA skeletal density by increasing the phosphate concentration in fish blood. An increased density of HA in simulated acidified oceans is, at first, an unexpected result when compared with the results of studies on calcifying invertebrates, but a plausible consequence of the effective buffering capacity of elasmobranchs during acidosis. In fact, the dentils.