Ocean acidification is elicited by anthropogenic carbon dioxide emissions and resulting oceanic uptake of excess CO2 and might constitute an abiotic stressor powerful enough to alter marine ecosystem structures. For surface waters in gas-exchange equilibrium with the atmosphere, models suggest increases in CO2 partial pressure (pCO2) from current values of ca. 390 μatm to ca. 700–1,000 μatm by the end of the century. However, in typically unequilibrated coastal hypoxic regions, much higher pCO2 values can be expected, as heterotrophic degradation of organic material is necessarily related to the production of CO2 (i.e., dissolved inorganic carbon). Here, we provide data and estimates that, even under current conditions, maximum pCO2 values of 1,700–3,200 μatm can easily be reached when all oxygen is consumed at salinities between 35 and 20, respectively. Due to the nonlinear nature of the carbonate system, the approximate doubling of seawater pCO2 in surface waters due to ocean acidification will most strongly affect coastal hypoxic zones as pCO2 during hypoxia will increase proportionally: we calculate maximum pCO2 values of ca. 4,500 μatm at a salinity of 20 (T = 10 °C) and ca. 3,400 μatm at a salinity of 35 (T = 10 °C) when all oxygen is consumed. Upwelling processes can bring these CO2-enriched waters in contact with shallow water ecosystems and may then affect species performance there as well. We conclude that (1) combined stressor experiments (pCO2 and pO2) are largely missing at the moment and that (2) coastal ocean acidification experimental designs need to be closely adjusted to carbonate system variability within the specific habitat. In general, the worldwide spread of coastal hypoxic zones also simultaneously is a spread of CO2-enriched zones. The magnitude of expected changes in pCO2 in these regions indicates that coastal systems may be more endangered by future global climate change than previously thought.

Future ocean acidification will be amplified by hypoxia in coastal habitats

Predicting the impact of ocean acidification on benthic biodiversity: What can animal physiology tell us?

Organisms living in coastal waters, and especially estuaries, have long been known to have behavioral or physiological mechanisms that enable them toexist in water containing low amounts of oxygen. However, the respiratory consumption of oxygen that generates hypoxia is also responsible for producing significant amounts of carbon dioxide. An elevation of carbon dioxide pressure in water will cause a significant acidosis in most aquatic organisms. Thus, the combination of low oxygen and elevated carbon dioxide that occurs in estuaries represents a significant environmental challenge to organisms living in this habitat. Organisms may maintain oxygen uptake in declining oxygen conditions by using a respiratory pigment and/or by making adjustments in the convective flow of water and blood past respiratory surfaces ( i.e. , increase cardiac output and ventilation rate). Severe hypoxia may result in an organism switching partially or completely to anaerobic biochemical pathways to sustain metabolic rate. There is also evidence to suggest that organisms lower their metabolism during hypoxic stress. Elevated water CO2 (hypercapnia) produces an acidosis in the tissues of organisms that breathe it. This acidosis may be wholly or partially compensated ( i.e. , mechanisms return pH to pre-exposure levels), or may be uncompensated. Some studies have examined the effects on organisms of exposure simultaneously to hypoxia and hypercapnia. This article reviews some of the specific adaptations and responses of organisms to low oxygen, to high carbon dioxide, and to the cooccurrence of low oxygen and high carbon dioxide

The challenges of living in hypoxic and hypercapnic aquatic environments

Respiratory responses of the salt marsh animals, Fundulus heteroclitus, Leiostomus xanthurus, and Palaemonetes pugio to environmental hypoxia and hypercapnia and to the organophosphate pesticide, azinphosmethyl☆

Hypoxia can have profound effects on individual organisms. This chapter focuses on the mechanisms different kinds of animals possess to avoid, tolerate, and adapt to low levels of oxygen in water; selected examples illustrate these mechanisms. While some organisms can detect and avoid hypoxic water, avoidance is not always possible, especially in the case of sessile organisms. When an organism cannot avoid hypoxia, its response may depend on the intensity and thz duration of the bout of low oxygen. Examples of responses to hypoxia include a depression in feeding as well as a decrease in molting and growth rates. During acute exposures to hypoxia some organisms can maintain aerobic metabolism by making effective use of a respiratory pigment, or increasing ventilation rates, or increasing the flow of blood past the respiratory surfaces or combinations of all three. Responses to chronic hypoxia are different and include the production of greater quantities of respiratory pigment and changing the structure of the pigment to one with an adaptive higher oxygen affinity. Many organisms respond to hypoxia by switching fiom aerobic to anaerobic metabolism and some simply reduce their overall metabolism. Hypoxia is often accompanied by hypercapnia (an elevation in water C02), which produces an acidification of the body tissues, including the blood, and has physiological implications that can also be profound and separate from the effects of low oxygen. Finally, there is evidence that hypoxia can inhibit immune responses, causing greater mortality than would otherwise occur when organisms are challenged with a pathogen.

Physiological Responses to Hypoxia

The effect of CO2 on hemocyanin-oxygen binding is not generally related to the effect of Cl-. Some hemocyanins respond to both and some to either one alone. The direction of the responses of O2 affinity of the various hemocyanins to CO2 is poorly correlated with the direction of responses to other effectors. The influence of CO2 on Busycon and Limulus hemocyanins reaches its maximum at high pH. Since the effect can be abolished by restoring divalent cation activities to the control levels prior to the addition of CO2, we suggest that the effect is not specific but rather indirect, by the pairing of the allosteric effectors Ca+2 and Mg+2 with the CO2 anions. In contrast the effect of CO2 on crustacean hemocyanins is greaterat low pH and it can be enhanced by maintaining HCO3- levels within narrow limits and permitting PCO2 to vary by a large factor. This finding suggests that the effective species is molecular CO2. While a influences only oxygen affinity, CO2 may influence cooperativity as well. Indifferen...

Louis E. Burnett

Papers

THE CO2 SENSITIVITY OF THE HEMOCYANINS AND ITS RELATIONSHIP TO Cl- SENSITIVITY