Rising levels of atmospheric carbon dioxide could be curbed by large-scale sequestration of CO 2 in the deep sea. Such a solution requires prior assessment of the impact of hypercapnic, acidic seawater on deep-sea fauna. Laboratory studies were conducted to assess the short-term hypercapnic tolerance of the deep-sea Tanner crab Chionoecetes tanneri, collected from 1000 m depth in Monterey Canyon off the coast of central California, USA. Hemolymph acidbase parameters were monitored over 24 h of exposure to seawater equilibrated with ~1% CO 2 (seawater P CO 2 6 torr or 0.8 kPa, pH 7.1), and compared with those of the shallow-living Dungeness crab Cancer magister. Short-term hypercapnia-induced acidosis in the hemolymph of Chionoecetes tanneri was almost uncompensated, with a net 24 h pH reduction of 0.32 units and a net bicarbonate accumulation of only 3 mM. Under simultaneous hypercapnia and hypoxia, short-term extracellular acidosis in Chionoecetes tanneri was completely uncompensated. In contrast, Cancer magister fully recovered its hemolymph pH over 24 h of hypercapnic exposure by net accumulation of 12 mM bicarbonate from the surrounding medium. The data support the hypothesis that deep-sea animals, which are adapted to a stable environment and exhibit reduced metabolic rates, lack the short-term acid -base regulatory capacity to cope with the acute hypercapnic stress that would accompany large-scale CO 2 sequestration. Additionally, the data indicate that sequestration in oxygen-poor areas of the ocean would be even more detrimental to deep-sea fauna.KEY WORDS: CO 2 · Deep sea · Physiology · Decapod crustacea · Acid-base regulation ·Chionoecetes tanneri · Cancer magister Resale or republication not permitted without written consent of the publisherThe ocean's large-scale absorption, as well as possible future anthropogenic sequestration of atmospheric CO 2 , will result in long-term acidification of the water. The deep-sea crab Chionoecetes tanneri (collected from Monterey Canyon at 1000 m depth) is unable to regulate extracellular pH during short-term CO 2 exposure. The results of Pane & Barry support the hypothesis that hypercapnia will have a profound physiological impact on deep-sea organisms.

We present evidence that Mg2+ antagonism is one mechanism for acute toxicity of waterborne Ni to Daphnia magna. Acutely, adult D. magna were exposed to either control or 694 microg Ni L(-1) as NiSO4 in moderately soft water (45 mg L(-1) as CaCO3; background Ni approximately 1 microg Ni L(-1)) for 48 h without feeding. Chronically, adults were exposed to either control or 131 microg Ni L(-1) for 14 days (fed exposure). These concentrations were approximately 65% and 12%, respectively, of the measured 48-h LC50 (1068 microg Ni L(-1)) for daphnid neonates in this water quality. The clearest effect of Ni exposure was on Mg2+ homeostasis, as whole-body [Mg2+] was significantly decreased both acutely and chronically by 18%. Additionally, unidirectional Mg2+ uptake rate (measured with the stable isotope 26Mg) was significantly decreased both acutely and chronically by 49 and 47%, respectively, strongly suggesting that Ni is toxic to D. magna due at least in part to Mg2+ antagonism. No impact was observed on the whole-body concentrations or unidirectional uptake rates of Ca2+ during either acute or chronic Ni exposure, while only minor effects were seen on Na+ and Cl- balance. No acute toxic effect was seen on respiratory parameters, as both oxygen consumption rate (MO2) and whole-body hemoglobin concentration ([Hb]) were conserved. Chronically, however, Ni impaired respiratory function, as both MO2 and [Hb] were significantly reduced by 31 and 68%, respectively. Acutely, Ni accumulation was substantial, rising to a plateau between 24 and 48 h of approximately 15 microg g(-1) wet weight--an increase of approximately 25-fold over control concentrations. Mechanisms of acute toxicity of Ni in D. magna differ from those in fish; it is likely that such mechanistic differences also exist for other metals.

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In a 21-d chronic toxicity test in which an F0 generation of Daphnia magna were exposed to waterborne Ni, the no-observable-effect concentration (for survival, reproduction, and growth) was 42 microg Ni L(-1), or 58% of the measured 21-d median lethal concentration (LC50) of 71.9 microg Ni L(-1) (95% confidence interval, 56.5-95.0). Chronic exposure to 85 microg Ni L(-1) caused marked decreases in survival, reproduction, and growth in F0 animals. In the F1 generation (daphnids born of mothers from the chronically exposed F0 generation), animals chronically exposed to 42 microg Ni L(-1) for 11 d weighed significantly less (20%) than controls, indicating increased sensitivity of F1 animals. Additionally, in this successive generation, significant decreases in whole-body levels of metabolites occurred following exposure to both 42 microg Ni L(-1) (decreased glycogen and adenosine triphosphate [ATP]) and 21 microg Ni L(-1) (decreased ATP). No significant changes were observed in whole-body total lipid, total protein, and lactate levels at any concentration. Whereas F1 neonates with mothers that were exposed to 21 microg Ni L(-1) showed increased resistance to acute Ni challenge, as measured by a significant (83%) increase in the acute (48-h) LC50, F1 neonates with mothers that were exposed to 42 microg Ni L(-1) were no more tolerant of acute Ni challenge than control animals were. Nickel accumulations in F1 animals chronically exposed to 21 and 42 microg Ni L(-1) were 11- and 18-fold, respectively, above control counterparts. The data presented suggest that chronic Ni exposure to two successive generations of D. magna lowered the overall energy state in the second generation. Whereas the quantity of neonates produced was not affected, the quality was; thus, environmentally meaningful criteria for regulating waterborne Ni concentrations in freshwater require consideration of possible multigenerational effects.