The response of two species of unionid mussels to extended exposure to elevated carbon dioxide

Hannan, Kelly D.; Jeffrey, Jennifer D.; Hasler, Caleb T.; Suski, Cory D.

doi:10.1016/j.cbpa.2016.07.009

Cited by 17 publications

(31 citation statements)

References 54 publications

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“…Hannan et al . (2016a, b) found that mussels experience acid–base regulation in response to short- and long-term exposures to elevated p CO 2 , and a stress response to long-term exposure to elevated p CO 2 . Previous studies on marine bivalves indicate that elevated p CO 2 causes internal acidosis (Michaelidis et al ., 2005; Bibby et al ., 2008) that is often buffered by increasing HCO 3 − in the fluids (Pörtner et al ., 2004).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies on marine bivalves indicate that elevated p CO 2 causes internal acidosis (Michaelidis et al ., 2005; Bibby et al ., 2008) that is often buffered by increasing HCO 3 − in the fluids (Pörtner et al ., 2004). Both marine (Michaelidis et al ., 2005) and freshwater mussels (Hannan et al ., 2016a, b) can increase haemolymph HCO 3 − by using CaCO 3 released from the shell as a result of decreased pH and elevated CO 2 (i.e. increases both haemolymph HCO 3 − and Ca 2+ ) or by reducing the activity of the Cl − –HCO 3 − exchanger to retain HCO 3 − at the cost of Cl − uptake (Byrne and Dietz, 1997; Hannan et al .…”

Section: Introductionmentioning

confidence: 99%

“…increases both haemolymph HCO 3 − and Ca 2+ ) or by reducing the activity of the Cl − –HCO 3 − exchanger to retain HCO 3 − at the cost of Cl − uptake (Byrne and Dietz, 1997; Hannan et al . 2016a, b). Another strategy to buffer acidosis is to alter the activity of Na + –H + exchangers to increase removal of H + ions, thus also increasing Na + uptake (Byrne and Dietz, 1997; Lannig et al ., 2010, Hannan et al .…”

Section: Introductionmentioning

confidence: 99%

“…2016a, b). Another strategy to buffer acidosis is to alter the activity of Na + –H + exchangers to increase removal of H + ions, thus also increasing Na + uptake (Byrne and Dietz, 1997; Lannig et al ., 2010, Hannan et al . 2016b).…”

Section: Introductionmentioning

confidence: 99%

“…Exposure to a chronic elevation in p CO 2 also appears to initiate the general stress response in mussels, because a decrease in haemolymph Mg 2+ and an increase in haemolymph glucose have been observed in unionid mussels (Hannan et al . 2016a, b). More importantly, previous studies (i.e.…”

Section: Introductionmentioning

confidence: 99%

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Physiological responses of three species of unionid mussels to intermittent exposure to elevated carbon dioxide

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Physiological responses of three species of unionid mussels to intermittent exposure to elevated carbon dioxide

et al. 2016

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Chronic exposure of a freshwater mussel to elevated pCO₂: Effects on the control of biomineralization and ion‐regulatory responses

Jeffrey

Hannan

Hasler

et al. 2017

Enviro Toxic and Chemistry

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Freshwater mussels may be exposed to elevations in mean partial pressure of carbon dioxide (pCO ) caused by both natural and anthropogenic factors. The goal of the present study was to assess the effects of a 28-d elevation in pCO at 15 000 and 50 000 μatm on processes associated with biomineralization, ion regulation, and cellular stress in adult Lampsilis siliquoidea (Barnes, 1823). In addition, the capacity for mussels to compensate for acid-base disturbances experienced after exposure to elevated pCO was assessed over a 14-d recovery period. Overall, exposure to 50 000 μatm pCO had more pronounced physiological consequences compared with 15 000 μatm pCO . Over the first 7 d of exposure to 50 000 μatm pCO , the mRNA abundance of chitin synthase (cs), calmodulin (cam), and calmodulin-like protein (calp) were significantly affected, suggesting that shell formation and integrity may be altered during pCO exposure. After the removal of the pCO treatment, mussels may compensate for the acid-base and ion disturbances experienced during pCO exposure, and transcript levels of some regulators of biomineralization (carbonic anhydrase [ca], cs, cam, calp) as well as ion regulation (na -k -ATPase [nka]) were modulated. Effects of elevated pCO on heat shock protein 70 (hsp70) were limited in the present study. Overall, adult L. siliquoidea appeared to regulate factors associated with the control of biomineralization and ion regulation during and/or after the removal of pCO exposure. Environ Toxicol Chem 2018;37:538-550. © 2017 SETAC.

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Temperature‐Related Responses of an Invasive Mussel and 2 Unionid Mussels to Elevated Carbon Dioxide

Waller

Bartsch

Lord

et al. 2020

Enviro Toxic and Chemistry

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Zebra mussels (Dreissena polymorpha) have exacerbated the decline of native freshwater mussels (order Unionida) in North America since their arrival in the 1980s. Options for controlling invasive mussels, particularly in unionid mussel habitats, are limited. Previously, carbon dioxide (CO 2) showed selective toxicity for zebra mussels, relative to unionids, when applied in cool water (12°C). We first determined 96-h lethal concentrations of CO 2 at 5 and 20°C to zebra mussels and responses of juvenile plain pocketbook (Lampsilis cardium). Next, we compared the time to lethality for zebra mussels at 5, 12, and 20°C during exposure to partial pressure of CO 2 (PCO 2) values of 110 to 120 atm (1 atm = 101.325 kPa) and responses of juvenile plain pocketbook and fragile papershell (Leptodea fragilis). We found efficacious CO 2 treatment regimens at each temperature that were minimally lethal to unionids. At 5°C, plain pocketbook survived 96-h exposure to the highest PCO 2 treatment (139 atm). At 20°C, the 96-h lethal concentration to 10% of animals (LC10) for plain pocketbook (173 atm PCO 2 , 95% CI 147-198 atm) was higher than the LC99 for zebra mussels (118 atm PCO 2 , 95% CI 109-127 atm). Lethal time to 99% mortality (LT99) of zebra mussels in 110 to 120 atm PCO 2 ranged from 100 h at 20°C to 300 h at 5°C. Mean survival of both plain pocketbook and fragile papershell juveniles exceeded 85% in LT99 CO 2 treatments at all temperatures. Short-term infusion of 100 to 200 atm PCO 2 at a range of water temperatures could reduce biofouling by zebra mussels with limited adverse effects on unionid mussels.

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The response of two species of unionid mussels to extended exposure to elevated carbon dioxide

Cited by 17 publications

References 54 publications

Physiological responses of three species of unionid mussels to intermittent exposure to elevated carbon dioxide

Physiological responses of three species of unionid mussels to intermittent exposure to elevated carbon dioxide

Chronic exposure of a freshwater mussel to elevated pCO₂: Effects on the control of biomineralization and ion‐regulatory responses

Temperature‐Related Responses of an Invasive Mussel and 2 Unionid Mussels to Elevated Carbon Dioxide

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The response of two species of unionid mussels to extended exposure to elevated carbon dioxide

Cited by 17 publications

References 54 publications

Physiological responses of three species of unionid mussels to intermittent exposure to elevated carbon dioxide

Physiological responses of three species of unionid mussels to intermittent exposure to elevated carbon dioxide

Chronic exposure of a freshwater mussel to elevated pCO2: Effects on the control of biomineralization and ion‐regulatory responses

Temperature‐Related Responses of an Invasive Mussel and 2 Unionid Mussels to Elevated Carbon Dioxide

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Chronic exposure of a freshwater mussel to elevated pCO₂: Effects on the control of biomineralization and ion‐regulatory responses