Chemical and Biological Effects Chemical and Biological Effects on Fishes in a High COon Fishes in a High CO22 World World

A. Ishimatsu, M. Hayashi, K. -S. Lee (Marine A. Ishimatsu, M. Hayashi, K. -S. Lee (Marine Research Institute, Nagasaki University)Research Institute, Nagasaki University)

T. Kikkawa (Marine Ecology Research Laboratory)T. Kikkawa (Marine Ecology Research Laboratory)

J. Kita (Research Institute of Innovative Technology J. Kita (Research Institute of Innovative Technology for the Earth)for the Earth)

Comparison of body fluid Comparison of body fluid PPCOCO22 in air- and in air- and

water-breatherswater-breathers

Air breathers

Water breathers

CO2

CO2

O2

O2

Air

Lung

Blood

Capillaries

Tissues

Blood

Capillaries

Gill

Water

Par

tial P

ress

ure

Par

tial P

ress

ure

Solubility (M/torr) at 20 C

O2 CO2

Air 54.7 54.7

Sea water 1.5 43.7

Arterial Blood PCO2

Air-breathers* 15 - 40 torr

Water-breathers 1 – 4 torr

PCO2 of air/water 0.2 torr

COCO22 reactions reactions and buffering in animal bodyand buffering in animal body

CO2 H2CO3 H+ + HCO3-

HCO3- H+ + CO3

2-

H+ + B- HBHCO3-

Cl-

Water

Fish Body

pH

Log Exposure Time (hrs)

Auerbach et al.1997

CA

LC90

LC0LC50

96 hrs

Na+

H+

Gills

Seawater Fish Freshwater Fish

Sea waterOsmolarity 1,000 mOsm/LNa+ 460 mmol/LCl- 550 mmol/L

BloodOsmolarity 330 mOsm/LNa+ 200 mmol/LCl- 160 mmol/L

Fresh waterOsmolarity 1 mOsm/LNa+ 0.08 mmol/LCl- 0.05 mmol/L

Drink SW

Excrete NaCl (Chloride cell)

BloodOsmolarity 300 mOsm/LNa+ 150 mmol/LCl- 120 mmol/L

Osmo- and iono-regulation in seawater and freshwater fish

NaClH2O

Take up NaCl Large volume of urine

H2O NaCl

Active transport

Passive transport

Differences in Biological Effects of CODifferences in Biological Effects of CO22 and H and H++ in in

WaterWater

Effects of CO2 Ocean Sequestration on Fishes

Comparison of fish mortality by CO2 and acid exposures

Lethal effect of CO2 and acid on embryos ( N = 5) and larvae (N = 3) of silver seabream at two pH conditions. Exposure period: embryo 360 min, larva 24 h*Significant difference between groups.

Kikkawa et al. (2004): Marine Pollution Bulletin 48, 108.

Acid-base responses to COAcid-base responses to CO22 and acid seawater in and acid seawater in

bastard halibut, bastard halibut, Paralichthys olivaceusParalichthys olivaceus

pH

a

6.8

7.2

7.6

Time (hr)

0 4 8 24 48 72

[ H

CO

3- ]p

(m

M)

0

20

40

60

80

Seawater was acidified by either bubbling with 5% CO2 in air ( ) or adding sulphuric acid ( ) to samepH of 6.2.

　 CO2 　 Exposure

Acid Exposure

pH = pK’ + log[HCO3

-]

x PCO2

[ H

CO

3- ]p

(m

M)

0

20

40

60

80

[ C

l- ]p

(m

M)

140

160

180

200

220

Effects of high COEffects of high CO22 plasma ions and chloride cells of plasma ions and chloride cells of

marine fishesmarine fishes

Gill chloride cells in bastard halibut

PCO2 37 torr Initial

24 hr

0 24 48 72

Japanese amberjack

PCO2 7 torr

22 torr37 torr

Effects of high COEffects of high CO22 on ion fluxes of on ion fluxes of

freshwater rainbow troutfreshwater rainbow trout

Hypercapnia

Efflux(Blood to water)

Influx(Water to blood)

Kidney

Gills

Hyperoxia-induced hypercapnia. Wood et al. (1984)

Control Recovery

Hypercapnia

Na+

Cl-

K+

Gills

Efflux

Influx

Control Recovery

Effect of acid water on ion fluxes of freshwater Effect of acid water on ion fluxes of freshwater rainbow troutrainbow trout

[Ca2+] 0.24 mEq/L, McDonald et al. 1983

Unidirectionalefflux

Unidirectionalinflux

Eq/

kg/h

r

Net flux

Na+ Cl-H+

Differences in Biological Effects of CODifferences in Biological Effects of CO22 and H and H++

Physiological responses to COPhysiological responses to CO22 and acids are different. and acids are different.

COCO22 readily diffuses into the body, and acidifies body flui readily diffuses into the body, and acidifies body flui

d of both intracellular and extracellular compartments. Fid of both intracellular and extracellular compartments. Fish kill mechanism by high COsh kill mechanism by high CO22 is not fully understood. is not fully understood.

Acid exposure inhibits active ion transports across the gilAcid exposure inhibits active ion transports across the gills, and increased passive ion movements.ls, and increased passive ion movements. 　　 The main cThe main cause of fish kill by acid exposure is thought not to be bloause of fish kill by acid exposure is thought not to be blood acidification but cardiac failure by hemoconcentration.od acidification but cardiac failure by hemoconcentration.

Differences in Biological Effects of CODifferences in Biological Effects of CO22 and H and H++

in Waterin Water

Effects of CO2 Ocean Sequestration on Fishes

COCO22 sequestration by the moving-ship method sequestration by the moving-ship method

Depth ca. 2,000-2,500 mTemperature ca. 2-3 C

Sato and Sato 2002

Initial exposure to high CO2 levelsfollowed by rapid decreases in CO2.

45

147

15

>377

PCO2

(torr)

Car

dia

c o

utp

ut

(m

l/min

/kg

)

0

40

80

Hea

rt R

ate

(b

eats

/min

)

40

80

120

Time (h)

0 2 4 6 8 24 48 72

Blo

od

Pre

ssu

re (

cmH

2O

)

0

40

80

120

10 20 30 40

Car

diac

out

put

(ml/m

in/k

g)

0

60

0

180

Blo

od p

ress

ure

(cm

H2O

)

1% CO2

37 torr

Effects of CO2 on cardiovascular system of amberjack

PCO2 7 torrPCO2 37 torr

Time (min)0 10 20 30

Fish mortality by unsteady exposures to COFish mortality by unsteady exposures to CO22

Effect of step-increase CO2 exposures on fish mortality: Japanese sillago1 kPa = 7.5 torr

PC

O2 (kP

a)

No mortality after pre-exposureto 1 kPa

ca. 100% mortality at 5 kPa

Mortality (%

)

Sudden drop of PCO2 quicklykilled the fish.

High Pressure Chamber (Max 50 MPa)

Known distribution depth 400-800 mWater temperature 2 C

Careproctus trachysoma: Liparididae

Experiments on deep-sea fish under high pressuresExperiments on deep-sea fish under high pressures

SummarySummary When tested at the same pH, COWhen tested at the same pH, CO22 and acids produce different effect and acids produce different effect

s on fish. Data on mineral acids cannot be used to evaluate effects s on fish. Data on mineral acids cannot be used to evaluate effects of COof CO22..

Still, useful information may be obtained from the literature on the effStill, useful information may be obtained from the literature on the effects of water acidification on fishes, which has already made great iects of water acidification on fishes, which has already made great impacts on freshwater ecosystems. mpacts on freshwater ecosystems.

Fish kill mechanism by lethal levels of COFish kill mechanism by lethal levels of CO22 must be clarified, particul must be clarified, particularly focusing on the role of cardiac response.arly focusing on the role of cardiac response.

Effects of ocean sequestration need to be investigated; on deep-sea Effects of ocean sequestration need to be investigated; on deep-sea animals, under high pressures, at low temperatures, and in unsteadanimals, under high pressures, at low temperatures, and in unsteady COy CO22 conditions. conditions.

Long-term effects at sublethal COLong-term effects at sublethal CO22 levels on fishes should also be in levels on fishes should also be investigated.vestigated.

COCO22 reception in fish reception in fish

PCO2 2 20 200 torr

PCO2 0.6 6.8 29 111 torr

Eel palatine CO2 receptors

pH of the test solution was 5.0Test solution acidified by HCl to pH 5.0 gave no response.

Yoshii et al. (1980)

0.5 torr

Effects of long-term COEffects of long-term CO22 exposure on growth of Japanese sillago exposure on growth of Japanese sillago

Low 3 torrMid 5 torrHi 9 torr

WT 25 C34 psuAlkalinity 2.3 mEq/L1 atm

Changes in arterial pH and mortality during Changes in arterial pH and mortality during hypercapnia in bastard halibuthypercapnia in bastard halibut

* *

pH

a

6.8

7.2

7.6

Time (h)

0 4 8 24 48 72

Su

rviv

al r

ate

(%)

0

20

40

60

80

100

*

*

*

*

* **

*

PCO2 7 torr

22 torr

37 torr

Effect of long-term COEffect of long-term CO22 exposure on fish growth exposure on fish growth

Species

Seawater

%BW

of Cont

PCO2

(torr)

Temp

(C)

Duration

(days)

Water

pH

Atlantic salmon 63 20 15-16 43 6.4

Spotted wolffish 64 20 6 70 6.5

Fresh water

Rainbow trout* 52 17 9 275 6.2-6.3

Rainbow trout** 76 17 9 275 6.2-6.3

White sturgeon 62 20 19 28 7.0AS: Fivelstad et al. (1998), SW: Foss et al. (2003), RT: Smart et al. (1979), WS: Crocker and Cech (1996).

*Fed normal mineral diet, **Fed low mineral diet

Branchial Ion Loss

Extracellular to Intracellular Fluid Shift

Reduced Plasma Volume

Red Blood Cell Swelling

Cardiac Failure?

Increased BloodViscosity

Increased BloodPressure

Adrenergic stimulation

CO2

Exposure

Cardiac output Decreases

Plasma Ion Imbalance Cl- DecreasesHCO3

- IncreasesNa+ Increases

Blood Pressure Increases

Body Fluid Acidification

H+ inhibits ion transport at the gills surface.

H+ Exposure

pH compensation

Body fluid acidificationmay be unimportant asa direct cause of death.

CO2 readily penetrates into the bodyto affect physiological functions.

Locomotor responses to COLocomotor responses to CO22 and H and H++

Avoided

Attracted

11 torr84

2

PCO2 0.2-1.2 torr

CO2 (carbonate water)

HCl (decarbonated water)

Arctic char (Jones et al. 1985)Avoidance threshold PCO2 2-4 torr