chemical and biological effects on fishes in a high co 2 world a. ishimatsu, m. hayashi, k. -s. lee...
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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