; Osmoregulation in fish and pollution by heavy metals
Learning Center
Plans & pricing Sign in
Sign Out
Your Federal Quarterly Tax Payments are due April 15th Get Help Now >>

Osmoregulation in fish and pollution by heavy metals


The water and ion balance of an aquatic animal is important for optimal physiological functioning, which is within rather narrow limits (Schmidt-Nielsen, 1997). The balance is strike by ionic and osmotic regulation of animal’s body fluid with respect to its external environment.

More Info
  • pg 1
       The water and ion balance of an aquatic animal is important for optimal physiological
functioning, which is within rather narrow limits (Schmidt-Nielsen, 1997). The balance is strike
by ionic and osmotic regulation of animal’s body fluid with respect to its external environment.
Osmoregulation is the process of regulating organism’s osmotic pressure of body fluid by
movement of solutes across biological membrane to control osmotic gradient. The process
generally involves ionic and osmotic regulation by (1) uptake of ions and (1) excretion of
metabolic waste products, toxic compounds, excess water and salt ion.
        Aquatic vertebrate has adapted different balancing strategies to survive different water
environment. There are two main strategies for osmotic regulation. Firstly, osmoconformer fish,
like marine elasmobranch and cyclostomes, strive to remain isosmotic gradient with the medium.
Secondly, osmoregulator fish, like the teleost, is able to regulate osmotic concentration of body
fluid regardless of external concentration changes.
        Fish gill epithelium, kidney, guts are the main sites of osmoregulation for gas exchange,
ionic regulation, acid-base balance, and nitrogenous waste excretion (Evans, 1987). Epithelial
tissues possess ion transporters that allow osmoregulation to occur. The type of transporters are:
Na+/K+ and H+ ATPase, various single ion channels, electroneutral cotransporters (Na+-K+-2Cl-
and K+-Cl- cotransporters) and, electroneutral exchangers (Na+/H+, NH4+/ H+ and Cl-/ HCO3-
exchangers). Osmoregulatory process is controlled by hormones, which regulate activity of ion
transporters at epithelium cells (Bern and Madsen, 1992).
        The fish gill lamellae is made up of mitochondria-rich chloride cells amongst
mitochondria-rich and low-mitochondrial-content pavement cells. Both mitochondria-rich
chloride and pavement cells participate in transport functions of the gills. Water salinity governs
the direction of ions and water transport in the gills. As teleost fishes maintain the NaCl content
of their body fluids at approximately 40% that of seawater, marine teleost is hyperosmotic and
freshwater teleost is hyposmotic to their respective environment (Evans, 1987).
        Freshwater fish, being hyperosmotic to its environment, need to take up ion from the
environment to maintain body fluid osmolity against steep electrochemical gradients. Pavement
cells absorb Na+ using ion channel and enhanced using H+ ATPase to create decrease pH, which
increases the electrochemical driving force for Na+ transport. Chloride cell imports Cl-/ HCO3-
exchanger, with Ca2+ uptake through ion channel. Both types of cells requires carbonic
anhydrase to produce HCO3- for changing pH or as counter ions.
       On the contrary, marine fish, being hyposmotic to seawater, need to prevent influx of
ions and excessive water loss. Marine teleost achieves osomoregulation by drinking seawater
constantly to replace water loss and excreting excess ions through Cl- ion channels and
paracellular transport of Na+ (Moyes, 2006).
      Interestingly, diadromous, catadromous and anadromous fish species that need to adapt
between seawater and freshwater environment in their life history, undergo smoltification to
remodel ion transporter types in the epithelium at the gills, kidney and gut using specific
hormones for difference in environment osmolarity (Moyes, 2006).
Heath (1984) found that freshwater fish exposed to copper experienced decreased plasma
osmolality as the uptake of sodium and chloride ions is greatly reduced by high concentration of
Cu in freshwater fish gills (McDonald et. al., 1988). The osmoregulation is upset by the rapid
decrease in plasma osmolality. Reduction is tested in vivo that enzyme Na+/K+ ATPase in the gill
tissue is inhibited (Lorz and McPherson, 1976). Coho salmon was able to adapt to prolonged and
gradual increase in concentration of copper, starting in sublethal concentration (Buckley et al.,

For anadromous Coho salmon (Onchorhynchus kisutch), chronic exposure to Cu during
migration result in organism becoming unable to osmoregulate because of reduction in activity
of Na+/K+ ATPase in the gills, which is activated during migration to seawater (Lorz and
McPherson, 1976). That might reduce survival of the salmon during migration.

Studies of Spry and Wood (1984 and 1985) showed that non-lethal dose of zinc causes drop in
intracellular calcium and efflux of sodium ions lead to osmoregulatory malfunction over long
period of time and to a physiological adaptation. Due to the efflux of sodium ions, the uptake of
ions from the water resulted in a raise in the rainbow trout’s gills ATPase activity (Watson and
Beamish, 1980). In seawater killifish, the zinc (and copper) restrains chloride transport at
concentration of 4x10-5 M and only the ATPase molecules at the basal area of the chloride cells
(Wilson and Taylor, 1993). Hence, that explains the low sensitivity of seawater-adapted fish to
zinc and copper (very high concentration needed to be lethal).

Young coho salmon in freshwater was exposed to 1-4weeks of chromium at the concentration of
0.5 mg Cr/L and released into seawater (Sugatt, 1980). The young fish survived the first week
but there was high mortality on the second week. When control fish was compared with Cr-
exposed fish, Cr-exposed has larger and longer increase in osmolality, hence the process of
adaptation to seawater was hindered by Cr. Similar to copper, Cr inhibit the enzyme Na+/K+
ATPase in the gill tissue (Lorz and McPherson, 1976).

The effect of Al depends on the pH and calcium content in the water. When exposed to Al
acutely to Al at pH 4 to 4.5, the rainbow and brook trout experienced inhibition of Na+/K+
ATPase in the gills reduced sodium and chloride uptake with increased passive efflux of ions
(Staurnes et al.,1984; Booth et al., 1988). When pH is increased to 4.5 to 5, the trout was known
to have more adverse effect at pH4.8 where it experience hypoxic condition coupled with loss of
ions (Malt and Weber, 1988). Interestingly, upon acclimation with chronic exposure to Al, trout
has physiological and histological adaptations that allow the gill cells to increase have greater
association with calcium and lead to reduce Al binding at the surface of the cells (Heath, 1995).

As mentioned earlier, marine fish rely on the gills to excrete excess sodium chloride. However,
the in vitro metabolic rate of this tissue can be decreased by 50% without any effect on the
plasma electrolytes (Thurberg and Dawson, 1974). Therefore, cadmium seems to affect other
osmoregulatory organs such the kidneys rather than the gills.
A relatively high concentration is required to change the concentration of plasma sodium and
chloride in marine fishes. How cadmium affects the kidneys of marine fish was studied by
Larsson et al. in 1981 where he investigated the effect of cadmium exposure on the flounder,
Platichthys flesus, a species of fish living in brackish water. The environment the flounder lives
in contains a higher concentration of magnesium but a lower concentration of potassium and
calcium than the blood plasma. Therefore, there is a net diffusion of magnesium into the blood
plasma and a net diffusion of potassium and calcium ions out. Excess magnesium is normally
excreted by the kidney (Heath, 1997). A rise in magnesium concentration in the plasma in
response to cadmium is an indicator of the kidney’s failure to excrete magnesium. The kidney is
therefore a target organ of cadmium and this heavy metal causes histological damage to the
kidney. Cadmium affects the kidney’s ability to regulate magnesium concentration of the plasma
and in turn affects osmoregulation.
On the other hand, calcium metabolism in freshwater fish is more drastically affected by
cadmium than in marine or brackish waters fish. Within a week of exposure to 0.3 ppm
cadmium, the plasma calcium of a species of the rainbow trout dropped by approximately 50%
(Roch and Maly, 1979). This concentration of cadmium causes only a small drop in the plasma
calcium of brackish water fish. Cadmium causes a decrease in plasma calcium by inhibiting the
influx of calcium at the gills (Reid and McDonald, 1988; Verbost et al., 1987). Cadmium
displaces calcium from protein carriers in the gill epithelium. The target organ of cadmium in
freshwater fish is essentially the gill in contrast to the kidneys in marine fish. However,
continued exposure to cadmium induces freshwater fish to increase prolactin secretion which
allows for the recovery of plasma calcium Therefore, exposure to modest amounts of cadmium
will not affect calcium regulation or osmoregulation to large extent.
Cadmium generally causes most harm to the early life stages of fish (Benoit et al.,1976;
Rombough and Garside, 1982). Exposure of larval fish to cadmium causes a reduction in uptake
rate of sodium, potassium calcium ions and water from the environment. Ion regulation and
osmoregulation may thus be drastically altered.

Mercury causes osmoregulation to alter in freshwater and marine fish to different degrees,
greater in marine species than freshwater species. When a freshwater fish, brook trout was
exposed to methylmercury at very low concentrations, there was an increase in plasma sodium
and chloride. On the other hand, another freshwater fish, rainbow trout suffers a decrease in
plasma sodium and chloride when exposed to higher concentrations of mercury.
Osmoregulatory failure may be one of the causes of death from mercury poisoning in freshwater
fish. Mercury cause osmoregulatory failure by causing an increased permeability of the gills to
water (Heath, 1997).
Freshwater fish, rainbow trout when exposed to lead in brackish water, show a dose-dependent
rise in plasma potassium. This potassium, from experimental results on the effect of lead on
mammalian erythrocytes cells, is inferred to have leaked out from tissue cells. The lead is
thought to inhibit the Na,K ATPase which controls the relative concentrations of potassium
between the body fluids and the cytoplasm of body cells (Heath, 1997). However, this increase in
plasma potassium has little effect on the regulation of sodium by the gills as the fish was in an
environment isotonic to its blood.
Tin compounds which are used in antifouling paints on ships were found to cause no change in
the plasma electrolytes (Pinkney et al., 1989). Even though tin compounds were observed in in
vitro conditions to inhibit the enzymes Na, K ATPase and Mg ATPase in the striped bass, these
enzymes are greatly stimulated by tin in in vivo conditions. This implies that the striped bass,
which lives in brackish water may have adapted to the presence of tin and induced more enzyme
synthesis. This is synonymous with the lack of effect tin has on the striped bass osmoregulation
and ion regulation.
The regulation of sodium is very adversely affected by manganese. Body and plasma sodium
concentrations fall by up to 50% before death. Therefore, it is highly likely that loss of plasma
sodium is a primary mode of death in acute doses of manganese (Heath, 1997). In contrast, iron
at high concentrations cause very little change to plasma sodium.

        Information on the toxicity of heavy metals can be applied to various fields of study,
particularly in health and commercial aspects. An interesting feature about fish which allows
them to survive in various concentrations of heavy metals pollution is their ability to
bioaccumulate heavy metal ions in their bodies. This bioaccumulation has various implications
on the survival of the fish themselves and their potential predators including humans. As
mentioned earlier, some heavy metals such as copper affect osmoregulation in fish by inhibiting
the enzyme Na+/ K+ ATPase. In addition to this inhibition, fish also accumulate copper in their
gills (Stagg and Shuttleworth, 1982; Wilson and Taylor, 1993) and in the intestine of marine fish
in response to high levels of copper in the water (Grosell et al., 2004). The bioaccumulation of
heavy metals in fish’s bodies causes many problems for human consumers as even low levels of
heavy metals such as mercury or lead can cause drastic effects to human body.
       A case study of the Minamata disease, which is a neurological disease caused by severe
mercury poisoning, revealed its origin to be in Minamata City in Japan. This disease was caused
by human consumption of fish and shellfish in Minamata Bay and Shiranui which had
bioaccumulated the extremely poisonous mercury. During the outbreak of the Minamata disease
in Minamata City in Japan, little was yet known about the toxicity of heavy metals and how high
concentrations could be bioaccumulated by fish and other marine organisms. The knowledge of
bioaccumulation is then useful not just to understand how fish survive in high concentrations of
heavy metal but to prevent future outbreaks of fatal diseases caused by heavy metals.
        Fish, unlike human or other mammals, have adapted to living in environment of certain
heavy metals concentration through bioaccumulation. It was found that heavy metals, such as
cadmium are normally taken up by the viscera, particularly the gut of marine fishes. This is due
to the fact that marine fish drink large amounts of saltwater to maintain their plasma osmotic
potential. The heavy metals taken up are then accumulated to a certain lethal concentration
before it kills them.
        This adaptation in fish to accumulate heavy metals without killing themselves is rather
interesting and the exact mechanism bioaccumulation and its concept could be applied to
biomedical research for perhaps a drug for human to safely accumulate certain heavy metals.
This would be extremely beneficial for people who constantly have to be exposed to heavy
metals due their profession
        The knowledge of the effect of heavy metals on fish osmoregulation also has potential
applications to commercial fish farming and fisheries. Commercial fisheries can develop
methods to test heavy metals content in the fish they capture. There are many different forms of
fish farming which is the principal form of aquaculture. A type of fish farming that could
potentially be affected by heavy metals pollution is the cage system farming method, whereby
the cages are placed in open water bodies such as rivers, lakes or open seas. One of the problems
of having fish farms in natural water bodies is that any pollutants such as heavy metals present or
polluting the water body will also pollute the water of the fish farms. Therefore, to ensure that
farmed fish are safe for consumption, it is important that commercial fish farms are informed
about the bioaccumulation of heavy metals in fish as well as how fish are affected by each type
of heavy metal. Being well-informed about the effects of heavy metals on fish also allows fish
farms to research and develop methods of keeping water in the farms free of heavy metals
        Recently, as an alternative to open oceans cage systems type of fish farms, recirculating
aquaculture system was developed. In this system, water is treated by continuous recycling,
whereby there was removal of particulate matter through the conversion on accumulated
chemicals to non-toxic ones. With further research on the relationship between osmoregulation
in fish and heavy metals pollution, more methods of efficient and safe fish farming could be

        Different heavy metals affect osmoregulation in fish to a different extent. Osmoregulation
in marine and freshwater fish is also altered to a different degree. Even within the large group of
freshwater fish, the ways heavy metals affect the ion and water regulation in each species is
different. Fish also have the ability to accumulate metal ions to until a certain lethal
concentration. From the Minamata incident, we can see how essential it is to understand the
reaction of fish to heavy metal pollution. This understanding also equips us with the necessary
knowledge to improve commercial fish farming methods and may have benefits in the
biomedical aspect as well
   1. Bern, H. A. and Madsen, S. S. (1992). A selective survey of the endocrine system of the
       rainbow trout (Oncorhynchus mykiss) with emphasis on the hormonal regulation of ion
       balance. Aquaculture, 100, 237.
   2. Buckley, J.T., Roch, M., McCarter, J.A., Rendell C.A., Matheson, A.T. (1982). Chronic
       exposure of coho salmon to sublethal concentrations of copper--I. Effect on growth, on
       accumulation and distribution of copper, and on copper tolerance. Comparative
       Biochemistry and Physiology Part C: Comparative Pharmacology, 72(1), 15-19.
   3. Evans, D. H. (1987). The fish gill: Site of action and model for toxic effects of
       environmental pollutants. Environmental Health Perspectives, Vol. 71, 47-58. Retrieved
       from www.scopus.com
   4. Grosell, M., McDonald, M. D., Walsh, P. J., & Wood, C. M. (2004a). Effects of
       prolonged copper exposure in the marine gulf toadfish (opsanus beta) II: Copper
       accumulation, drinking rate and Na+/K +-ATPase activity in osmoregulatory tissues.
       Aquatic Toxicology, 68(3), 263-275. Retrieved from www.scopus.com
   5. Grosell, M., McDonald, M. D., Wood, C. M., & Walsh, P. J. (2004b). Effects of
       prolonged copper exposure in the marine gulf toadfish (opsanus beta) I. hydromineral
       balance and plasma nitrogenous waste products. Aquatic Toxicology, 68(3), 249-262.
       Retrieved from www.scopus.com
   6. Heath, A.G. (1984). Ghanges in tissue adenylates and water content of bluegill, Lepomis
       macrochirus, exposed to copper. J.Fish Biol., 24, 299
   7. Karnaky, K.J. (1998) osmotic and ionic regulation. The physiology of fishes. Evans D.
       and McPherson, B.P. (1976). Effects of copper and zinc in fresh water on the adaptation
       to seawater and ATPase activiy, and the effects of copper on migratory disposition of
       coho salmon (Oncorhynchus kisutch). J. Fish Res. Ed. Can, 33, 2023.
   8. Malt, H. and Weber, R.E. (1988). Respiratiory stress in rainbow trout dying from
       aluminum exposure in soft, acid waer, with or without added sodium chloride. Fish
       physiol. Biochem., 8, 187
   9. Monserrat, J.M., Martí P.E., Geracitano, L.A., Lund Amado, L., Martinez Gaspar
       Martins, C., Lopes Leã Pinho, G., Soares Chaves, I., Ferreira-Cravo, M., Ventura-
       Lima, J., Bianchini, A. (2007). Pollution biomarkers in estuarine animals: Critical
       review and new perspectives. Comparative Biochemistry and Physiology - C Toxicology
       and Pharmacology, 146 (1-2 SPEC. ISS.), pp. 221-234.
   10. Moyes, C.D. and Schulte, P.M. (2006). Principles of Animal physiology. Pearson
       Benjamin Cummings.
   11. Pickney, A., Wright, D.A., Jepson, M.A., and Towle, D.W. (1989). Effects of tributyltin
       compounds on ionic regulation and gill ATPase activity in estuarine fish. Comp Biochem
       Physiol C. 92(1), 125.
   12. Reid S.D. and McDonald D.G. (1991). Effects of cadmium, copper, and low pH on ion
       fluxes in the rainbow trout, Salmo Gairdneri. Can. J. Fish. Aquatic Science, 45, 244.
   13. Roch, M. and Maly, E.J. (1979). Relationshop of cadmium-induced hypocalcemia with
       mortality in rainbow trout (salmo gairdneri) and the influence of temperature on toxicity.
       J.Fish. Res. Bd. Can., 36, 1297.
   14. Rombough, P.J and Garside, E.T. (1982). Cadmium toxicity and accumulation in eggs
    and alevins of Atlantic salmon Salmo salar. Can. J. Zool. 60(8): 2006-2014.
15. Schmidt-Nielsen, K. (1997). Animal physiology: Adaptation and envionment 5th edition.
    Cambridge University Press.
16. Spry, D.J. and Wood, C.M.(1984). Acid-base, plasma ion and blood gas changes in
    rainbow trout during short term toxic zinc exposure. J. Comp. Physiol. B., 154(2), 149-
17. Staurnes, M., Sigholt, T. and Reite, O.B. (1984). Reduced carbonic anhydrase and
    Na−K-ATPase activity in gills of salmonids exposed to aluminium-containing acid water.
    Cellular and Molecular Life Sciences (CMLS), 40(2), 226-227.
18. Stagg, R.M. and Shuttleworth, T.J. (1982). The accumulation of copper in Platichthys
    flesus :. And its effects n plasma electrolyte concentrations. J.fish biol., 20, 491-505
19. Sugatt R.H. (1980). Effects of sublethal sodium dichromate exposure in freshwater on the
    salinity tolerance and serum osmolality of juvenile coho salmon,Oncorhynchus kisutch,
    in seawater. Archives of Environmental Contamination and Toxicology, 9(1), 41-52.
20. Thurberg, P. and Dawson, M.A. (1974). Changes in osmoregulation and oxygen
    consumption in physiological response if the cunner, tautogolabrus adspersus, to
    cadmium. NOAA technical report NMFS SSRF-681, chapIII, 11-13.
21. Verbost, P. M., Flik, B., Lock, R. A. and Wendelaar Bonga, S. E.(1987). Cadmium
    inhibition of Ca2+ uptake in rainbow trout gills. Am J Physiol Regul Integr Comp
    Physiol, 253 (2), : R216-R221.
22. Watson, T.A. and Beamish, F.W.H. (1981). The effects of zinc on branchial adenosine
    triphosphatase enzymes in vitro from rainbow trout, salmo gairdneri. Comparative
    Biochemistry and Physiology Part C: Comparative Pharmacology, 68(2), 167-173.
23. Wilson, R. and Taylor, E. (1993). The physiological responses of freshwater rainbow
    trout, Oncorhynchus mykiss, during acutely lethal copper exposure. J. comp. Physiol. B.,
    163(1), 38-47.

To top