Fish obtain the oxygen that they require for their metabolic processes from the gas dissolved in water. The solubility of oxygen in water is low and depends on the temperature; at 5, 15 and 25°C the dissolved oxygen concentration is 12.8, 10.0 and 8.4 mg per litre respectively. These amounts are those for water in equilibrium with air, and are known as air saturation values. They will vary slightly with changes in barometric pressure. The saturation value for oxygen per se is about five times that for the air equilibrium value.
Because of this low concentration of dissolved oxygen in water, the fish has to have an extensive and efficient respiratory mechanism. This is shown diagrammatically in Fig. 2. Water flows through a sieve of parallel plates; each plate, or secondary lamellum, consists of a central sheet of pillar cells with concave sides that form blood spaces. These cells are covered by a thin epithelium. Oxygen diffuses from the water across the epithelial cells and the extensions of the pillar cells into the blood space.
To increase the efficiency further, the blood flows in the opposite direction to the water flow. This counter-current arrangement enables the almost fully utilized water of low oxygen content to come into close contact with (venous) blood with a low partial pressure of oxygen.
Fig. 2: Diagrammatic structure of fish gills (from Lloyd, 1992)
At the same time, carbon dioxide diffuses from the blood into the interlamellar space. Again, the counter current flows maximize the diffusion gradients, which may be enhanced still further by the presence of the enzyme carbonic anhydrase at the gill surface, which converts some of the gaseous CO2 to carbonic acid.
When a fish is inactive, the respiratory apparatus is more than sufficient to supply the necessary amount of oxygen to the blood. Under such conditions, only a proportion of the secondary lamellae may be utilized for respiration, and the concentration of red blood cells may be reduced. The latter may assist the heart in that it will reduce the viscosity of the blood being pumped through the gill capillaries before then passing via the arteries to the capillaries of the various tissues.
In response to a high energy demand, or a low concentration of dissolved oxygen in the water, the fish can respond in two ways: the blood flow can be increased by opening up further secondary lamellae to increase the effective respiratory area (it may be difficult to increase significantly the blood flow rate through the capillaries themselves), and the concentration of red blood corpuscles can be increased to raise the oxygen carrying capacity of the blood per unit volume. The latter can be achieved by reducing the blood plasma volume (e.g. by increasing the urine flow rate) in the short term, and by releasing extra blood corpuscles from the spleen in the longer term.
At the same time, the ventilation rate is increased to bring more water into contact with the gills within a unit time. There are, however, limits on the increased flow attainable; the space between the secondary lamellae is narrow (in trout it is about 20μm) and water will tend to be forced past the tips of the primary lamellae when the respiratory water flow is high, thus by-passing the respiratory surfaces.
These reactions are quite adequate to compensate for the normal fluctuations of energy demands of the fish and of dissolved oxygen concentrations in the water. One of the consequences, however, of an increased ventilation rate is that there will be an increase in the amount of toxic substances in the water reaching the gill surface where they can be absorbed.
Because the osmotic pressure of the body fluids of fish is considerably higher than that of freshwater, there will be a continuous influx of water across the surface epithelium and a corresponding loss of ions into the water. These fluxes occur over the whole body surface, but particularly at the gills which are relatively unprotected in this respect. Elsewhere, fluxes can be relatively high in the fins, but the remainder of the body is protected by a tough epithelium (and usually scales), and a covering of mucus.
The influx of water is balanced by a copious discharge of urine, from which as much sodium and chloride as possible has been re-absorbed in the kidneys. These organs do not control the osmotic pressure of the internal fluids; such control is exerted by special cells in the gill epithelium, whereby sodium is taken up in exchange for hydrogen ions, and chloride in exchange for bicarbonate. The internal hydrogen and bicarbonate is derived from respiratory carbon dioxide in the blood. These processes are shown in Fig. 3.
Fig. 3: The osmotic balance in fish (after Lloyd, 1992)
It is clear that damage to the integument, the fins, the ability to secrete mucus or its removal from the body surface, will lead to an osmotic imbalance. Similarly, damage to the gill epithelium will affect the ability of the fish to control their internal osmotic pressure.
It is not the purpose of this document to deal with this aspect of adaptation in any depth. The following brief summary describes the salient features.
Fish have become genetically adapted to live in such diverse environments as cold, soft, arctic waters to warm muddy rivers in the tropics. Transfer of fish between these environments is not possible. In the same way, there is a limited potential for genetic adaption to extreme conditions within a particular environment; for example, to extreme acidity in waters affected by acid rain, or to elevated levels of zinc in waters affected by historic mining activities.
In general, however, most of the adaptations that do occur are due to the limited ability of individual fish to detoxify the harmful chemicals entering the body, e.g. by enhancing the biochemical processes involved. For example, high levels of ammonia in the water are toxic to fish; however, the end-product of protein catabolism in fish is ammonia which is excreted by the gills. A limited adaptation to ammonia can be obtained by enhancing the excretory mechanism.
Similarly, elevated levels of zinc and copper in the water can be harmful, although at lower levels they are essential elements for fish. The internal concentrations of these metals are maintained by translocating them as complexes with metallothioneins (proteins) and perhaps by depositing surplus metals in the form of inert granules. These mechanisms can be enhanced to a certain extent to cope with limited increased metal levels in the surrounding water.
Many organic compounds can be metabolized and detoxified in the liver; residues can be excreted in the urine or via the bile through the gut. Again, there is a limited capacity for these mechanisms to become enhanced to cope with increased uptake of potentially harmful chemicals from the water. The existence of such mechanism can be demonstrated by placing fish which have been exposed to sub-lethal concentrations of a toxicant into higher concentrations and comparing their survival times with those not previously exposed. In general, it is unusual to find that fish can achieve more than a four-fold increase in resistance to a toxic substance.
It is very important to bear these adaptive potentials in mind when considering the effects of pollution on fish. In particular, the rate of change in the water quality may be important in determining whether the change is harmful; it may take some time for the adaption to be completed. This will be considered later in the context of temperature variations.
It is also important to remember that the natural environment is rarely stable and that fish have to constantly adapt to the changes. If these changes are made within the natural limits and rates, then the fish are not placed under stress. It is only when these limits and rates are exceeded, or the normal physiological functions and controls become damaged, that stress occurs. Such damage, especially to the integument, can lead to an increased susceptibility to disease.
