Old immunization protocols used additives, termed adjuvants, that included bacterial PAMPs. There are a few positive indications in mental health, but I have yet to see verifiable studies. Antibody diversity is thus caused by a DNA-based random generator. The majority of vaccines against viral diseases contain attenuated live viruses. The omega-3 fatty acids in flaxseed oil do not include any GLA; therefore, utilization of flaxseed is totally dependent on the unpredictable delta 6 enzymatic conversion of its LA to GLA. If more evidence indicates eating omega-3s from fish is going to preserve my health longer than not eating it, I owe it to myself to that. Thanks for this link.
Also of Interest
For example, red cabbage contains about 85 percent of the daily vitamin C our bodies need, while the green variety provides 47 percent. In fact, red cabbage has more vitamin C than oranges, believe it or not. Red and green cabbage are two different cabbage varieties, but they have a similar flavor.
Red cabbage tends to be more peppery and is usually smaller and denser than green cabbage heads. In acidic soils, the leaves usually grow more reddish, while in neutral soils, they grow more purple. This explains why the same plant is known by different colors in various regions. Red cabbage needs well-fertilized soil and sufficient humidity to grow at its best. However, if you are concerned at all about pesticide use, go for organic cabbage. Red cabbage contains 10 times more vitamin A than green cabbage.
It may also aid aid in keeping the skin and immune system healthy. Vitamin A can help maintain healthy teeth, skeletal tissue and mucous membranes. Green cabbage contains almost twice as much vitamin K as red cabbage. Vitamin K regulates bone mineralization by increasing bone density and helps the blood to coagulate. Both contain a good amount of vitamin C, which provides antioxidants and collagen protein. T he body needs vitamin C to help repair wounds and injuries as well as keeping bones, cartilage and teeth strong and healthy.
Iron delivers oxygen to your cells, which helps your muscles perform well during exercise and general day-to-day activities. L ack of iron in your diet could cause anemia , leading to fatigue. Red cabbage is the winner when it comes to antioxidants. The purple color in red cabbage comes from anthocyanins, and these nutrients provide further evidence of the cancer-fighting flavonoids it contains.
Anthocyanins are noted in research studies for protection against various types of memory loss, as well as other disease-preventing benefits like the ones I discussed above. Depending on the acidity of the soil in which a plant containing anthocyanin is grown, this pigment can look red, purple or even blue.
The original version of the wild cultivar of red cabbage was grown originally in the Mediterranean region. Many figures in history have contributed to the popularity of cabbage, including the Roman statesman, Cato, who is probably the person responsible for creating the cole slaw dish when he insisted on eating raw cabbage with vinegar.
Pliny the Elder, a famous Roman citizen who served in the military, wrote philosophy and recorded common health practices of the ancient Romans, wrote about cabbage in Natural History , noting its medicinal properties both as a food and in poultice form.
People in the southern parts of the Mediterranean probably developed cultivars of cabbage that could stand warmer temperatures than its original home. Jacques Cartier likely brought cabbage to the Americas in the s, where it was re-planted by colonists in the United States. However, it was before this plant would be written about in pre-United States records.
Native Americans and United States citizens alike were known to plant and eat this valuable veggie by the 18th century. There are numerous ways to prepare red cabbage, such as red cabbage slaw, braised red cabbage, steamed red cabbage or simply eating it raw in salads. When cooking, red cabbage normally turns blue.
However, if you want to retain the red color, you need to add apple cider vinegar or acidic fruit to the pot. In winter, fish are commonly killed by suffocation in polluted storage ponds and in summer this often happens in polluted water courses with high temperatures and low flow rates.
In severely eutrophicated ponds, oxygen deficiency often occurs during the summer early in morning as a result of the night time oxygen consumption by bacteria for the decomposition of organic substances and the respiration of aquatic plants.
In heavily fertilized ponds e. Even in ponds where the oxygen levels have been satisfactory during the summer, when plant growth was vigorous, severe oxygen deficiencies can occur in the autumn when the plants begin to die and decompose.
This deficiency can be more pronounced if the sky is heavily overcast during the day, so that the limited oxygen production by photosynthesis is further reduced. In these cases, the maximum oxygen deficiency occurs just before daybreak. In summary, the oxygen levels in water depend on the balance between the inputs from the air and plants, and the consumption by all forms of life.
Inputs from the air depend on the turbulence of the air-water interface, and the oxygen deficiency of the water. Inputs from plants depend on photosynthetic activity which increases with temperature and sunlight; excess oxygen can be lost to the atmosphere. Oxygen consumption depends on the respiration of aquatic organisms, including plants, and the aerobic decomposition of organic material by bacteria; these rates also increase with temperature.
This balance needs to be clearly understood; a satisfactory oxygen level recorded during the day is no guarantee that the levels will be maintained during the night. Moderate levels recorded in calm eutrophic waters on a warm, sunny afternoon will almost always indicate that severe oxygen deficiencies will occur during the night.
Also, lower than expected daytime pH values due to high levels of CO 2 may indicate high levels of bacterial respiration which could lead to low night-time oxygen levels. Oxygen deficiency causes asphyxiation and fish will die, depending on the oxygen requirements of the species and to a lesser extent on their rate of adaptation. Fish exposed to oxygen deficient water do not take food, collect near the water surface, gasp for air cyprinids , gather at the inflow to ponds where the oxygen levels are higher, become torpid, fail to react to irritation, lose their ability to escape capture and ultimately die.
The major pathologico-anatomic changes include a very pale skin colour, congestion of the cyanotic blood in the gills, adherence of the gill lamellae, and small haemorrhages in the front of the ocular cavity and in the skin of the gill covers.
In the majority of predatory fishes the mouth gapes spasmodically and the operculum over the gills remains loosely open. Remedial action is to either reduce the input of degradable material, or to aerate the water. The latter is usually the best option; aeration can be with air or oxygen pumps, or by spraying the water into the air in the form of a fountain, or by increasing the input of aerated water.
It must be remembered that these remedial actions are most important at night when the oxygen deficiency is likely to be at its greatest. Damage caused to fish by too much oxygen dissolved in water is seldom encountered. However, it may happen, for example, when fish are transported in polythene bags with an oxygen-filled air space. The gills of such affected fish have a conspicous light red colour and the ends of the gill lamellae fray.
When such fish are used for stocking waters they may suffer from secondary fungus infections and some of them may die. It is possible that fish adapted to such high oxygen levels need to be progressively acclimatized to more normal concentrations. The condition described here should not be confused with the supersaturation of water with dissolved gas, which can cause gas bubble disease.
Supersaturation with dissolved gas occurs when the pressure of the dissolved gas exceeds the atmospheric pressure. It occurs when water is equilibrated with air under pressure, e. It can also occur if cold air-equilibrated water is warmed up without re-equilibration to the higher temperature. A bottle containing such water will show either minute bubbles forming as a cloudy suspension which will clear from the bottom upwards, or larger bubbles forming on the glass wall.
This is analogous to that seen in an opened bottle of carbonated drinking water. If fish are exposed at a lower atmospheric pressure to such water, their blood equilibrates with the excess pressure in the water. Bubbles form in the blood and these can block the capillaries; in sub-acute cases the dorsal and caudal fin can be affected, and bubbles may be visible between the fin rays. The epidermal tissue distal to the occlusions then becomes necrotic and cases are known where the dorsal fins of trout have become completely eroded.
In severe cases, death occurs rapidly as a result of blockage of the major arteries, and large bubbles are clearly seen between the rays of all the fins. A similar effect of gas bubbles forming in the blood can be experienced by deep-sea divers when they return to the surface. The remedy is either to remove the fish to normally equilibrated water or to provide vigorous aeration to strip out the excess gas.
Ammonia pollution of water courses, ponds and lakes may be of organic origin domestic sewage, agricultural wastes, or the reduction of nitrates and nitrites by bacteria in anoxic waters or of inorganic origin industrial effluents from gas works, coking plants and power generator stations. The ratio between these two forms depends on the pH and temperature of the water Table 1. Also, under normal conditions there is an acid-base balance at the water-tissue interface.
If this balance is altered, the side on which the pH is lower will attract additional molecular ammonia. This explains how molecular ammonia passes from water through the epithelium of the gills to the blood and also how it passes from the blood to the tissues. Ammonia has a particular toxic effect on the brain; this is why nervous symptoms are so pronounced in cases of ammonia toxicity to fish.
Water quality monitoring of water courses, lakes and fish culture facilities includes the measurement of total ammonia concentrations. To assess the potential toxicity of these concentrations it is important to know the amount of nondissociated ammonia NH 3 present. Alternatively, the values can be interpolated from Table 1 compiled from calculations on the basis of this formula.
Besides water temperature and pH, other factors that influence ammonia toxicity include the concentration of dissolved oxygen in water; the lower the oxygen concentration in water, the greater the toxicity of ammonia Fig. To a lesser extent, the toxicity of ammonia is affected by the amount of free CO 2 in the water. This is because the diffusion of respiratory CO 2 at the gill surface reduces the pH of the water, thus reducing the proportion of nondissociated ammonia there.
The extent of the reduction in pH depends on the amount of CO 2 already present in the water. In general, Table 1 shows that the toxicity of ammonia will be much greater in warm alkaline waters than in cold acid waters. Non-dissociated ammonia is highly toxic to fish.
The LC 50 values, determined in acute toxicity tests, are in the range of 1. The maximum admissible ammonia NH 3 concentration is 0. It should be emphasized here that these standards apply to ammonia as a toxic substance. Other standards for total ammonia are applied to control eutrophication of waters and prevent excessive algal and plant growth that can cause physical problems and affect the oxygen balance. With low levels of oxygen in the water, lower concentrations non-dissociated ammonia can kill fish:.
The first signs of ammonia toxicity include a slight restlessness, and increased respiration; the fish congregate close to the water surface. In later stages, cyprinids gasp for air, their restlessness increases with rapid movements and respiration becomes irregular; then follows a stage of intense activity.
Finally, the fish react violently to outside stimuli; they lose their balance, leap out of the water, and their muscles twitch in spasms. Affected fish lie on their side and spasmodically open wide their mouths and gill opercula.
Then follows a short period of apparent recovery. The fish return to normal swimming and appear slightly restless. This stage is then replaced by another period of high activity; the body surface becomes pale and the fish die. The skin of ammonia poisoned fish is light in colour, and covered with a thick or excessive layer of mucus. In some cases small haemorrhages occur, mainly at the base of the pectoral fins and in the anterior part of the ocular cavity.
The gills are heavily congested and contain a considerable amount of mucus; fish exposed to high ammonia concentrations may have slight to severe bleeding of the gills. Intense mucus production can be observed on the inner side of the gill opercula, mainly at the posterior end.
The organs inside the body cavity are congested and parenchymatous, and show dystrophic changes. In recent years, considerable losses among farmed carp have been caused by the so-called toxic necrosis of the gills. The factors responsible for the occurence of this disease include ammonia poisoning in which the ammonia level in the blood is considerably increased.
As stated earlier, ammonia is the final product of nitrogen metabolism in carp as it is in other species and most of it is excreted via the gills into the water. If the diffusion rate is reduced for some reason or another high water pH, oxygen deficit, damaged gills etc. A very interesting case of autointoxication among carp yearlings C 1 where extremely high ammonia N levels were found in the blood serum occurred after their transfer from a pond to well water in large aquarium tanks.
Some of the fish caught and transferred during the morning exhibited typical symptoms of ammonia poisoning the following morning. These symptoms included considerable restlessness, increased respiration, leaping out of the water, uncoordinated activity, and tonic-clonic spasms of the muscles.
The skin of the affected fish was light in colour; the gills were heavily congested, dark red and showed oedematous swellings particularly severe on the edges of the gill filaments.
It is known that ammonia toxicity is accompanied by an increase in the permeability of the fish epithelium to water, as measured by an increase in the flow of urine. If the kidneys cannot cope with the increased water influx, oedema is likely to occur. An increased water influx may also occur if the skin or the mucus coating of the fish is damaged by handling and during transport. The histopathological changes in the gills corresponded with what had been described for toxic necrosis of carp gills.
The digestive tract of those fish with severe poisoning symptoms was filled with undigested food. On the other hand, fish that had cleared their gut faeces found on the bottom of the tank, the gut almost empty , were free from symptoms of toxic damage.
On the basis of this case of ammonia poisoning of carp, some other unexplained incidents of rapid death among fish may be ascribed to a similar cause. Such events may occur mainly in carp farms where there is an intensive feeding with a high-nitrogen diet, if the fish are also exposed to other stresses caused by e. The clinical signs of toxic gill necrosis in carp included the congregation of the fish in the deeper and shaded part of the pond and subsequently, in the advanced stage of disease the body surface darkened and there was a reduced or total absence of the escape response.
Respiration was laboured and the fish did not feed. Pronounced hyperaemia, oedematic swelling and increased accumulation of mucus in the gills are typical features of the patho-anatomic picture. These are followed by a gill necrosis and separation of the epithelium from the gill lamellae.
The pillar cells of the gill lamellae are completely exposed over the whole lamellar surface. In the later stages of the disease, necrotic gill lamellae become detached and the margins of the gills are distorted.
Histological and pathological examination reveals venostasis, swelling, vacuolization and separation of the respiratory epithelial cells from basal membrane in the gills. Associated with these effects is an increase in the activity of chloride cells in the lamellar epithelium.
Dystrophic and necrobiotic cells from the respiratory epithelium including chloride cells create a compact mass of debris in the interlamellar space of gills. Extensive effects are characterized by a total lysis and necrotic changes in the cell nucleus. A significant increase in the ammonia level of blood serum in fish is a specific feature of these effects.
In other gill diseases that cause necrosis, the following levels of ammonia in blood serum have been found as N per ml: The diagnosis of toxic necrosis is based on a detailed examination of fish.
The main specific effect in carp is the elevated ammonia level in the blood serum. However, because such toxic gill necrosis can be caused by other unfavourable conditions in the pond environment Fig. Preventive measures to control frequent outbreaks of gill necrosis in carp in highly eutrophic ponds are centred on optimizing of the hydrobiological and hydrochemical conditions and ensuring the healthy state of fish stock e.
Stocking the ponds with fish at the correct time in the spring, and preventing or oxygen deficiency, are among the most important preventive measures.
In this context a simple biological test has been developed to determine the optimum timing for the spring stocking of two-year-old carp into ponds with a history of toxic gill necrosis. This test is based on the ability of carp to eliminate ammonia under the existing physical and chemical conditions of the pond water given as an oral dose of mg.
If the ammonia level in the blood serum decreases to the original value within 6 hours of the dose being given, the fish can be stocked in pond. On the other hand, if the ammonia level in the blood serum remains at a threefold higher level than the original value, the stocking of fish must be postponed until the physical and chemical conditions of pond water allow the fish to eliminate the toxic ammonia.
Application of the pesticide Soldep at a rate ml ha -1 depth of pond l m on average can ensure the survival of the fish stock when an overproduction of zooplankton, followed by an oxygen deficiency, is expected.
Soldep is effective in controlling the daphnid zooplankton and should be applied when there is still a reasonable phytoplankton community in the pond. Nitrites as a rule are found together with nitrates and ammonia nitrogen in surface waters but their concentrations are usually low because of their instability. They are readily oxidized to nitrate or reduced to ammonia, both chemically and biochemically by bacteria.
Nitrates are the final product of the aerobic decomposition of organic nitrogen compounds. They are present in low concentrations in all surface waters.
There is almost no nitrate retention in soil, so it is readily leached to watercourses, ponds and lakes. The main sources of nitrate pollution of surface waters is the use of nitrogenous fertilizers and manures on arable land leading to diffuse inputs, and the discharge of sewage effluents from treatment works. Nitrite can be associated with ammonia concentrations in the water.
In normal aerobic conditions, ammonia is oxidized to nitrite and then to nitrate by two separate bacterial actions.
If the second stage of oxidation is inhibited by bactericidal chemicals in the water, nitrite concentrations will increase. This may be important in small ponds or aquaria where water is recirculated through a purification filter; the ammonia-oxidizing bacteria need to become established for the filter to function, and they may be affected by the use of antibiotics to control fish diseases.
The toxic action of nitrite on fish is incompletely known; it depends on a number of internal and external factors such as fish species and age, and general water quality. The importance and role of these factors have been frequently studied and reviewed. Different authors often come to contradictory conclusions, and usually fail to offer a definitive explanation of either the mechanism of nitrite toxic action on fish or the modifying effects of different environmental factors.
It is now clear that nitrite ions are taken up into the fish by the chloride cells of the gills. In the blood, nitrites become bound to haemoglobin, giving rise to methaemoglobin: The increase in the amount of methaemoglobin can be seen as a brown colour of the blood and gills.
Nevertheless, the fish may still be able to survive because the erythrocytes in their blood contain the enzyme reductase which can convert methaemoglobin to haemoglobin.
This process can return the haemoglobin to its normal level within 24—48 hours, if the fish are put into nitrite-free water. Hydrobiological and hydrochemical conditions in the Dremliny Pond before and during the course of toxic gill necrosis in carp. Toxic necrosis was diagnosed on 2 May Several authors have shown that nitrite toxicity to fish can be affected by certain water quality characteristics e. Lewis and Morris, In this investigation, the 96h LC50 for rainbow trout ranged from 0.
The effect of chloride on nitrite toxicity is so marked that the results of tests made without recording the chloride concentrations in the water cannot be compared with those of other tests. It is now known that the chloride cells in the fish gills cannot distinguish between nitrite and chloride ions; both are transported across the gill epithelium. The rate of nitrite uptake depends therefore on the nitrite-chloride ratio in the water.
Nitrite toxicity can be also influenced by bicarbonate, potassium, sodium, calcium and other ions, but their effect is not so great as that of chloride. Among these, potassium is the more significant, and that of sodium and calcium is less. These monovalent ions are also involved in the ionic fluxes across the gill epithelium and so directly or indirectly influence the uptake of nitrite. The pH value has also been considered as important for nitrite toxicity; pH and temperature control dissociation between NO 2 and nondissociated HNO 2 and it was believed that the uptake of nitrites into fish blood plasma depended on the diffusion of nondissociated HNO 2 across the gill epithelium.
However, the results of later experiments refuted these theories and showed that within the acidity-alkalinity range encountered in natural waters the pH is of little importance in nitrite toxicity. Another factor that influences nitrite toxicity is the dissolved oxygen concentration and water temperature. This is associated with the fact that fish need a fully oxygenated water when the oxygen-carrying capacity of the blood is reduced by the formation of methaemoglobin, and the oxygen requirement of fish increases with temperature.
Long exposure to sublethal concentrations of nitrites does not cause much damage to the fish. For estimating the safe nitrite concentration for particular locations, it is necessary to measure the ratio of chloride to nitrite. These ratios expressed as mg l -1 Cl: The toxicity of nitrates to fish is very low, and mortalities have only been recorded when concentrations have exceeded mg per litre; 80 mg per litre is considered to be the maximum admissible nitrate concentration for carp and 20 mg per litre for rainbow trout.
In surface waters and in fish farms where the water contains ample oxygen with no danger of denitrification i. However, as with ammonia, water quality standards need to be set for nitrate to prevent eutrophication, and the excessive growth of algae and plants, which can have a secondary effect on fish.
Hydrogen sulphide occurs in organically polluted waters from the decomposition of proteins. It is also present in industrial effluents including those from metallurgical and chemical works, paper pulp plants, and tanneries. It has a high to very high toxicity to fish; the lethal concentrations for different fish species range from 0. The toxicity of H 2 S decreases with increasing water pH, because of a reduction in the ratio of the nondissociated toxic H 2 S to the less toxic HS ions.
For natural water it is about 0. Hydrogen sulphide can be formed in decomposing rich organic mud, and escapes into the overlying water together with other gases e. In aerobic waters the H 2 S is rapidly oxidized to sulphate; however, it is possible for fish living close to the surface of such muds to be exposed to hydrogen sulphide.
These two forms of carbon dioxide together constitute what is termed free CO 2. The ionic forms, i. Their presence is important for the buffering capacity of the water.
The amounts of CO 2 present in flowing surface waters are typically in the order of a few mg per litre, and seldom rise above 20 to 30 mg per litre. In stagnant surface waters the CO 2 levels are stratified because of photosynthetic assimilation by phytoplankton, the upper strata usually having less free CO 2 than the lower strata.
If all the free CO 2 in the surface strata is used for photosynthesis, the pH of the water there may rise above 8. Ground waters from limestone or chalk strata usually contain several tens of mg of free CO 2 per litre, and this may be important where well water is used for fish culture. The toxic action of carbon dioxide is either direct or indirect. The indirect action of both free and bound CO 2 is exerted on fish through its influence on water pH, especially where, as described earlier, the values rise to toxic levels.
Also, changes in pH affect the toxicity of those chemicals which exist in the dissociated and nondissociated forms of which only one is toxic, such as H 2 S and ammonia. A direct adverse effect occurs when there is an excess or absence of free CO 2.
In waters of low oxygen content, such as where intensive biodegradation is taking place, or where fish are kept or transported in a high density, or when poorly aerated ground waters are used, free CO 2 may reach harmful levels. In such cases the diffusion of CO 2 from the fish blood into the respiratory water is reduced, the blood CO 2 rises and acidosis develops. If the rise in CO 2 concentration is relatively slow e.
Adapted fish can then suffer from alkalinosis if returned to water of low CO 2 content. In water of low O 2 and high CO 2 , where gaseous exchange at the respiratory surface is limited, the fish increase their ventilation rate, become restless, lose equilibrium, and may die.
Twenty mg free CO 2 per litre is considered the maximum permissible concentration for trout higher concentrations can cause kidney problems and 25 mg free CO 2 per litre is the maximum for carp if the acid capacity is 0. The sensitivity of fish to free carbon dioxide declines with increasing acid capacity of water.
However, the more frequent occurrence is a lack of free carbon dioxide in water. Carbon dioxide deficiency occurs when too much free CO 2 is utilized for photosynthetic activity by the phytoplankton, or when the water used in thermal power plants is artificially softened or when water is aerated more vigorously than necessary with CO 2 free air. Free carbon dioxide concentrations below 1 mg per litre affect the acid-base balance in the fish blood and tissues, and cause alkalosis.
A lack of free carbon dioxide is particularly harmful to cyprinid fry when they pass from endogenous to exogenous nutrition. Cyprinid fry respire through their body surface and are unable to regulate their acid-base balance by gill respiration. A low partial pressure of free CO 2 in water is conductive to a high CO 2 diffusion rate from the body, leading to alkalosis and finally to death. If the fry of cyprinids suffer from free CO 2 deficiency, they gather close to the water surface and show symptoms of suffocation even though the concentration of oxygen in the water is adequate Taege, The factors considered in this Chapter have been those which can occur in the natural environment, and which can be enhanced by man's activities.
Fish have a limited ability to adapt to changes in these factors, if they occur sufficiently slowly; rapid changes can be harmful. If fish are affected to some extent by such changes, a full recovery is possible on return in some cases, e.
Unless irreparable damage has been caused to fish tissues, there are unlikely to be any long-term consequences to their health. This section briefly describes the toxicity to fish of chemicals that are likely to occur in surface waters. Where possible, the acute toxic concentrations are given to provide information useful for cases of sporadic discharges where high concentrations may exist for a short time, and maximum admissible concentrations which are relevant for low-level continuous discharges.
Clinical and patho-anatomic effects are also described. For more detailed information standard reference works should be consulted.
Their principal function is to help the fish swim. Fins can also be used for gliding or crawling, as seen in the flying fish and frogfish. Fins located in different places on the fish serve different purposes, such as moving forward, turning, and keeping an upright position. For every fin, there are a number of fish species in which this particular fin has been lost during evolution.
In bony fish, most fins may have spines or rays. A fin may contain only spiny rays, only soft rays, or a combination of both. If both are present, the spiny rays are always anterior. Spines are generally stiff, sharp and unsegmented. Rays are generally soft, flexible, segmented, and may be branched. This segmentation of rays is the main difference that distinguishes them from spines; spines may be flexible in certain species, but never segmented. Spines have a variety of uses.
In catfish , they are used as a form of defense; many catfish have the ability to lock their spines outwards. Triggerfish also use spines to lock themselves in crevices to prevent them being pulled out. Lepidotrichia are bony, bilaterally-paired, segmented fin rays found in bony fishes. They develop around actinotrichia as part of the dermal exoskeleton.
Lepidotrichia may have some cartilage or bone in them as well. They are actually segmented and appear as a series of disks stacked one on top of another. The genetic basis for the formation of the fin rays is thought to be genes coding for the proteins actinodin 1 and actinodin 2.
As with other vertebrates, the intestines of fish consist of two segments, the small intestine and the large intestine. In most higher vertebrates, the small intestine is further divided into the duodenum and other parts. In fish, the divisions of the small intestine are not as clear, and the terms anterior intestine or proximal intestine may be used instead of duodenum. It commonly has a number of pyloric caeca , small pouch-like structures along its length that help to increase the overall surface area of the organ for digesting food.
There is no ileocaecal valve in teleosts, with the boundary between the small intestine and the rectum being marked only by the end of the digestive epithelium. Instead, the digestive part of the gut forms a spiral intestine , connecting the stomach to the rectum. In this type of gut, the intestine itself is relatively straight, but has a long fold running along the inner surface in a spiral fashion, sometimes for dozens of turns.
This fold creates a valve-like structure that greatly increases both the surface area and the effective length of the intestine. The lining of the spiral intestine is similar to that of the small intestine in teleosts and non-mammalian tetrapods. Hagfish have no spiral valve at all, with digestion occurring for almost the entire length of the intestine, which is not subdivided into different regions.
The pyloric caecum is a pouch, usually peritoneal , at the beginning of the large intestine. It receives faecal material from the ileum , and connects to the ascending colon of the large intestine.
It is present in most amniotes , and also in lungfish. Their purpose is to increase the overall surface area of the digestive epithelium, therefore optimizing the absorption of sugars, amino acids, and dipeptides, among other nutrients.
As with other vertebrates, the relative positions of the esophageal and duodenal openings to the stomach remain relatively constant. As a result, the stomach always curves somewhat to the left before curving back to meet the pyloric sphincter.
However, lampreys , hagfishes , chimaeras , lungfishes , and some teleost fish have no stomach at all, with the esophagus opening directly into the intestine. These fish consume diets that either require little storage of food, or no pre-digestion with gastric juices, or both.
The kidneys of fish are typically narrow, elongated organs, occupying a significant portion of the trunk. They are similar to the mesonephros of higher vertebrates reptiles, birds and mammals. The kidneys contain clusters of nephrons , serviced by collecting ducts which usually drain into a mesonephric duct.
However, the situation is not always so simple. In cartilaginous fish there is also a shorter duct which drains the posterior metanephric parts of the kidney, and joins with the mesonephric duct at the bladder or cloaca. Indeed, in many cartilaginous fish, the anterior portion of the kidney may degenerate or cease to function altogether in the adult. They consist of a row of nephrons, each emptying directly into the mesonephric duct. The spleen is found in nearly all vertebrates.
It is a non-vital organ, similar in structure to a large lymph node. It acts primarily as a blood filter, and plays important roles in regard to red blood cells and the immune system. Even in these animals, there is a diffuse layer of haematopoeitic tissue within the gut wall, which has a similar structure to red pulp, and is presumed to be homologous with the spleen of higher vertebrates. The liver is a large vital organ present in all fish. It has a wide range of functions, including detoxification , protein synthesis , and production of biochemicals necessary for digestion.
It is very susceptible to contamination by organic and inorganic compounds because they can accumulate over time and cause potentially life-threatening conditions. Because of the liver's capacity for detoxification and storage of harmful components, it is often used as an environmental biomarker. Fish have what is often described as a two-chambered heart ,  consisting of one atrium to receive blood and one ventricle to pump it,  in contrast to three chambers two atria, one ventricle of amphibian and most reptile hearts and four chambers two atria, two ventricles of mammal and bird hearts.
Ostial valves, consisting of flap-like connective tissues, prevent blood from flowing backward through the compartments. The ventral aorta delivers blood to the gills where it is oxygenated and flows, through the dorsal aorta , into the rest of the body.
In tetrapods , the ventral aorta has divided in two; one half forms the ascending aorta , while the other forms the pulmonary artery. The circulatory systems of all vertebrates , are closed. Fish have the simplest circulatory system, consisting of only one circuit, with the blood being pumped through the capillaries of the gills and on to the capillaries of the body tissues.
This is known as single cycle circulation. In the adult fish, the four compartments are not arranged in a straight row but, instead form an S-shape with the latter two compartments lying above the former two. This relatively simpler pattern is found in cartilaginous fish and in the ray-finned fish. In teleosts , the conus arteriosus is very small and can more accurately be described as part of the aorta rather than of the heart proper.
The conus arteriosus is not present in any amniotes , presumably having been absorbed into the ventricles over the course of evolution. Similarly, while the sinus venosus is present as a vestigial structure in some reptiles and birds, it is otherwise absorbed into the right atrium and is no longer distinguishable. The swim bladder or gas bladder is an internal organ that contributes to the ability of a fish to control its buoyancy, and thus to stay at the current water depth, ascend, or descend without having to waste energy in swimming.
The bladder is found only in the bony fishes. In the more primitive groups like some minnows , bichirs and lungfish , the bladder is open to the esophagus and doubles as a lung.
It is often absent in fast swimming fishes such as the tuna and mackerel families. The condition of a bladder open to the esophagus is called physostome , the closed condition physoclist. In the latter, the gas content of the bladder is controlled through a rete mirabilis , a network of blood vessels effecting gas exchange between the bladder and the blood.
Fishes of the superorder Ostariophysi possess a structure called the Weberian apparatus , a modification which allow them to hear better. This ability which may well explain the marked success of otophysian fishes. This allows the transmission of vibrations to the inner ear. A fully functioning Weberian apparatus consists of the swim bladder, the Weberian ossicles, a portion of the anterior vertebral column, and some muscles and ligaments.
Fish reproductive organs include testes and ovaries. In most species, gonads are paired organs of similar size, which can be partially or totally fused. The genital papilla is a small, fleshy tube behind the anus in some fishes, from which the sperm or eggs are released; the sex of a fish often can be determined by the shape of its papilla. Most male fish have two testes of similar size.
In the case of sharks , the testis on the right side is usually larger. The primitive jawless fish have only a single testis, located in the midline of the body, although even this forms from the fusion of paired structures in the embryo. Under a tough membranous shell, the tunica albuginea , the testis of some teleost fish, contains very fine coiled tubes called seminiferous tubules. The tubules are lined with a layer of cells germ cells that from puberty into old age, develop into sperm cells also known as spermatozoa or male gametes.
The developing sperm travel through the seminiferous tubules to the rete testis located in the mediastinum testis , to the efferent ducts , and then to the epididymis where newly created sperm cells mature see spermatogenesis. The sperm move into the vas deferens , and are eventually expelled through the urethra and out of the urethral orifice through muscular contractions.
However, most fish do not possess seminiferous tubules. Instead, the sperm are produced in spherical structures called sperm ampullae. These are seasonal structures, releasing their contents during the breeding season, and then being reabsorbed by the body.
Before the next breeding season, new sperm ampullae begin to form and ripen. The ampullae are otherwise essentially identical to the seminiferous tubules in higher vertebrates, including the same range of cell types. In terms of spermatogonia distribution, the structure of teleosts testes has two types: Fish can present cystic or semi-cystic spermatogenesis in relation to the release phase of germ cells in cysts to the seminiferous tubules lumen.
Many of the features found in ovaries are common to all vertebrates, including the presence of follicular cells and tunica albuginea There may be hundreds or even millions of fertile eggs present in the ovary of a fish at any given time. Fresh eggs may be developing from the germinal epithelium throughout life. Corpora lutea are found only in mammals, and in some elasmobranch fish; in other species, the remnants of the follicle are quickly resorbed by the ovary.
In some elasmobranchs , only the right ovary develops fully. In the primitive jawless fish , and some teleosts, there is only one ovary, formed by the fusion of the paired organs in the embryo. Fish ovaries may be of three types: In the first type, the oocytes are released directly into the coelomic cavity and then enter the ostium , then through the oviduct and are eliminated. Secondary gymnovarian ovaries shed ova into the coelom from which they go directly into the oviduct.
In the third type, the oocytes are conveyed to the exterior through the oviduct. Cystovaries characterize most teleosts, where the ovary lumen has continuity with the oviduct. Fish typically have quite small brains relative to body size compared with other vertebrates, typically one-fifteenth the brain mass of a similarly sized bird or mammal. Fish brains are divided into several regions. At the front are the olfactory lobes , a pair of structures that receive and process signals from the nostrils via the two olfactory nerves.
The olfactory lobes are very large in fish that hunt primarily by smell, such as hagfish, sharks, and catfish. Behind the olfactory lobes is the two-lobed telencephalon , the structural equivalent to the cerebrum in higher vertebrates.
In fish the telencephalon is concerned mostly with olfaction. The forebrain is connected to the midbrain via the diencephalon in the diagram, this structure is below the optic lobes and consequently not visible. The diencephalon performs functions associated with hormones and homeostasis. This structure detects light, maintains circadian rhythms, and controls color changes. These are very large in species that hunt by sight, such as rainbow trout and cichlids.
The hindbrain or metencephalon is particularly involved in swimming and balance. The brain stem or myelencephalon is the brain's posterior. Vertebrates are the only chordate group to exhibit a proper brain. A slight swelling of the anterior end of the dorsal nerve cord is found in the lancelet , though it lacks the eyes and other complex sense organs comparable to those of vertebrates. Other chordates do not show any trends towards cephalisation. The front end of the nerve tube is expanded by a thickening of the walls and expansion of the central canal of spinal cord into three primary brain vesicles: The prosencephalon forebrain , mesencephalon midbrain and rhombencephalon hindbrain , further differentiated in the various vertebrate groups.
Vesicles of the forebrain are usually paired, giving rise to hemispheres like the cerebral hemispheres in mammals. The circuits in the cerebellum are similar across all classes of vertebrates , including fish, reptiles, birds, and mammals. There is considerable variation in the size and shape of the cerebellum in different vertebrate species.
In amphibians , lampreys , and hagfish , the cerebellum is little developed; in the latter two groups, it is barely distinguishable from the brain-stem. Although the spinocerebellum is present in these groups, the primary structures are small paired nuclei corresponding to the vestibulocerebellum.
The cerebellum of cartilaginous and bony fishes is extraordinarily large and complex. In at least one important respect, it differs in internal structure from the mammalian cerebellum: The fish cerebellum does not contain discrete deep cerebellar nuclei.