PIGMENTAL EXCHANGE (Latin pigmentum paint) — set of processes of education, transformation and disintegration in an organism of pigments (the colored compounds performing the most various functions). P.'s disturbance by the lake is the reason of a large number of diseases, including diseases of accumulation, or a consequence of some diseases (e.g., a viral hepatitis, etc.).
The most important aspect of exchange pigments (see) at animals and the person exchange of a gemsoderzhashchy chromoproteid is hemoglobin (see) and related to it pigments — myoglobin (see), tsitokhrom (see), catalases (see) and peroxydase (see), many respiratory pigments (see). Synthesis gem is carried out from suktsinil-KOA and glycine through a mode of formation 6-aminolevulinic to - you at which condensation of two molecules there is a porphobilinogen — the direct predecessor of protoporphyrin (see. Porphyrines ). After end of a porphyrinic cycle there is an inclusion in porphyrias of atom of the iron delivered by transport protein ferritin (see), with education hematin , which, connecting to specific protein, turns into hemoglobin or another gemso the holding pigment. Chromoproteids of food (hemoglobin, a myoglobin, a chlorophyll proteids etc.), getting in went. - kish. a path, are split on the proteinaceous part which is exposed then to proteolytic splitting, and prosthetic group. Gem is not used for resynthesis of chromoproteids and is oxidized in the hematin which is emitted with a stake in not changed look or in the form of the connections which are formed of hematin under the influence of intestinal microflora. In fabrics disintegration of hemoglobin and other gemsoderzhashchy pigments proceeds in other way. The hemoglobin which is formed at an erythrocytolysis is delivered by protein of plasma gaptoglobiny (see) in cells of reticuloendothelial system where after oxidation of hemoglobin to formation of verdohaemoglobin there is eliminating from a molecule of a pigment of a proteinaceous part which then collapses under the influence of proteolytic enzymes, and release of the iron which is filling up the general reserve of iron in an organism.
Excess formation of a yellowy-brown pigment of hemosiderin — a product of exchange of hemoglobin and its adjournment in fabrics conducts to to a hemosiderosis (see) and to hemochromatosis (see). Disturbance of metabolism of hemoglobin in a liver leads to a pigmental hepatosis (see. Hepatoses ). At intensive destruction of a large number of erythrocytes (e.g., at poisonings, infections, burns) arises haemoglobinuria (see) — emergence in urine of a significant amount of hemoglobin. Numerous cases of synthesis of the abnormal hemoglobin consisting, e.g., in replacement of amino acids in primary structure of a globin — a squirrel of a molecule of hemoglobin are known (see. Anemias ; Gemoglobin, haemo globins unstable ; Hemoglobinopathies ). At some patol, states at the person and animals escaping of muscles and allocation with urine of a myoglobin is observed (see. Myoglobinuria ).
The bilious pigment of green color the biliverdin representing linear derivative a tetrapirrol is formed of verdohaemoglobin. It is found in bile, and also in tissues of animals and the person. At recovery of biliverdin other bilious pigment of reddish-yellow color is formed bilirubin (see). The bilious pigments getting into intestines with bile are partially soaked up in blood and come to a liver on system of a portal vein (see. Bilious pigments ). Free (indirect) bilirubin is slightly soluble and toxic; it is neutralized in a liver by formation of soluble diglucuronide — pair compound of bilirubin with glucuronic to - that (direct bilirubin). In a digestive tract at recovery of bilirubin the main pigments a calla and urine — urobilinigen and stercobilinogen are formed, to-rye on air are oxidized in stercobilin (see) and urobilin (see). The normal maintenance of an indirect bilirubin in blood makes 0,2 — 0,8 mg / 100 ml. At increase in content of bilirubin in blood it is higher than 2 mg / 100 the ml develops jaundice (see). At jaundice in urine through the renal filter there passes direct bilirubin (see. Bilirubinurea ). At disturbance of functions of a liver in urine a large amount of urobilin sometimes is found (see. Urobilinuria ). Disturbance of porphyrinic exchange leads to development of the diseases relating to group porphyrias (see). At the purpurinuria accompanying a number of diseases note the increased allocation r urine of porphyrines.
Melanina (see) — dark brown and black pigments of the person and animals — are formed of tyrosine in pigment cells (see). Also the way of formation of melanin from 3 oxykynurenines is found. The insufficient formation of melanin caused by hl. obr. genetically caused hypoactivity of a tyrosinase, it is noted at albinism (see). At addisonovy disease (see) observe the strengthened formation of melanin leading to the raised xanthopathy. Treat the morbid conditions connected with disturbance of exchange of melanin melanosis (see) — excess accumulation of melanin, and also Melanoma (see) — the tumor consisting of the malignizirovanny cells producing melanin — melanoblasts. Disturbances of a xanthopathy — dyschromias of skin (see) can be caused not only by disturbance of exchange of melanin, but also anomalies of exchange of other pigments defining skin color — carotene (see) and hemoglobin.
Disturbance of exchange of tyrosine can lead to allocation with urine homogentistic to - you at which oxidation the dark pigment (is formed see. Alkaptonuria ). At the same time often there is a pigmentation of cartilages and other connecting fabric (see. Ochronosis ).
At some patol, states (e.g., at the E-hypovitaminosis), and also during the aging in nervous, muscular and connecting fabrics the pigment of the lipidic nature collects lipofuscin (see). At animals excess formation of the pigments of the lipidic nature arising obviously, as a result of an autookisleniye of unsaturated lipids and afterpolymerization of products of their oxidation, is revealed at action of ionizing radiation and malignant tumors.
The animal organism is not capable to synthesize a number of the pigments found in plants. However biosynthesis chlorophyll (see) in vegetable fabrics has common features with formation of porphyrines at animals. Carotinoids (see) are synthesized at consecutive condensation of molecules atsetil-KOA through education mevalonovy to - you. At oxidation of karotin xanthophylls are formed. The carotinoids which came to an organism of animals with vegetable food are exposed to oxidizing splitting (this process happens hl. obr. in a wall of guts) with formation of a retinal, aldehyde of vitamin A. Formed then vitamin A comes to blood and collects in various fabrics, including in a liver. In photoreceptors of a retina a retinal, connecting to protein opsin, forms rhodopsin (see), providing distinguishing of light (see. Rhodopsins ).
At disturbance of transformation of carotinoids into vitamin A a hypovitaminosis And, followed by considerable changes of an epithelium, damage of eyes etc. develops. The exogenous form of insufficiency of vitamin A meets seldom (see. Vitamin deficiency). Excess of carotene brings in a human body to carotenemias (see).
Flavonoids and antotsianidina (see. Flavones , Anthocyans ) in a vegetable organism are synthesized from shikimic to - you or at condensation of two molecules malonil-KOA with one molecule atsetil-KOA. In a human body flavonoids of food break up to smaller fragments; sometimes decomposition products of flavonoids are found in urine as a part of gomopirokatekhovy, gomovanilinovy and m - hydroxy-phenyl-acetic to - t.
Methods of definition — see in articles devoted to the description of separate pigments or groups of pigments.
N. V. Gulyaeva.