HYPOXANTHINE (6 hypoxanthine) — the nitrogen base which is taking part in creation of nucleic acids:
It is eurysynusic in an animal and flora in a stand-at-ease, and also in connection with phosphoric to - that and a D-ribose in the form of so-called inosinic to - you are an inozinmonofosfata (see. Inosinic acids ) or in the form of a riboside of hypoxanthine — inosine (hypoxanthosine).
It is found in 5' - the provision of an anti-codon of many transport ribonucleic to - t (TRNK) as a minor component.
Represents colourless acicular crystals, t ° pl (with decomposition) 150 °, a pier. weight (weight) 136,11. Let's badly dissolve in water, alcohol and ether and it is good — in alkalis and to-takh. In the UF-range it is characterized by maxima of absorption at the wavelength of 248 nanometers (pH 1,0) and 258 nanometers (pH 11,0). It is amphoteric.
In an animal organism of G. it is formed at deamination of adenine (see. Purine bases) or adenosine with the participation of specific enzymes dezaminaz (KF 3. 5. 4).
Unlike adenine, G. can complementary form couples of bases not only with uracil, but also with tsitoziny and with adenine. In some TRNK instead of G. 1 methyl hypoxanthine which sometimes in a free look is defined in urine is found. At hydrolysis nucleinic to - t strong to-tami and alkalis a quantity of G. is found in a hydrolyzate.
It is noted that at ischemia of a myocardium adenosine in cells is deaminized more intensively, than normal therefore in the blood flowing from a zone of ischemia the concentration of inosine and G. Polagayut increased in comparison with norm is defined that this test can serve as an exponent of ischemia. At disturbances of purine exchange the characteristic encephalopathy (Lesh's disease — Naykhana) which is clinically shown mental retardation, loss of coordination of movements and so forth is observed; increase in contents uric to - you in blood serum and urine is observed. In fibroblasts of people with Lesh's disease — Naykhana is found hypoactivity hypoxanthine-fosforiboziltransferazy (KF 2. 4. 2. 8), what is proved by sharp reduction of inclusion 3N-G or 3H-guanine in kernels and cytoplasm of fibroblasts of patients in comparison with norm. It demonstrates the broken exchange nucleinic to - t at such patients.
At an inherited disorder or total absence of synthesis of enzyme of a xanthineoxidase (KF 1. 2. 3. 2) with urine G. and xanthine is allocated (a clinical syndrome a xanthinuria). At disturbance of purine exchange develops gout (see), at a cut in various fabrics (cartilages, ligaments, sinews, kidneys, etc.) almost insoluble crystals of salts uric to - you are postponed.
Bibliography: Venkstern T. V. Primary structure of transport RNA, M., 1970, bibliogr.; Mardashev S. R. Biochemical problems of medicine, page 52, M., 1975; Chemistry and biochemistry of nucleic acids, under the editorship of I. B. Zbarsky and S. S. Debov, L., 1968, bibliogr.; H and 1 1 R. N of The modified nucleosides in nucleic acids, N. Y. — L., 1971, bibliogr.
B. F. Vanyushin.