[Mechanisms of the early effect of biologically active hydroxysterols: calcitriol and ecdysterone. Modulation of systems which generate low molecular weight activators of guanylate cyclase]. / Doslidzhennia mekhanizmiv rann'oï diï biolohichno aktyvnykh oksysteryniv: kal'tsitriolu ta ekdysteronu. Moduliatsiia sistem, shcho heneruiut' nyz'komolekuliarni aktyvatory guanilattsyuklazy.

Three metabolic channels producing active forms of oxygen (OH.), carbon (CO) and nitrogen (NO) were studied for their contribution to the mechanism of early activation of guanylate cyclase by hydroxysterols: ecdysterone (20-hydroxyecdysone) and calcitriol (1 alpha, 25-dihydroxyvitamin D3) which are steroid agonists of phospholipid signal system in target tissues. It is established that in the cells of target tissues (brain, heart, liver) affected by the mentioned hydroxysterols only NO- and CO- metabolic lipid channels are activated while the nucleotide metabolic channel of generation of OH--radical is blocked. It is supposed that the nucleotide OH. metabolic channel activation due to oxidation of oxypurines and dihydroorotic acid most probably takes no part in formation of the negative feedback and termination of the signal of phospholipid signalling system by means of activation of soluble guanylate cyclase in contrast to the lipid channel of OH. formation due to oxidation of arachidonic acid.