SYNTHETIC POLYMERS AS POTENTIAL SUSTAINED-RELEASE COATINGS.
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The functional state of the adrenal cortex (cortisol and 11-OCS in blood, 17-OCS in 24-hours' urine) was studied in 105 patients with chronic relapsing pancreatitis in the acute state. An increase of adrenal cortex glucocorticoid activity was determined in 46.7% of the patients. A decrease of glucocorticoid activity was observed in 10% of the patients. During remission a tendency towards hormone normalization was noted in most of the patients, except for 5 patients with marked exocrine pancreatic insufficiency in whom the hormone content of adrenal cortex remained low. The type of pancreatitis as well as the severity and duration of the disease were noted to exert no regular impact upon the changes of the indices. Since exacerbation of chronic pancreatitis is frequently accompanied by elevated glucocorticoid activity of the adrenal cortex, the prescription of glucocorticoid hormones in such patients seems undesirable. The administration of such hormones is possible only for the patients with exocrine pancreas insufficiency.
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The conversion of deoxycorticosterone to 18-hydroxycorticosterone was examined by using sonicated mitochondrial suspension of bovine adrenocortex. The KM's of deoxycorticosterone for the 11 beta- and 18-hydroxylations were in the same range (1 microM), while the turnover number for the 11 beta-hydroxylation (50 nmol/min/nmol cytochrome P-450) was 6 times as great as that for the 18-hydroxylation (7.3). The KM and turnover number for the 18-hydroxylation of corticosterone were 6 microM and 0.4, respectively. Those for the 11 beta-hydroxylation of 18-hydroxy-11-deoxycorticosterone were 120 microM and 5. When products were analysed in the incubation of deoxycorticosterone with the mitochondrial suspension containing a larger amount of cytochrome P-450, the formation of 18-hydroxycorticosterone was observed in addition to the formation of corticosterone and 18-hydroxy-11-deoxycorticosterone. The kinetic interrelation between the two pathways was further examined together with consideration of the cytochrome P-450-linked hydroxylation system. The result suggests that the pathway via 18-hydroxy-11-deoxycorticosterone substantially participates in the formation of 18-hydroxycorticosterone from deoxycorticosterone. The perturbation of this network by an artificial means, such as the addition of Triton X-100, revealed that the detergent (0.02%) facilitated the production of 18-hydroxycorticosterone from deoxycorticosterone, regardless of its inhibitory effect on the production of corticosterone and 18-hydroxy-11-deoxycorticosterone from deoxycorticosterone. These studies provide an important insight into the regulation mechanism of 18-hydroxycorticosterone formation from the precursors on the mitochondrial level.
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