Steroidal Inactivator Research Articles

Effects of Protein, Lipids, and Surfactants on the Antimicrobial Activity of Synthetic Steroids

Three 4-azacholestanes and two A-norcholestanes were inactivated by 10 and 20% bovine serum and by 1.0, 2.5, and 5.0% sheep blood. The five compounds exhibited hemolytic properties when tested with 2% sheep blood and 2% human blood. These cholestanes inhibited Streptococcus pyogenes and were completely inactivated by 0.1% lecithin. Tween 80 was comparable to lecithin in causing the inactivation of steroids; 1% polyethylene glycol-4000 was inert; 1% Tween 20 and 1.0% Span 20 caused the inactivation of 3beta,4-dimethyl-4-aza-5alpha-cholestane (ND-307). The sodium salts of four fatty acids, oleate, stearate, deoxycholate, and lauryl sulfate (0.1 to 1.0 mg/ml), effectively interfered with the action of ND-307. The steroids appear to have some properties similar to those of antimicrobial surfactants of the cationic type but have certain distinct features.

Hepatic regulation of adrenal cortical function.

Under many different experimental and physiological conditions, a close correlation has been found between the size of the adrenal glands and the ca-pacity of the liver to inactivate adrenal cortical hormones by ring A reduction in vitro. We have concluded from this close correlation that there is a similar parallel relationship between the in vivo capacity of the liver to inactivate corti-costeroids, and the adrenal cortical secretion rate. This conclusion is based on several assumptions which are discussed. The present experiments demon-strate that this relationship denotes secondary responses of the adrenal cortex to primary, independent variations in hepatic inactivation of corti-costeroids. Neither ACTH nor adrenal cortical hormones increases the capacity of the liver to inactivate corticosteroids. In contrast, however, a primary diminution of hepatic capacit for adrenal steroid inactivation by surgical removal of 65% of the liver tissue can cause secondary adrenal atrophy. Therefore, the parallel re...

Effect of antigonadotrophic serum on recent intrasplenic ovarian implants of castrate mice.

IF TECHNICAL error is excluded, tumors appear with consistent regularity in the laboratory rodent ovary when it is transplanted to the spleen of a castrate animal. This frequently confirmed response was first recorded by Biskind and Biskind (1), who suggested that tumors arise in ovaries transplanted to the spleen as a result of excessive and continuous gonadotrophic stimulation. In their opinion, enhanced gonadotrophic secretion follows hepatic inactivation of gonadal steroids which must pass through the liver en route to the general circulation from the ovarian implant in the spleen. The ensuing loss of the well-known inhibiting effect of ovarian hormones on the gonadotrophic secretions of the pituitary gland leads to exposure of the intrasplenic grafts to heightened gonadotrophic stimulation which eventually terminates in tumor formation. Support for the postulation of Biskind and Biskind has been derived from widely different experimental approaches. The literature has been summarized (3, 6, 7, 8).

Studies on the function of liver cell (especially about inactivation of steroid hormones) in the course of experimental liver cancer production.

Studies on the function of liver cell (especially about inactivation of steroid hormones) in the course of experimental liver cancer production.