The effect of hydrocortisone acetate on the development of mouse embryos.

Hydrocortisone (Kendall's compound F, 17-hydroxycorticosterone, Cortisol) and cortisone (Kendall's compound E, 17-hydroxy-ll-dehydrocorticosterone) have been widely used in medicine for about 20 years, first as adrenal hormones in substitution therapy. Since the discovery of Hench, Kendal, Slocumb & Polley (1949) that cortisone is beneficial against a wide range of rheumatic diseases and against all forms of arthritis, many more types of diseases have been added in later years to the list of ailments curable with cortisone, namely bronchitis, bronchial asthma, pulmonary tuberculosis, colitis, various inflammatory conditions and certain skin, blood and eye diseases. Hydrocortisone is used against the same diseases as cortisone; in fact, it is believed that cortisone becomes pharmacologically active only after conversion to hydrocortisone in the liver (Cope, 1964). Particularly in the inflammatory conditions cortisone must be converted to hydrocortisone to become antiphlogistic (Applezweig, 1962). The biochemical mode of action of these drugs was not understood for many years. More recently, hydrocortisone in particular has been used extensively in investigations in the field of cell biology, particularly in investigations of protein synthesis. In general, it is believed that at the cellular level hydrocortisone influences many metabolic processes. First, it has a cell-stabilizing effect which can be expressed for instance in its antihaemolytic activity. It stabilizes lipoprotein membranes in general, and in particular prevents lysosomes from releasing the hydrolytic enzymes contained inside these organelles (de Duve, Wattiaux & Wibo, 1961). The latter effect may explain the mechanism of the protective properties of hydrocortisone against cell damage induced by such factors as irradiation with ultraviolet light or X-rays or intoxication with bacterial toxins or chemical agents (Weissmann & Dingle, 1961; Weissmann & Fell, 1962; Weissmann & Thomas, 1963). However, hydrocortisone does not always protect cells from injury or alleviate damage. On the contrary, in some cases it delays the repair of cellular injury. This paradoxical phenomenon is most probably due to occasional stimulation of the synthesis of enzymes deaminating amino acids, which is followed by delayed protein synthesis (Kenney, 1962 a, b; Segal & Kim, 1963; Schimke,