ABSTRACT
BACKGROUND: Previous studies have demonstrated that sex hormones modulate epidermal permeability barrier homeostasis, and when the balance of these hormones is altered at menopause or during the menstrual cycle, skin sensitivity or barrier function is changed. OBJECTIVES: To observe the direct effects of sex hormones on epidermal homeostasis. METHODS: We examined the effects of topical application of sex hormones on permeability barrier recovery after tape stripping in the hairless mouse. To avoid the influence of systemic hormonal alteration, we employed male animals. RESULTS: Application of androgen (testosterone or androsterone) delayed the barrier recovery, and the delay was overcome by co-application of beta-estradiol. Progesterone also delayed the barrier recovery, but in this case the delay was enhanced by beta-estradiol. CONCLUSIONS: These results suggest that changes in sex hormone balance might be associated with the skin dysfunction that often occurs during menopause, and at certain points during the menstrual cycle.
Subject(s)
Epidermis/drug effects , Estradiol/pharmacology , Water Loss, Insensible/drug effects , Androsterone/antagonists & inhibitors , Androsterone/pharmacology , Animals , Epidermis/physiology , Homeostasis/drug effects , Male , Mice , Mice, Hairless , Permeability/drug effects , Skin Absorption/drug effects , Testosterone/antagonists & inhibitors , Testosterone/pharmacologyABSTRACT
Se reporta una vía alternativa para la síntesis del 3-etilencetal-androsta-3, 17-diona, el cual es un intermedio importante para la obtención de corticoides por construcción de la cadena lateral de 17-ceto esteroides. En nuestro caso, partiendo de la androsta-4-ene-3, 17-diona, se obtuvo el producto deseado en 3 pasos de síntesis con buenos rendimientos
Subject(s)
Androsterone/antagonists & inhibitors , Androsterone/chemical synthesis , Cholesterol Side-Chain Cleavage Enzyme , Complement Pathway, AlternativeABSTRACT
Se reporta una vía alternativa para la síntesis del 3-etilencetal-androsta-3, 17-diona, el cual es un intermedio importante para la obtención de corticoides por construcción de la cadena lateral de 17-ceto esteroides. En nuestro caso, partiendo de la androsta-4-ene-3, 17-diona, se obtuvo el producto deseado en 3 pasos de síntesis con buenos rendimientos(AU)
Subject(s)
Complement Pathway, Alternative , Cholesterol Side-Chain Cleavage Enzyme , Androsterone/antagonists & inhibitors , Androsterone/chemical synthesisSubject(s)
Androgen Antagonists , Androgen-Insensitivity Syndrome/prevention & control , Tamoxifen/pharmacology , Androgen-Insensitivity Syndrome/chemically induced , Androsterone/antagonists & inhibitors , Animals , Chick Embryo , Dihydrotestosterone/antagonists & inhibitors , Etiocholanolone/analogs & derivatives , Etiocholanolone/antagonists & inhibitors , MaleABSTRACT
Androsterone sulfate (5alpha-androstan-3alpha-ol-17-one, 3-sodium sulfate) administered to freely moving rats via cerebroventricular cannulae induced analgesia, wet-dog shakes, body jerks, rigidity, Straub tail, hypermotility, excessive grooming, hyperreactivity to stimuli, aggression, escape behavior, EEG spiking, and behavioral and EEG seizures. These responses resemble those produced by certain opiate drugs and by beta-endorphin, an endogenous peptide; they appear during the 5-min infusion period, persist in some cases for several hours, and are diminished by pretreatment with the narcotic antagonist naloxone. These findings indicate that steroid hormones can act upon at least some of the same central pathways influenced by recognized opiate compounds.
