Age and seasonal differences in the synthesis and metabolism of testosterone by testicular tissue and pineal HIOMT activity of Uinta ground squirrels (Spermophilus armatus).
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to L C Ellis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Rat pituitary MAO activity was reduced by constant darkness and by additions of melatonin in vitro and was increased by constant light and by pinealectomy. Hypothalamic MAO activity followed the same pattern but was less dramatically affected. The data suggest that MAO may be a target enzyme for melatonin.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The frequency of spontaneous in vitro contractions of seminiferous tubules of the rat appeared to be increased in a dose-dependent manner by prostaglandin F1alpha. PGF1alpha treatment increased the tonus of the smooth muscle cells in the wall of the tubules as indicated by a reduction in the diameter of the tubules. When the tubules were rinsed successively with fresh Tyrode's solution, the contractile frequency was diminished. Returning the original bathing medium to the tubules restored their contractile frequency, as did treatment of the rinsed tubules with PGF1alpha (10(-7) M). Preinjecting ther rats with indomethacin tended to reduce the contractile frequency of the extirpated tubules. Treating the tubules with a solution of indomethacin for 90 min. in vitro was more effective than pretreatment in vivo in reducing contractile frequency, but a combination of these two procedures produced the greatest inhibition. PGF1alpha restored the contractile frequency of the indomethacin-treated tubules. Our results indicate that PGs modulate the in vitro contractility of the tubules.
Contractions of rabbit testicular capsules in vitro and in vivo in response to prostaglandin F2a, epinephrine, and acetylcholine were measured in the presence of prostaglandin E1 (PGE1). Contractions induced by these agents were markedly inhibited at 10-7 M concentrations of PGE1 in both preparations. Even so, lower levels of PGE1 (10-8 or 10-9 M) potentiated epinephrine- or acetylcholine-induced stimulation of increased tonus in vovo. Epinephrine, PGE1, and PGF2a caused increased tonus and contractions in vitro and in vovo; however, acetylcholine stimulated the testicular capsule much more in vivo than in vitro. The control log dose-response curve for epinephrine stimulation showed a slight decrease in the upper concentration range. Propranolol, a beta-adrenergic blocking agent, more than overcame this decrease and also prevented a theophylline inhibition of epinephrine-induced contraction. Prostaglandin E1's bimodal effect gives it the ability to modulate testicular contractions by increasing stimulation by other agonists in vovo at low concentrations of PGE1 but inhibiting it at higher concentrations. Thus PGE1 is a potential regulator of testicular capsular motility and possibly sperm transport and hemodynamics.
Liver mitochondria from alphatocopherol deficient rats swell more rapidly, both spontaneously and in the presence of GSH, than those from control animals. The increased swelling of deficient mitochondria induced by GSH was completely eliminated when mitochondria were left longer than two hours at 0 degrees in the suspending medium. GSH-induced swelling of liver mitochondria from alpha-tocopherol deficient rats is reversed by ATP, polyvinyl pyrrolidone (PVP) and by oral administration alpha-tocopherol (2 mg/day per rat). Swelling of mitochondria in the above system was completely inhibited by the respiratory chain inhibitor, cyanide (.001 M), and partially by azide (0.001 M). We suggest that the swelling tendency of liver mitochondria from alpha-tocopherol deficient rats might be associated with an altered respiratory mechanism and/or an alteration in membrane permeability.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.