Neuroprotective action and free radical scavenging activity of Guttiferone-A, a naturally occurring prenylated benzophenone.

Reactive oxygen species (ROS) are important mediators in a number of neurodegenerative diseases and molecules capable of scavenging ROS may be a feasible strategy for protecting neuronal cells. We previously demonstrated a powerful iron-chelating action of Guttiferone-A (GA), a naturally occurring polyphenol, on oxidative stress injuries initiated by iron overload. Here we addressed the neuroprotective potential of GA in hydrogen peroxide and glutamate-induced injury on rat's primary culture of cortical neurons and PC12 cells, respectively, and antioxidant properties concerning scavenging and anti-lipoperoxidative activities in cell-free models. The decrease in cell viability induced by each of the toxins, assessed by [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] (MTT) assay, was significantly attenuated by GA. In addition, GA was found to be a potent antioxidant, as shown by (i) inhibition of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical reduction (EC50=20.0 µM), (ii) prevention against chemically or electrochemically generated superoxide radicals, (iii) inhibition of spontaneous brain lipid peroxidation and (iv) interference with the Fenton reaction. These results indicate that GA exerts neuroprotective effects against H2O2 or glutamate toxicity and its antioxidant activity, demonstrated in vitro, could be at least partly involved. They also suggest a promising potential for GA as a therapeutic agent against neurodegenerative diseases involving ROS and oxidative damage.

[Liver function and iatrogenic anovulation]. / Función hepática y anovulación iatrogénica.

PIP: 58 postpartum patients between the ages of 20-35 were selected from a series of 208 oral contraceptive users for liver function studies. They had been treated with 1 of 3 anovulatory combined oral contraceptives for a period of 1 year. The preparations used were: 1) .05 mcg of ethinyl estradiol + 1 mcg of ethinyl-nortestosterone acetate (25 patients), 2) .075 mcg of ethinyl estradiol + 1 mcg of ethinyl-nortestosterone acetate (16 patients), and 3) .50 mcg of ethinyl estradiol + .50 mcg of norgestrel (17 patients). Studies were done trimestrally and included direct bilirubing, total bilirubin, turbidity of timol, SGOT, SGFT, alkaline phosphatase, and sulfobromophthalien retention. Menstruation was induced on the 28th day postpartum by administering 20 mcg of nortestosterone acetate and .04 mcg of ethinyl estradiol (Duogynon). The assigned contraceptives was taken on a normal basis thereafter. No changes in liver function that could be attributed to the pills were observed. Pathological modifications were, however, observed in the tests for turbidity (in 52.5%, 31.3%, and 25%, respectively), SGOY (0%, 0%, and 12.5%, respectively), and sulfobromophthalien retention (0%, 13.3%, and 11.76%); in some instances the changes persisted throughout the study. Alterations in turbidity, SGOT and SGFT that occurred in 1 patient with a history of hepatitis were an indication to the authors that hepatitis should be a contraindication for use of orals. Graphs of test results are included.^ieng