Removal of the toxic effects of chlormadinon acetate on the development of Drosophila melanogaster via the use of nordihydroguaiaretic acid.

In this study, the effects of chlormadinon acetate (CMA) and CMA + nordihydroguaiaretic acid (NDGA) on various developmental stages of Drosophila melanogaster were investigated. Different concentrations of CMA (1.0; 3.0; 5.0 and 10.0 µM/100 mL medium) and CMA + NDGA as the concentrations of CMA (1.0 + 1.0; 3.0 + 3.0; 5.0 + 5.0 and 10.0 + 10.0 µM/100 mL medium) were carried out during the developmental periods of the flies. When F(1) progeny of control and application groups were compared, CMA was found to extend the process of metamorphosis and decrease the total offspring numbers. However, these negative effects were inhibited by NDGA treatment at different concentrations. These results suggest that NDGA could effectively inhibit CMA-induced abnormalities in developmental stages of D. melanogaster. It was found that the difference between the groups was significantly important (p < 0.05).

Binding of chlormadinone acetate to cytosol from human benign prostatic hypertrophy.

Chlormadinone acetate was bound to cytosol from the human benign prostatic hypertrophy in a high affinity fashion. The kd and number of maximum binding site of the binding were 5.4 +/- 0.7 X 10(-9) M and 67.9 +/- 5.8 fmol/mg protein, respectively. When compared with the binding to dihydrotestosterone, the Kd for chlormadinone acetate was greater. The number of maximum binding site for chlormadinone acetate was observed to be smaller than that for dihydrotestosterone, but these two values were not different statistically. The binding of chlormadinone acetate was inhibited significantly by the addition of R 1881 or cyproterone acetate. However, dihydrotestosterone revealed itself to be a weak inhibitor of the binding. The cytosol prelabelled with chlormadinone acetate was not bound to the nuclei of the human prostate.