ductase, an enzyme which converts testosterone to 5-?-dihydrotestosterone (DHT), which is the more active form of the hormone (1).
Ripple, Henry, Rago and Wilding studied the effects of androgens in LNCaP androgen-responsive prostate carcinoma cell lines to show that androgens can increase their oxidative stress (1). They used LNCaP androgen-responsive cells and the androgen-independent DU145 line, exposing both to the androgen Sa-dihydroxytestosterone (DHT) and the synthetic androgen, R1881 androgens on the glutathione system, catalase, and ?-glutamyl transpeptidase. Oxidation reactions were carried out using the dye 2',7'-dichlorofluorescein diacetate, which fluoresces in the presence of H2O2 (hydrogen peroxide) and hydroxyl radicals, to measure the generation of reactive oxygen species. Oxygen consumption was measured using a Clarktype electrode (1). The chromagen specific for malonaldehyde and 4-hydroxy-2(E)-nonenal was used to evaluate lipid peroxidation, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazonium bromide (MTT) reduction was assayed to determine mitochondrial activity. A spectrophotometer was used to assay catalase, ?-glutamyl transpeptidase, and intracellular glutathione activity in the antioxidant reactions.
The results showed that in the LNCaP androgen-responsive cells, both DHT and R1881 produced a proliferative response and a change in oxidative state, along with a significant increase in mitochondrial activity (1). These effects were not seen in the androgen-independent DU145 cell line. Also, the synthetic androgen R1881 affected the LNCaP cells by producing an increase in oxygen consumption, an increase in the activities of catalase and ?-glutamyl transpeptidase, and a decrease in the intracellular concentration of glutathione. It was also noted that H2O2 or menadione as an oxidizing agent increased ?-glutamyl transpeptidase activity in LNCaP cells, while ascorbic acid, an antioxidant, red...