Flow-cytometric analysis of reactive oxygen species in cancer cells under treatment with brassinosteroids.

To explore the underlying mechanism of cancer cell growth inhibition by brassinosteroids (BS), reactive oxygen species (ROS) generation under treatment with 28-homocastasterone and its synthetic derivatives (22S,23S)-28-homocastasterone was measured in A549 human lung adenocarcinoma cells. BS induced ROS generation in A549 cells and their growth in a time and dose-dependent manner. The maximal effect was observed for (22S,23S)-28-homocastasterone which at 30μM concentration showed a 6-fold increase of ROS generation in comparison with the control.

Inhibition of 17β-estradiol activation by CYP1A1: genotype- and regioselective inhibition by St. John's Wort and several natural polyphenols.

Several epidemiological studies associate certain CYP1A1 genotypes, alone or in combination, with an increased risk of estrogen-related cancers. Previously we demonstrated that metabolic activation of estrogens by CYP1A1 is a genotype-dependent reaction with the CYP1A1.2 (Ile462Val) variant being the most efficient catalyst (Kisselev et al.

Human CYP1A1 variants lead to differential eicosapentaenoic acid metabolite patterns.

To answer the question whether the most common allelic variants of human CYP1A1, namely CYP1A1.1 (wild type), CYP1A1.2 (Ile462Val), and CYP1A1.

Association of CYP1A1 polymorphisms with differential metabolic activation of 17beta-estradiol and estrone.

Several epidemiologic studies associate certain CYP1A1 genotypes, alone or in combination, with an increased risk of estrogen-related cancers. To answer the question of whether genotype-dependent activation of estrogens by CYP1A1 could be the underlying mechanism, we studied the hydroxylation activity of the most common allelic variants of human CYP1A1 towards both endogenously occurring estrogens, 17beta-estradiol (E2) and estrone (E1). We expressed and purified CYP1A1.

CYP1A1 genotype-selective inhibition of benzo[a]pyrene activation by quercetin.

Epidemiological studies suggest that food rich in quercetin and naringin may protect against certain types of lung cancer, and that genotype dependent inhibition of cytochrome P450 1A1 (CYP1A1)-mediated bioactivation of procarcinogens could be the underlying mechanism. We studied the inhibitory effects of quercetin and naringin on the terminal bioactivation step of benzo[a]pyrene (B[a]P), a member of the major class of lung carcinogens. This reaction (epoxidation of (+/-)-trans-7,8-dihydro-7,8-dihydroxy-B[a]P to the ultimate carcinogenic product, (+/-)-B[a]P-r-7,t-8-dihydrodiol-t-9,10-epoxide (diolepoxide 2)) was examined using three of the most common allelic variants of human CYP1A1, namely wild-type CYP1A1.