Assessment of filtration efficiency and physiological responses of selected plant species to indoor air pollutants (toluene and 2-ethylhexanol) under chamber conditions.

Three common plant species (Dieffenbachia maculata, Spathiphyllum wallisii, and Asparagus densiflorus) were tested against their capacity to remove the air pollutants toluene (20.0 mg m-3) and 2-ethylhexanol (14.6 mg m-3) under light or under dark in chamber experiments of 48-h duration. Results revealed only limited pollutant filtration capabilities and indicate that aerial plant parts of the tested species are only of limited value for indoor air quality improvement. The removal rate constant ranged for toluene from 3.4 to 5.7 L h-1 m-2 leaf area with no significant differences between plant species or light conditions (light/dark). The values for 2-ethylhexanol were somewhat lower, fluctuating around 2 L h-1 m-2 leaf area for all plant species tested, whereas differences between light and dark were observed for two of the three species. In addition to pollutant removal, CO2 fixation/respiration and transpiration as well as quantum yield were evaluated. These physiological characteristics seem to have no major impact on the VOC removal rate constant. Exposure to toluene or 2-ethylhexanol revealed no or only minor effects on D. maculata and S. wallisii. In contrast, a decrease in quantum yield and CO2 fixation was observed for A. densiflorus when exposed to 2-ethylhexanol or toluene under light, indicating phytotoxic effects in this species.

Induction of apoptosis in HeLa cells via caspase activation by resveratrol and genistein.

Selectively inducing apoptosis in cancer cells is a much desired strategy when tolerance toward side effects is minimal during chemotherapy. In our search for natural products that can induce apoptosis in human cervical cancer cells (HeLa), we selected resveratrol and genistein for our study. We conducted several experiments to test whether genistein can synergistically enhance the apoptotic potential of resveratrol at doses lower than the usual cytotoxic dose. Both resveratrol and genistein were able to induce apoptosis by enhancing the activities of caspase-9 and caspase-3 by themselves and also in combination. After 24 h of exposure to resveratrol and genistein, individually or in combination, lowered mitochondrial membrane potential was observed in HeLa cells. In addition, the mitochondrial membrane potential in HeLa cells was decreased, forcing JC-1 to stay in the monomeric form. The monomeric JC-1(5,5',6,6' -tetrachloro-1,1',3,3'-tetraethyl benzimedazolyl carbocyanine iodide) emitted green fluorescence. In the control group, the color of the fluorescence was red due to aggregation of JC-1 in the physiological pH. The treatment groups exhibited DNA fragmentation as the hallmark of apoptotic nuclear features. We also detected an obvious decrease in the level of HDM2 gene expression after both individual and combination treatments with resveratrol and genistein. Our findings suggest that resveratrol and genistein when combined can induce apoptosis at doses lower than usual doses, through the activation of caspases cascade, and by decreasing the expression of HDM2.

Anticancer activities of genistein-topotecan combination in prostate cancer cells.

Prostate cancer is one of the leading causes of death in men aged 40 to 55. Genistein isoflavone (4', 5', 7-trihydroxyisoflavone) is a dietary phytochemical with demonstrated anti-tumour activities in a variety of cancers. Topotecan Hydrochloride (Hycamtin) is an FDA-approved chemotherapy drug, primarily used for secondary treatment of ovarian, cervical and small cell lung cancers. This study was to demonstrate the potential anticancer efficacy of genistein-topotecan combination in LNCaP prostate cancer cells and the mechanism of the combination treatment. The LNCaP cells were grown in complete RPMI medium, and cultured at 37°C, 5% CO(2) for 24-48 hrs to achieve 70-90% confluency. The cells were treated with varying concentrations of genistein, topotecan and genistein-topotecan combination and incubated for 24 hrs. The treated cells were assayed for (i) post-treatment sensitivity using MTT assay and DNA fragmentation, (ii) treatment-induced apoptosis using caspase-3 and -9 binding assays and (iii) treatment-induced ROS generation levels. The overall data indicated that (i) both genistein and topotecan induce cellular death in LNCaP cells, (ii) genistein-topotecan combination was significantly more efficacious in reducing LNCaP cell viability compared with either genistein or topotecan alone, (iii) in all cases, cell death was primarily through apoptosis, via the activation of caspase-3 and -9, which are involved in the intrinsic pathway, (iv) ROS generation levels increased significantly with the genistein-topotecan combination treatment. Treatments involving genistein-topotecan combination may prove to be an attractive alternative phytotherapy or adjuvant therapy for prostate cancer.

Genistein-selenium combination induces growth arrest in prostate cancer cells.

The prognosis for patients with metastasized prostate cancer is still poor, despite conventional aggressive therapeutic modalities. Several in vitro studies together with animal models and epidemiological studies have indicated that phytochemicals can be antitumorigenic and may be protective against human cancers. However, the potential antitumor effects of genistein isoflavone, a widely studied nutrient phytochemical, have been equivocal. In this study, we investigated the effects of genistein-selenium (Gn-Se) combination on chemosensitivity and matrix metalloproteinase-2 (MMP-2) expression levels in PC3 (hormone-independent) and LNCaP (hormone-dependent) prostate cancer cells. 3-(4,5-Dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium staining and ATP bioassay showed that genistein, selenium, and Gn-Se combination significantly inhibited growth of LNCaP and PC3 cells in a dose- and time-dependent manner, independent of hormonal status, and with no significant differences in chemosensitivity between LNCaP and PC3. Gn-Se combination induced significantly the greatest growth inhibition in both cell lines. Growth inhibition was through apoptosis induction. The treatment-induced apoptotic cascades are caspase-dependent, with evidence of an alternative non-caspase pathway(s). Treatment also induced a dose- and time-dependent decrease in MMP-2 expression levels in PC3 and LNCaP with no significant differences between the two cells. Gn-Se combination induced the greatest depression in MMP-2. Overall, none of the treatment modalities had any significant inhibitory effect in normal prostate epithelial cells. The data obtained from the present study indicate that Gn-Se combination may have chemopreventive value and/or may be adjuvant to standard therapy for prostate tumors independent of hormonal status. MMP-2 expression in cancer cells has been associated with active invasion and metastasis.