Parasitic plants, such as toji acquire nutrients through xylem of the host plants. To investigate the influence of parasitic-host interactions on phenolic composition and antioxidant activity from arid sites of Sonora, Mexico is the objective of this research. Organic and aqueous extracts from trees (stems) such as Prosopis glandulosa (Mesquite), Olneya tesota (Palo fierro), Parkinsonia aculeata (Palo verde), Acacia farnesiana (Vinorama), Quercus sp. (Encino o Oak), and Phoradendron californicum (toji) were collected in an arid zone. Each plant was analyzed for phytochemical screening, phenolic composition using Folin-Ciocalteu, AlCl3, DNP methods and reversed phase high performance liquid chromatography. In vitro the antioxidant properties were determined by 1,1-diphenyl-2-picryl hydrazyl radical scavenging (DPPH), ferric reducing antioxidant power (FRAP) and superoxide radical scavenging (O-2(center dot)). Pearson correlation was used for quantifying the relationship between phenolic content and antioxidant activity in toji compared to their non-parasitic hosts. The highest content of phenolic compounds and antioxidant capacity was found in the parasitic toji (Phoradendron californicum) compared to their hosts. Some correlations (r > 0.5, P < 0.01) between Mesquite or Vinorama (hosts) and toji secondary compounds (flavonoids and tannins) and between Oak and toji phenols and tannins could indicate that toji (parasite) might get some chemical compounds transferred from the host xylem.
Background: Throughout the years humanity has used plants to treat different illnesses. Plants have several secondary metabolites such as phenol compounds, which have important biological activities. In this work, we evaluated the phytochemical screening, the phenol content and the antiproliferative activity of nine methanolic plants extract: Bucida buceras, Haemotoxylon brasiletto, Bursera hindsiana, Bursera microphylla, Ambrosia ambrosioides, Phoradendron californicum, Annona muricata, Morinda citrifolia, and Larrea tridentata, in murine cell lines: RAW 264.7 and L929; and human cell lines: A549, HeLa, 22Rv-1, BxPc-3, LS-180 and ARPE-19. Methods: The type metabolites in the sample were evaluated in a phytochemical screening. The phenols content present in the plant was evaluated by the Folin-Ciocalteu´s method and the antiproliferative activity wad determinate by MTT method, searching the IC50 value in each extract for each cell line. Results: The most abundant secondary metabolites in these plants were lactonic groups, saponins, phenols/tannins and flavonoids. The phenolic content fell in a range from 43.11 ± 6.22 to 827.74 ± 3.48 µgGAE/mg, the order from best to worst was: P. californicum (oak) > L. tridentata > B. buceras > H. brasiletto > B. microphylla > B. hindsiana > P. californicum (mesquite) > A. ambrosioides > A. muricata > M. citrifolia. While the better extracts in antiproliferative activity were: A. muricata, B. buceras, L. tridentata, H. brasiletto (range from 13.35 ± 0.74 to 163.73 ± 8.42 µg/mL), showing IC50 value similars to the cisplatin drug in the different cell lines. Conclusions: In this study was possible observe that the richest plants in secondary metabolites were B. buceras, H. brasiletto, B. hindsiana, M. citrifolia and P. californicum. The plant extract with the highest phenolic content was P. californicum of oak. While in the antiproliferative activity the best extracts were: A. muricata and L. tridentata in murine and human cell lines, and also B. buceras and H. brasiletto only in the case of human cell lines.
BACKGROUND:Reactive Oxygen Species (ROS) impair the physiological functions of Retinal Pigment Epithelial (RPE) cells, which are known as one major cause of age-related macular degeneration and retinopathy diseases. The purpose of this study is to explore the cytoprotective effects of the antioxidant Bucida buceras extract in co-treatment with hydrogen peroxide (H2O2) delivery as a single addition or with continuous generation using glucose oxidase (GOx) in ARPE-19 cell cultures. The mechanism of Bucida buceras extract is believed to be associated with their antioxidant capacity to protect cells against oxidative stress.METHODS:A comparative oxidative stress H2O2-induced was performed by addition and enzymatic generation using glucose oxidase on human retinal pigment epithelial cells line. H2O2-induced injury was measured by toxic effects (cell death and apoptotic pathway) and intracellular redox status: glutathione (GSH), antioxidant enzymes (catalase and glutathione peroxidase) and reducing power (FRAP). The retino-protective effect of co-treatment with Bucida buceras extract on H2O2-induced human RPE cell injury was investigated by cell death (MTT assay) and oxidative stress biomarkers (H2O2, GSH, CAT, GPx and FRAP).RESULTS:Bucida buceras L. extract is believed to be associated with the ability to prevent cellular oxidative stress. When added as a pulse, H2O2 is rapidly depleted and the cytotoxicity analyses show that cells can tolerate short exposure to high peroxide doses delivered as a pulse but are susceptible to lower chronic doses. Co-treatment with Bucida buceras was able to protect the cells against H2O2-induced injury. In addition to preventing cell death treatment with antioxidant plant could also reverse the significant decrease in GSH level, catalase activity and reducing power caused by H2O2.CONCLUSION:These findings suggest that Bucida buceras could protect RPE against ocular pathogenesis associated with oxidative stress induced by H2O2-delivered by addition and enzymatic generation.
The present investigation evaluated 4 different solvent compositions for their relative capacity to extract total phenolic and total flavonoid (TF) components of the leaves, trunks, and stems of Bucida buceras L. (Combretaceae), and the stems of Phoradendron californicum (Viscaceae), plus mesquite and oak species endemic to the Southwestern United States, northern Mexico, and tropical regions of Central and South America, as well as to profile the composition of these plant materials and to measure their antioxidant capacity.