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Molecular effects of fermented papaya preparation on oxidative damage, MAP Kinase activation and modulation of the benzo[a]pyrene mediated genotoxicity

2006; Wiley; Volume: 26; Issue: 2 Linguagem: Inglês

10.1002/biof.5520260205

1872-8081

Okezie I. Aruoma, Renato Colognato, Ilaria Fontana, Joanne Gartlon, Lucia Migliore, Keiko Koike, Sandra Coecke, Evelyn Lamy, Volker Mersch‐Sundermann, Incoronata Laurenza, Luca Benzi, Fumihiko Yoshino, Kyo Kobayashi, Masaichi‐Chang‐il Lee,

Nanoparticles: synthesis and applications

The involvement of oxidative and nitrosative stress mechanisms in several biological and pathological processes including aging, cancer, cardiovascular and neurodegenerative diseases has continued to fuel suggestions that processes can potentially be modulated by treatment with free-radical scavengers and antioxidant. The fermented papaya preparation (FPP) derived from Carica papaya Linn was investigated for its ability to modulate oxidative DNA damage due to H2O2 in rat pheochromocytoma (PC12) cells and protection of brain oxidative damage in hypertensive rats. Cells pre-treated with FPP (50 μg/ml) prior to incubation with H2O2 had significantly increased viability and sustenance of morphology and shape. The human hepatoma (HepG2) cells exposed to H2O2 (50 μM) showed an olive tail moment of 10.56 ± 1.44 compared to 1.37 ± 0.29 of the solvent control. A significant reduction (P ⩽ 0.05) of DNA damage was observed at concentrations ⩾ 10 μg/ml FPP, with 50 μg/ml FPP reducing the genotoxic effect of H2O2 by about 1.5-fold compared to only H2O2 exposed cells. Similarly, concentrations≥50μg/ml FPP significantly reduced DNA migration in co-treated cells compared with only the benzo[a]pyrene treated cells with a dose of 100μg/ml FPP reduced the DNA damage 2-fold. The potential of FPP to regulate the phosphorylation status of ERK 1/2, Akt, and p38 was analyzed by Western blot analysis. FPP showed the potential to modulate the H2O2-induced ERK, Akt and p38 activation with the reduction of p38 phosphorylation induced by 250μMH2O2 being more pronounced. Supplementation with FPP significantly inhibited the increased decay rate constant of the MC-PROXYL (a blood brain barrier permeable nitroxyl spin probe) ESR signal in the spontaneously hypertensive rat brain suggesting modulation of oxidative stress. These studies indicate that FPP can modulate oxidative injury supporting the view that prophylactic potentials in neurodegenerative diseases could be facilitated by FPP.