Prevention Of Oxidative Stress-related Diseases Research Articles

Red cabbage anthocyanins may protect blood plasma proteins and lipids

Abstract The present in vitro study was designed to examine the antioxidative activity of red cabbage anthocyanins (ATH) in the protection of blood plasma proteins and lipids against damage induced by oxidative stress. Fresh leaves of red cabbage were extracted with a mixture of methanol/distilled water/0.01% HCl (MeOH/H2O/HCl, 50/50/1, v/v/w). Total ATH concentration [µM] was determined with cyanidin 3-glucoside as a standard. Phenolic profiles in the crude red cabbage extract were determined using the HPLC method. Plasma samples were exposed to 100 µM peroxynitrite (ONOO−) or 2 mM hydrogen peroxide (H2O2) in the presence/absence of ATH extract (5–15 µM); oxidative alterations were then assessed. Pre-incubation of plasma with ATH extract partly reduced oxidative stress in plasma proteins and lipids. Dose-dependent reduction of both ONOO− and H2O2-mediated plasma protein carbonylation was observed. ATH extract partly inhibited the nitrative action of ONOO−, and significantly decreased plasma lipid peroxidation caused by ONOO− or H2O2. Our results demonstrate that anthocyanins present in red cabbage have inhibitory effects on ONOO− and H2O2-induced oxidative stress in blood plasma components. We suggest that red cabbage ATH, as dietary antioxidants, should be considered as potentially usable nutraceuticals in the prevention of oxidative stress-related diseases.

Extract of the mushroom Mycoleptodonoides aitchisonii induces a series of anti-oxidative and phase II detoxifying enzymes through activation of the transcription factor Nrf2

Activation of the transcriptional factor Nrf2 is a powerful strategy for protecting oxidative stress-related disease. To find novel compounds from mushrooms, the NAD(P)H:quinone oxidoreductase 1 (NQO1)-inducing activity of 43 ethyl-acetate extracts of mushrooms were examined using Hepa1c1c7 cells. In this screening, an extract of Mycoleptodonoides aitchisonii significantly induced NQO1. This extract also increased ARE reporter activity and inhibited H 2O 2-induced cell death in RAW264.7 cells. The induction of anti-oxidative and phase II enzymes was attenuated in peritoneal macrophages from Nrf2-deficient mice, so these activities were probably mediated by Nrf2 activation. Oral administration of the extract upregulated expression of these genes in the liver and small intestinal epithelium of mice. We purified 11 active compounds (including three novel ones), and dihydro-4-phenyl-2(3H)-furanone was the most effective NQO1-inducer. These results suggest that dietary intake of M. aitchisonii may contribute to the prevention of oxidative stress-related diseases by inducing anti-oxidative and phase II enzymes.

Prolonged red wine consumption changes hepatic redox status and inflammation

To understand the utility of red wine (RW) in the prevention of oxidative stress‐related diseases we investigated its effect on hepatic redox status and inflammation and determined the involvement of procyanidins in the effects. Groups of 5 male Wistar rats were treated with: water (control, C); aqueous procyanidin solution (PW, 200 mg/L); 13% ethanol (E); alcoholic procyanidin solution (PE, 200 mg/L of 13% ethanol); or RW (with 13% ethanol). Lipid, protein and DNA oxidation, glutathione status and the activity of enzymatic antioxidant defenses were determined in liver homogenates. Enzyme expression was assessed by RT‐PCR and NFκB activation by ELISA. RW prevented protein oxidation and changed glutathione (GSH) status and enzymatic antioxidant defenses. PE and RW treatments increased GSH synthetase expression (when compared to E). GSH reductase expression was decreased in all groups, while GSH peroxidase was decreased by PE and increased by RW. RW increased NFκB although TNFα was unchanged in RW group and reduced by PE. In conclusion, chronic consumption of RW altered hepatic redox status, its effects being partially justified by procyanidins in an alcoholic matrix. Ethanol seems critical for the effects of procyanidins, highlighting the importance of food matrix for the effects of these compounds.Supported by FCT (PTDC/QUI/65501/2006, SFRH/BPD/40110/2007) and Instituto de Bebidas e Saúde (iBeSa).