1-1-diphenyl-2-picrylhydrazyl and 4-hydroxy-2-nonenal

The aim of the study was to investigate the in vitro antioxidant properties Moringa oleifera Lam. (MO) extracts and its curative role in acetaminophen (APAP)-induced toxic liver injury in rats caused by oxidative damage. The total phenolic content and antioxidant properties of hydroethanolic extracts of different MO edible parts were investigated by employing an established in vitro biological assay. In the antihepatotoxic study, either flowers or leaves extract (200 mg/kg or 400 mg/kg, i.p) were administered an hour after APAP administration, respectively. N-Acetylcysteine was used as the positive control against APAP-induced hepatotoxicity. The levels of liver markers such as alanine aminotransferase (ALT) and the levels of oxidative damage markers including malondialdehyde (MDA), 4-hydroxynonenal (4-HNE) protein adduct, reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were analysed and compared between experimental groups. Among MO edible parts the flower extracts contain the highest total phenolic content and antioxidant capacity, followed by leaves extract. The oxidative marker MDA, as well as 4-HNE protein adduct levels were elevated and GSH, SOD and CAT were significantly decreased in groups treated with hepatotoxin. The biochemical liver tissue oxidative markers measured in the rats treated with MO flowers and leaves hydroethanolic extracts showed a significant (p < 0.05) reduction in the severity of the liver damage. The results of this study strongly indicate the therapeutic properties of MO hydroethanolic extracts against acute liver injury and thereby scientifically support its traditional use.

Topics: Acetaminophen; Aldehydes; Animals; Antioxidants; Biomarkers; Biphenyl Compounds; Ethanol; Flowers; Fluorescence Recovery After Photobleaching; Free Radical Scavengers; Glutathione; Liver; Liver Diseases; Liver Function Tests; Male; Malondialdehyde; Moringa oleifera; Oxidative Stress; Phenols; Phytotherapy; Picrates; Plant Extracts; Rats; Rats, Sprague-Dawley; Water

This study describes the antioxidant activities and antigenotoxic effects of garlic extracts prepared by different processing methods. Aged-garlic extract (AGE) showed a significantly higher total phenolic content (562.6 +/- 1.92 mg/100 g garlic acid equivalents) than those of raw garlic extract (RGE) or heated garlic extract (HGE). The SC(50) for DPPH RSA in HGE was significantly the highest at 2.1 mg/ml. The SC(50) for SOD-like activity in garlic extracts was, in decreasing order, RGE (7.3 mg/ml) > AGE (8.5 mg/ml) > HGE (9.2 mg /ml). The ED(50) of AGE was the highest (19.3 microg/ml) regarding H2O2 induced DNA damage and its inhibition rate was 70.8%. The ED(50) of RGE for 4-hydroxynonenal (a lipid peroxidation product) induced DNA damage was 38.6 microg/ml, followed by AGE > HGE. Although the heat treatment of garlic tended to decrease the TPC and SOD-like activity and increased DPPH RSA, garlic, in general, has significant antioxidant activity and protective effects against oxidative DNA damage regardless of processing method.

Topics: Aldehydes; Antimutagenic Agents; Antineoplastic Agents, Phytogenic; Antioxidants; Biphenyl Compounds; DNA Damage; Food Handling; Garlic; Hot Temperature; Humans; Hydrogen Peroxide; Leukocytes; Phenols; Picrates; Plant Extracts; Superoxide Dismutase

The mechanism of metal ion-catalyzed oxidative modification of apolipoprotein E (apoE) in human very-low-density lipoprotein (VLDL) and its inhibition by glycosaminoglycan (GAG) was investigated in vitro. The VLDL oxidation catalyzed by Cu2+ led to the lipid peroxidation, the formation of aggregates, and covalent modification of apoE. The modified apoE lost heparin-binding activity. These results suggest that the lipid peroxidation of VLDL and modification of apoE cause impairment of lipid uptake by cells and deposit the oxidized lipids in the tissues. The lipid peroxidation and oxidative modification of apoE in VLDL mediated by Cu2+ and an aqueous radical generator were suppressed by GAG, heparan sulfate, heparin, and chondroitin sulfate A, even though GAGs demonstrated no ability to scavenge alpha,alpha-diphenyl-beta-picrylhydrazyl radical. There were no relationships between inhibitory activity of GAGs in the VLDL oxidation and their number of sulfate groups which possess chelating activity of metal ion. Therefore, it can be considered that the inhibition of VLDL oxidation by GAGs is possibly due to the interaction between GAG and VLDL which bring about the steric hindrance, interference with the reaction between VLDL particle and the reactive oxygen species. These studies suggest that GAGs preserve the biological functions of apoE from oxidative stress.

Topics: Adult; Aldehydes; Alzheimer Disease; Amidines; Apolipoproteins E; Bepridil; Biphenyl Compounds; Chelating Agents; Cholesterol Esters; Chondroitin Sulfates; Copper Sulfate; Dextrans; Free Radical Scavengers; Glutathione; Glycosaminoglycans; Heparin; Hippocampus; Humans; Hydrogen-Ion Concentration; Lipid Peroxidation; Lipoproteins, VLDL; Male; Picrates; Reactive Oxygen Species; Thiobarbituric Acid Reactive Substances