8-hydroxy-2--deoxyguanosine and Hemolysis

To compare the effects of lotus root and cucumber on antioxidant function in aged subjects.. Pilot comparative study.. Research setting with vegetable intervention.. Healthy aged subjects over the age of sixty.. 30-day supplementation of lotus root or cucumber powder.. Plasma value of ferric reducing antioxidant power assay, activity of antioxidant enzymes, contents of some antioxidants, oxidation products, hemolysis, blood mononuclear cell DNA damage and urinary excretion of 8-hydroxy-2'-deoxyguanosine were measured before and after the intervention.. Plasma glutathione peroxidase activity, contents of vitamin C, total phenolics were significantly increased, while plasma uric acid content significantly decreased in both groups at the end of the intervention. Meanwhile, hemolysis was significantly reduced in both groups and DNA injury rate of blood mononuclear cells in lotus root group and the ratio of comet tail length to total length in cucumber group were also declined significantly post-intervention. However, plasma value of ferric reducing antioxidant power assay, contents of reduced glutathione, vitamin E, malondialdehyde, oxidized low density lipoprotein, carbonyls and activity of superoxide dismutase and catalase were not changed significantly in both group after the intervention.. These results suggest that lotus root and cucumber are not remarkably different in improving antioxidant function in aged subjects, though they are significantly different in antioxidant capacity in vitro. The benefits observed in this study may come from the additive or synergistic combinations of antioxidants contained in vegetables.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Aged; Antioxidants; Ascorbic Acid; Catalase; Comet Assay; Cucumis sativus; Deoxyguanosine; Dietary Supplements; DNA Damage; Female; Glutathione; Glutathione Peroxidase; Healthy Volunteers; Hemolysis; Humans; Leukocytes, Mononuclear; Lipoproteins, LDL; Lotus; Male; Malondialdehyde; Middle Aged; Oxidation-Reduction; Phenols; Pilot Projects; Superoxide Dismutase; Uric Acid; Vegetables; Vitamin E

Acrylamide has a variety of toxicities, including carcinogenicity, and can be present in food via the Maillard reaction in processing of certain foods. Previous studies have demonstrated that co-existing Maillard reaction products (MRPs) ameliorated acrylamide-induced abnormal physiological status in mice. This study is focused on the effects on hematological parameters, erythrocyte osmotic fragility, oxidative stress in plasma and liver, and contents of 8-hydroxy-2-deoxyguanosine (8-OHdG) in mice exposed to acrylamide and to acrylamide and MRPs derived from arginine and glucose. Acrylamide alone caused significant increases in liver indexes, erythrocyte osmotic fragility, malonaldehyde level in liver and 8-OHdG level in testis, and significant decreases in weight gain, hematological parameters, levels of glutathione, glutathione peroxidase and total superoxide dismutase in plasma. Whether MRPs and acrylamide were physically mixed or when the solution is prepared from heating the mixture of arginine, glucose and acrylamide, the presence of MRPs effectively reduced the adverse changes caused by acrylamide. These results suggest that the toxicity of acrylamide to mice can be ameliorated by MRPs, the common compositions simultaneously generated with acrylamide in food matrix.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Acrylamide; Animals; Arginine; Body Weight; Erythrocytes; Female; Glucose; Glutathione; Glutathione Peroxidase; Hemolysis; Liver; Maillard Reaction; Male; Malondialdehyde; Mice; Mice, Inbred ICR; Oxidative Stress; Superoxide Dismutase; Testis

2-Butoxyethanol has been reported to induce an increase in liver tumors in male B6C3F1 mice following chronic inhalation while rats, similarly treated, showed no increase in liver tumors. The mechanism for the selective induction of cancer in mouse liver is unknown, however, 2-butoxyethanol has been shown to induce hemolysis in mice, resulting in an accumulation of hemosiderin (iron) in the liver. Previous studies by our group and others have shown that mouse liver compared to other rodent species has a lower antioxidant capacity and appears to be more susceptible to chemically-induced oxidative damage. Since iron is known to produce hydroxyl radicals (through the Fenton reaction), we have proposed that the 2-butoxyethanol-induced iron overload (through hemolysis) may contribute to the induction of liver neoplasia in the mouse. In the present studies, 2-butoxyethanol induced oxidative stress in the liver of mice following 7-day treatment by gavage. These studies also examined whether 2-butoxyethanol, 2-butoxy acetic acid (a major metabolite of 2-butoxyethanol) or iron (FeSO(4)) produced oxidative stress in mouse and rat hepatocytes. Oxidative stress was examined by measuring oxidative DNA damage (OH8dG), lipid peroxidation (MDA formation) and cellular vitamin E concentrations. Neither 2-butoxyethanol or 2-butoxyacetic acid induced changes in the oxidative stress parameters examined in either rat or mouse hepatocytes. In contrast, FeSO(4) produced a dose-related increase in OH8dG and MDA and a decrease in vitamin E levels following 24 h treatment. Mouse hepatocytes were more sensitive than rat hepatocytes to the oxidative damage induced by the FeSO(4). FeSO(4)-induced oxidative stress was not increased by co-treatment of FeSO(4) with either 2-butoxyethanol or 2-butoxy acetic acid. These results support the proposal that the induction of hepatic oxidative stress by 2-butoxyethanol in vivo occurs secondary to induction of hemolysis and iron deposition in the liver rather than as a direct action of 2-butoxyethanol or its main metabolite, 2-butoxy acetic acid.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Deoxyguanosine; Ethylene Glycols; Ferrous Compounds; Glycolates; Hemolysis; Hepatocytes; L-Lactate Dehydrogenase; Lipid Peroxidation; Liver Neoplasms, Experimental; Male; Malondialdehyde; Mice; Oxidative Stress; Rats; Rats, Inbred F344; Vitamin E