The effect of granulocyte macrophage-colony stimulating factor on glutathione and lipid peroxidation in a rat model

Kılıç, Diclehan; Sayan, Hale; Gönül, Bilge; Egehan, Îbrahîm

doi:10.1053/ejso.2000.0984

Cited by 20 publications

(9 citation statements)

References 15 publications

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“…Although the decreased GSH levels with the concomitant increased lipid peroxides, as we have observed, agrees with what has been reported in previous in vitro and in vivo models (Kilic et al, 2000; Lin et al, 2003), our findings represent the first of such an observation in leukemia cells. This suggests that perhaps both normal and leukemic cells may respond identically to the agents.…”

Section: Discussionsupporting

confidence: 93%

Lipid peroxides and glutathione status in human progenitor mononuclear (U937) cells following exposure to low doses of nickel and copper

Boadi

Harris

Anderson

et al. 2012

Drug and Chemical Toxicology

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Effects of Cu2+, Ni2+ or Cu2+ + Ni2+ on lipid peroxide and glutathione (GSH) levels in U937 cells were investigated. Cells were treated with 0, 5,10, and 20 µM of Cu2+ and/or Ni2+ and H2O2 (0.01 mM) and incubated for 24 hours at 37°C. Lipid peroxides were measured by the thiobarbituric acid assay (TBA). GSH intracellular levels were assayed by the GSH assay kit from EMD/Calbiochem (San Diego, California, USA). Cu2+ or Ni2+ significantly (P < 0.01) increased lipid peroxides in a dose-dependent manner, compared to controls. The effect was more pronounced for Cu2+, compared to the Ni2+-treated samples. Cu2+ + Ni2+ increased lipid peroxides in a significant (P < 0.001), dose-dependent manner, compared to Cu2+ or Ni2+ alone (i.e., ratio of 2.5:1-fold for combined versus single treatments, respectively). Cu2+ or Ni2+ significantly decreased GSH levels in U937 cells, with the effect being pronounced for Cu2+. Cu2+ + Ni2+ metal ions significantly (P < 0.001) depleted cells of GSH in a dose-dependent manner. Ethylene diamine tetraacetic acid (EDTA) at 50 or 100 µM moderately reduced the Cu2+- or Ni2+-induced effects on GSH levels. Interestingly, GSH levels generally decreased to half (except for the combined metal dose of 20 µM at 100 µM EDTA) of its level at the highest metal concentration tested for both the single or combined treatments. In conclusion, multiple exposures of cells to metal ions may be lethal to cells, compared to their single treatments.

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Section: Discussionsupporting

confidence: 93%

Lipid peroxides and glutathione status in human progenitor mononuclear (U937) cells following exposure to low doses of nickel and copper

Boadi

Harris

Anderson

et al. 2012

Drug and Chemical Toxicology

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“…Such observation is contrary to what has been reported by Sachan et al (1996), who showed that chelation therapy decreased GSH levels in lead-poisoned rats. Although the decreased GSH levels with the concomitant reduced lipid peroxides that we have observed may support what has been reported in differential in vitro and in vivo models (Kilic et al, 2000;Lin et al, 2003), our findings represent perhaps the first of such observation in leukemia cells. This may lead to the suggestion that perhaps both normal and leukemic cells require an identical response to these agents.…”

Section: Discussionsupporting

confidence: 91%

“…In some cases, ROS are the direct cause of a disease state (e.g. tissue damage initiated by exposure to ionization radiation) (Shimoi et al, 1994;Devi et al, 2000;Kilic et al, 2000). In other cases such as rheumatoid arthritis, ROS may perpetuate cellular damage caused by another process (Yuting et al, 1991;Shimoi et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells

Boadi

Iyere

Adunyah

2005

J of Applied Toxicology

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The effects of flavonoids quercetin and genistein were investigated according to their potency to inhibit the oxidation of U937 cells via Fenton's pathway through the analysis of lipid peroxides and glutathione (GSH) levels. Human leukemia (U937) cells from the American Type Culture Collection were maintained at 37 degrees C for 24 h under 5% CO2 tension in RPMI-1640 medium containing 10% fetal bovine serum and 50 units ml(-1) each of penicillin and streptomycin. Cells were oxidized with iron 50 microM) or copper (50 microM) in H2O2 (0.01 mM) without or with a flavonoid sample (10 or 20 microM) for the lipid peroxidation studies. The GSH levels were measured (GSH Kit) before and after oxidation as above with different concentrations of flavonoids (0-40 microM). Lipid peroxide was measured by the thiobarbituric acid assay. Both quercetin and genistein at either the 10 or 20 microM level decreased lipid peroxidation significantly compared with their respective controls (P < 0.01). Lipid peroxides by Fe compared to the Cu-treated samples did not differ significantly from each other. However, the combination of flavonoids at the doses tested significantly (P < 0.001) decreased lipid peroxides, the effect being the same for both metal ions. The GSH levels increased significantly before exposure to the metal ions (for the different doses for the differences between the flavonoid samples and their respective untreated levels). For quercetin and genistein the increases in GSH above their untreated levels were 4.5, 8.3, 11.7 and 15 and 3.8, 7.9, 12.5 and 14.6 nmol 10(-6) cells, respectively, for the 5-40 microM levels tested for each flavonoid. Following the exposure to the metal ions, GSH levels remained almost the same for the different concentrations for each of the flavonoids tested but significantly above all of the controls and same for those of the untreated samples. The results indicate that both flavonoids inhibited lipid peroxides and the inhibition may be attributed to the prevention of loss of intracellular GSH levels in U937 cells.

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“…This conclusion is supported by the increased activities of antioxidant enzymes such as GST, GSHPx, GSH reductase, SOD, and CAT. GSH has been inversely correlated with LPx in several previous studies [Kilic et al, 2000;Jagetia et al, , 2004. The Environmental and Molecular Mutagenesis.…”

Section: Discussionmentioning

confidence: 80%

Evaluation of the radioprotective effect of Liv 52 in mice

Jagetia

Ganapathi

Venkatesh

et al. 2006

Environ and Mol Mutagen

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Liv 52 is a mixture of botanicals that is used clinically to treat various hepatic disorders. In this study, the radioprotective activity of Liv 52 was evaluated in mice given whole-body exposure to different doses of gamma-radiation. In addition, a series of studies was conducted to explore the mechanism of radioprotection. Radioprotection was evaluated by the ability of Liv 52 to reduce both the frequency of bone marrow micronucleated erythrocytes and the lethality produced by (60)Co gamma-radiation. Mice were treated by oral gavage once daily for seven consecutive days with 500 mg/kg body weight Liv 52 or carboxymethylcellulose vehicle prior to radiation. Micronucleated polychromatic erythrocytes (MPCEs), micronucleated normochromatic erythrocytes (MNCEs), and the PCE/NCE ratio were measured at 0.25-14 days after exposure to whole-body radiation doses of 0, 0.5, 1.5, 3.0, or 4.5 Gy; animal survival was monitored after doses of 7, 8, 9, 10, 11, or 12 Gy. Pretreatment of mice with Liv 52 significantly reduced the frequency of radiation-induced MPCEs and MNCEs. Irradiation reduced the PCE/NCE ratio in a dose-related manner for up to 7 days following irradiation; Liv 52 pretreatment significantly mitigated against these reductions. Liv 52 treatment also reduced the symptoms of radiation sickness and increased mouse survival 10 and 30 days after irradiation. Liv 52 pretreatment elevated the levels of reduced glutathione (GSH), increased the activities of glutathione transferase, GSH peroxidase, GSH reductase, superoxide dismutase, and catalase, and lowered lipid peroxidation (LPx) and the activities of alanine amino transferase and aspartate aminotransferase 30 min after exposure to 7 Gy of gamma-radiation. Liv 52 pretreatment also reduced radiation-induced LPx and increased GSH concentration 31 days following the exposure. The results of this study indicate that pretreatment with Liv 52 reduces the genotoxic and lethal effects of gamma-irradiation in mice and suggest that this radioprotection may be afforded by reducing the toxic effects of the oxidative products of irradiation.

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The effect of granulocyte macrophage-colony stimulating factor on glutathione and lipid peroxidation in a rat model

Cited by 20 publications

References 15 publications

Lipid peroxides and glutathione status in human progenitor mononuclear (U937) cells following exposure to low doses of nickel and copper

Lipid peroxides and glutathione status in human progenitor mononuclear (U937) cells following exposure to low doses of nickel and copper

In vitro exposure to quercetin and genistein alters lipid peroxides and prevents the loss of glutathione in human progenitor mononuclear (U937) cells

Evaluation of the radioprotective effect of Liv 52 in mice

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