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Vivo Oxidative Stress (vivo + oxidative_stress)
Selected AbstractsEffect of Exogenous and Endogenous Antioxidants on 3-Nitropionic Acid-Inducedin vivo Oxidative Stress and Striatal LesionsJOURNAL OF NEUROCHEMISTRY, Issue 4 2000Insights into Huntington's Disease Abstract: 3-Nitropropionic acid (3-NP) is an irreversible inhibitor of complex II in the mitochondria. 3-NP toxicity has gained acceptance as an animal model of Huntington's disease (HD). In the present study, we confirmed that rats injected with 3-NP (20 mg/kg, i.p., daily for 4 days) exhibit increased oxidative stress in both striatum and cortical synaptosomes as well as lesions in the striatum. Synaptosomal membrane proteins from rats injected with 3-NP exhibited a decrease in W/S ratio, the relevant electron paramagnetic resonance (EPR) parameter used to determine levels of protein oxidation, and western blot analysis for protein carbonyls revealed direct evidence of increased synaptosomal protein oxidation. Treatment of rats with the brain-accessible free radical spin trap 5-diethoxyphosphoryl-5-methyl-1-pyrroline N -oxide (DEPMPO; 30 mg/kg, i.p., daily 2 h before 3-NP injection) or with N -acetylcysteine (NAC; 100 mg/kg, i.p., daily 2 h before 3-NP injection), a known glutathione precursor, before 3-NP treatments protects against oxidative damage induced by 3-NP as measured by EPR and western blot analysis for protein carbonyls. Furthermore, both DEMPMPO and NAC treatments before 3-NP administration significantly reduce striatal lesion volumes. These data suggest oxidative damage is a prerequisite for striatal lesion formation and that antioxidant treatment may be a useful therapeutic strategy against 3-NP neurotoxicity and perhaps against HD as well. [source] Oxidative stress during leukocyte absorption apheresisJOURNAL OF CLINICAL APHERESIS, Issue 2 2003Aki Hirayama Abstract Leukocyte absorption apheresis absorbs leukocytes to the apheresis columns involving leukocyte activation. This process is regarded as bioincompatible and avoided in hemodialysis or other extracorporeal circulation processes. Thus, leukocyte apheresis has a potential risk to exacerbate in vivo oxidative stress. We evaluated the changes in plasma oxidative stress during leukocyte apheresis. Patients diagnosed as ulcerative colitis (UC) and treated with leukocyte apheresis were studied. Adacolumn (celluloseacetate beads) or Cellsorba EX (polyethylenephtarate fiber) was used for the leukocyte absorption device. Oxidative stress was measured by thiobarbituric acid reactive substances (TBARS) and hydroxyl radical (,OH) scavenging activity. Plasma samples were collected from the pre- and post-column sampling port at the start, and from the pre-column sampling port at the end of the treatment. The ,OH signal intensities (OHRI) significantly increased during a column passage, indicating a loss of plasma ,OH scavenging activity. However, OHRI was reduced at the end, suggesting a recovery of radical scavenging activity during leukocyte apheresis. Significant decreases of OHRI and TBARS were only observed in the early phase of the therapeutic course. No differences of OHRI and TBARS levels were observed between the two columns. These results indicate that though the plasma antioxidant activity was diminished by a column passage, plasma antioxidant activity recovers during the procedure. This efficient antioxidative effect is limited to the early phase of the therapeutic course. J. Clin. Apheresis 18:61,66, 2003. © 2003 Wiley-Liss, Inc. [source] Reduced in vivo oxidative stress following 5-methyltetrahydrofolate supplementation in patients with early-onset thrombosis and 677TT methylenetetrahydrofolate reductase genotypeBRITISH JOURNAL OF HAEMATOLOGY, Issue 1 2005Antonio Coppola Summary The protective role of folate in vascular disease has been related to antioxidant effects. In 45 patients with previous early-onset (at age <50 years) thrombotic episodes and the 677TT methylenetetrahydrofolate reductase genotype, we evaluated the effects of a 28d-course (15 mg/d) of 5-methyltetrahydrofolate (MTHF) on homocysteine metabolism and on in vivo generation of 8-iso-prostaglandin F2, (8-iso-PGF2,), a reliable marker of oxidative stress. At baseline, patients' fasting total homocysteine (tHcy) was 11·5 ,mol/l (geometric mean) and urinary excretion of 8-iso-PGF2, was 304 pg/mg creatinine, with the highest metabolite levels in the lowest quartile of plasma folate distribution (P < 0·05). After 5-MTHF supplementation, plasma folate levels increased approximately 13-fold (P < 0·0001 versus baseline); tHcy levels (6·7 ,mol/l, P < 0·0001) and urinary 8-iso-PGF2, (254 pg/mg creatinine, P < 0·001) were both significantly lowered, their reduction being proportional to baseline values (r = 0·98 and r = 0·77, respectively) and maximal in patients with the lowest pre-supplementation folate levels (P < 0·05). The effects on folate (P < 0·0001) and tHcy (P = 0·0004) persisted for at least up to 2 months after withdrawing 5-MTHF. In parallel with long-lasting tHcy-lowering effects, a short-course 5-MTHF supplementation reduces in vivo formation of 8-iso-PGF2, in this population, supporting the antioxidant protective effects of folate in vascular disease. [source] 3243: In vivo quantitative measurement of oxidation repair of glutaredoxin-1ACTA OPHTHALMOLOGICA, Issue 2010PG SÖDERBERG Purpose Quantitative determination of the impact of glutaredoxin-1 on sensitivity to oxidative stress induced by in vivo exposure to ultraviolet radiation in the 300 nm wavelength region. Methods Altogether, 20 glutredoxin-1 knockout mice (Grx1 -/-) and 20 wild type C57BL/6, bred on the same background were in vivo exposed unilaterally to ultraviolet radiation in the 300 nm wavelength region (UVR-300 nm). For both the Grx1-/- and the Grx1+/+ groups, respectively, the animals were subdivided into 5 dose groups of four receiving 0.0, 2.1, 2.9, 3.6 or 4.1 kJ m^-2, depending on group belonging. At 48 hrs after exposure the animals were sacrificed, the lenses were extracted and measured for intensity of forward light scattering. The threshold dose for damage was estimated as the Maximum Tolerable Dose-2.3:16. The protection factor (PF), defined as the ratio between the threshold with protection and the threshold without protection was calculated. Results The MTD-2.3:16 was for the Grx1+/+ estimated to 3.81 kJ/m2 (95% CI, 2.82 , 6.37) and for the Grx1-/- estimated to 2.99 kJ/m2 (95% CI, 2.33 , 4.00). The PF factor for the Grx1 gene thus was 1.3. Conclusion The Grx-1 gene provides a higher tolerance to in vivo oxidative stress induced by in vivo exposure to ultraviolet radiation, allowing a 1.3 longer exposure times at the same intensity before cataract develops. [source] | ||||||||||