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PubMed2004

Resveratrol reduces oxidative stress induced by platinum compounds in blood platelets.

The effects of resveratrol (trans-3,4',5-trihydroxystilbene) on the oxidative stress in blood platelets induced by platinum compounds [cisplatin and selenium-cisplatin conjugate] were studied in vitro. The production of thiobarbituric acid reactive substances (TBARS), the level of conjugate diene, the generation of superoxide anion radicals (O2-*) and other reactive oxygen species (O2-*, H2O2, singlet oxygen and organic radicals) were measured by chemiluminescence in blood platelets treated with platinum compounds. Cisplatin at the concentration of 10 microg/ml, as well as selenium-cisplatin conjugate (10 microg/ml) induced oxidative stress in blood platelets: an increase in TBARS, conjugate diene, chemiluminescence and generation of O2-*. In the presence of resveratrol (a natural compound with antioxidant activity) at the concentrations of 1-25 microg/ml, the chemiluminescence, the levels of O2-*, conjugate diene and TBARS were reduced (p < 0.05). We showed that resveratrol at different concentrations (1-25 microg/ml) had a protective effect against oxidative stress in platelets caused by platinum compounds (10 microg/ml) and it diminished platelet lipid peroxidation and reactive oxygen species generation induced by platinum compounds.

Animals↗
PubMed1979

Cataractogenic and lethal effect of selenite in rats during postnatal ontogenesis.

Male rats aged 5, 10, 15, 20, 30, 40, 50 and 60 days were injected with a single dose of sodium selenite (20 or 40 mumol/kg b.w.). For two months after the injection, all the rats were observed daily for mortality (acute up to 24 h after the injection, subacute 2--7 days after) and the incidence of permanent and intermittent cataract. With the higher dose, both forms of lethal effect were found to shift to earlier phases of ontogenetic development, subacute mortality appearing sooner than acute mortality. The cataractogenic effect produced by the administration of both 20 and 40 mumol/kg b.w. dependent on the age of the experimental animals. It appeared only in the early phases of ontogenetic development (up to the age of 15 days); cataract was not observed during later development.

Age Factors↗
PubMed1991

Lipid hydroperoxide involvement in copper-dependent and independent oxidation of low density lipoproteins.

The involvement of lipid hydroperoxides in the oxidation of human low density lipoproteins (LDL) induced by Cu++ or azoperoxyl radicals was studied. Concurrent or pretreatment of LDL with the synthetic peroxidase Ebselen and its cofactor glutathione totally prevented Cu+(+)-dependent oxidation, as measured by the formation of thiobarbituric acid reactive substances and LDL mobility on agarose gels. LDL could be oxidized in the absence of metals with peroxy radicals generated via homolysis of azo compounds. With the azo initiator, 2,2'-azobis-2-amidinopropane hydrochloride, Ebselen plus glutathione prevented lipid oxidation when present during oxidation. However, if LDL were first pretreated with Ebselen plus glutathione and these reagents removed before oxidation, they did not prevent oxidation. Analysis by high-performance liquid chromatography of lipids extracted from Cu+(+)- or azoperoxyl radical-modified lipoproteins indicated that the major lipid oxidation products were derived from linoleate and that Ebselen-glutathione addition reduced linoleate hydroperoxides. Oxidation of LDL by human monocyte-derived macrophages was also prevented by coincubation with Ebselen-glutathione or the antioxidant, probucol. These results demonstrate that initiation of Cu+(+)-dependent oxidation absolutely requires the presence of trace amounts of lipid hydroperoxides in the lipoprotein and that hydroperoxides play a major role in the propagation reactions even in the absence of added transition metals.

Azo Compounds↗
PubMed1990

Phagocytosis, bactericidal activity, and oxidative metabolism of milk neutrophils from dairy cows fed selenium-supplemented and selenium-deficient diets.

Six primiparous Holstein cows were fed a Se-deficient diet, beginning at least 90 days before their first calving, and 6 other primiparous cows were given the same diet plus a supplement of 2 mg of Se/cow/d as sodium selenite. All cows were fed their diets for the duration of the experimental period. One uninfected quarter of each cow was injected with 25 micrograms of Escherichia coli endotoxin at postpartum week 5. Leukocytes were isolated by centrifugation from milk collected at postinjection hour 16. Isolated cells were 92 +/- 3% neutrophils and were incubated with Staphylococcus aureus or E coli in a 1:300 ratio. Phagocytosis and intracellular killing by neutrophils were assessed after 0, 30, 60, and 90 minutes by a fluorochrome assay, using acridine orange. Viability of neutrophils was assessed by use of trypan blue. Superoxide anion production and hydrogen peroxide production by neutrophils also were determined. Cows fed Se-deficient diets had significantly (P less than 0.05) lower blood Se concentration and blood glutathione peroxidase activity than cows fed Se-supplemented diets. Selenium status had no effect on the phagocytic capacity of neutrophils. Neutrophils obtained from cows fed Se-supplemented diets killed a significantly (P less than 0.05) higher percentage of ingested bacteria than did neutrophils from cows fed the Se-deficient diet. Viability was significantly (P less than 0.05) reduced by incubation with S aureus in neutrophils from both groups of cows, with neutrophils from Se-deficient cows having lower viability.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1988

A facile one-step synthesis of delta 1,4-3-keto bile acid esters by iodoxybenzene and benzeneselenic anhydride.

A facile one-step conversion of stereoisomeric methyl 3-hydroxycholanoates to 1,4-dien-3-one, by treatment in boiling toluene with iodoxybenzene catalyzed by benzeneselenic anhydride, is described. The direct oxidation-dehydrogenation at C-3 is applicable to other cholanoates (hyodeoxycholic, chenodeoxycholic, ursodeoxycholic, deoxycholic, and cholic) when the hydroxyl groups at C-6, C-7, or C-12 are protected. Without protection at C-6 and C-7, the products from hyodeoxycholic, chenodeoxycholic, ursodeoxycholic, and cholic esters are complex mixtures, whereas, methyl deoxycholate yields the 1,4-dien-3,12-dione cleanly.

Benzene Derivatives↗
PubMed1997

Effect of doxazosin on endothelial dysfunction in hypercholesterolemic/antioxidant-deficient rats.

Hypertension, hypercholesterolemia, atherosclerosis, and coronary heart disease are associated with abnormal endothelium-dependent, nitric oxide-mediated vasorelaxation. In rats, hypercholesterolemia in combination with deficiencies of vitamin E and selenium results in increased endogenous lipid oxidation and endothelial dysfunction. Two hydroxymetabolites of doxazosin, an alpha 1-adrenergic blocking antihypertensive agent, inhibit human lipid oxidation in vitro in a dose-dependent fashion. The present studies were performed to determine the effect of in vivo treatment with doxazosin on endothelial dysfunction in hypercholesterolemic/ antioxidant-deficient rats. Dahl rats were fed 1) a standard diet, 2) a high cholesterol (4%) diet, or 3) a high cholesterol, vitamin E- and selenium-deficient diet. A subgroup of animals in each group were administered doxazosin (3.5 mg/100 g/day) for 16 weeks. In the aortas, vascular relaxations induced by acetylcholine were significantly decreased (P < .05) in high cholesterol/antioxidant-deficient rats compared with normal and high cholesterol animals. Doxazosin treatment prevented the impairment in endothelium-dependent vascular relaxation in the high cholesterol/antioxidant-deficient group. Vasorelaxation in response to the exogenous nitric oxide donor diethylamine nanoate, which was significantly impaired (P < .05) in aortas from high cholesterol/antioxidant-deficient animals compared with normal and high cholesterol animals, was normalized in aortas from high cholesterol/ antioxidant-deficient animals that had received doxazosin. The antioxidant effect of doxazosin may have therapeutic implications in diseases associated with endothelial dysfunction linked to products of lipid oxidation.

Adrenergic alpha-Antagonists↗
PubMed2002

Increase in total blood antioxidant status and selenium levels in black patients with active vitiligo.

BACKGROUND: Oxidative stress could be an important phenomenon leading to melanocyte death in vitiligo. The accumulation of hydrogen peroxide (H2O2) and low catalase levels have recently been demonstrated in the epidermis of vitiligo patients. Few abnormalities of antioxidants have been found in the blood of patients with vitiligo, except for an elevation of selenium. No studies on oxidative stress have been performed so far on patients with skin phototype VI (Fitzpatrick classification). AIM: To study the blood antioxidant status of black patients with active generalized vitiligo. METHODS: Randox total antioxidant status, selenium, ferritin, transferrin, ceruloplasmin, tocopherol, and retinol levels were evaluated in blood samples obtained from 11 dark-skinned patients from the French West Indies (Isle of Martinique) with recent active lesions of vitiligo and from 11 age- and sex-matched healthy volunteers. RESULTS: Total blood antioxidant status and selenium levels were significantly increased in vitiligo patients, compared to those in sex- and age-matched controls (P < 0.01 and P < 0.02, respectively). Blood levels of ferritin, transferrin, ceruloplasmin, retinol, and tocopherol were not significantly modified. CONCLUSIONS: This is the first report on the global blood antioxidant status in vitiligo. The increase in total blood antioxidant status observed in black patients was an unexpected result that needs to be confirmed and explained by further studies. The spontaneous increase in selenium levels could be of interest, as it has been recommended in the treatment of vitiligo.

Adult↗
PubMed1995

Protective effect of selenium on hemoglobin mediated lipid peroxidation in vivo.

The toxicity of hemoglobin (Hb) solutions is related, at least in part, to the generation of oxygen free radicals with consequent induction of lipid peroxidation. The present study was designed to examine whether selenium (Se) may prevent the oxidative damage observed after Hb administration. Three groups of rats were compared; (I) the negative control group receiving autotransfusion; (II) the positive control group with replacement of 40% total blood volume (TBV) with modified bovine Hb solution; and (III) the experimental group which received dietary supplemented selenium (Na2SeO3) in daily doses of 5 micrograms.kg body wt-1 in drinking water, 4 days before and 3 days after administration of Hb solution in the same volume as in group II. Three days after Hb injection, all animals were sacrificed. Oxidative stress was determined by measuring conjugated dienes (CD) and thiobarbituric acid reactants (MDA) in homogenates of the perfused liver, heart, lungs, kidney, brain and plasma. Additionally, the 45k x g supernatants of the organs homogenates and plasma were assayed for the antioxidant enzymes activity: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the intracellular level of reduced glutathione (GSH). Also, a measurement of nonprotein bound intracellular free iron (Fe) and tissue Se concentrations was performed. Simultaneously, injury dysfunction of vital organs was assessed by the measurement of plasma LDH, SGPT, creatinine, blood PaO2 and by histopathological studies. Results indicate that the exchange transfusion with Hb solution introduced significant increases in CD and MDA formation, particularly in the liver and heart tissues, and in plasma. While the values of the SOD and CAT in the liver and heart tissue were generally altered, the SOD/CAT ratio was also increased. After the Hb injection, activity of GSH-Px remained unchanged and was associated with significant depletion of GSH. The plasma levels of SGPT and LDH were increased, but the creatinine and PaO2 was similar to that of the control and corresponded with histopathological findings. The liver and heart intracellular free Fe was found to be higher than that of control. Treatment with Se was very effective in the prevention of oxidative damage introduced by Hb. Full protection from MDA formation was noted in liver tissue (p < 0.001). Also, plasma levels of MDA, SGPT and LDH were significantly decreased and appeared similar to that of the control group (I). Treatment with Se increased liver (p < 0.05) and plasma (p < 0.1) level of GSH-Px.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗