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C Calzada

Publications and source records attributed to C Calzada.

5 recordsLinked to original sources

Lower levels of lipid peroxidation in human platelets incubated with eicosapentaenoic acid.

The modulatory effects of eicosapentaenoic acid (EPA) on platelet arachidonic acid (AA) metabolism were applied to an in vitro model of oxidant stress. Unstimulated normal human blood platelets were first treated with a thiol-oxidizing agent, azodicarboxylic acid bis(dimethylamide) (diamide) (1 microM), and then incubated with a low concentration of EPA (100 nM). Diamide treatment led to a lower alpha-tocopherol content compared to control. Formation of MDA, a marker of the overall lipid peroxidation, as well as formation of 12-hydroxyeicosatetraenoic acid (12-HETE), the 12-lipoxygenase end-product of AA, were both higher in diamide-treated platelets. Subsequent incubation of diamide-treated platelets with EPA counteracted the effects of oxidant stress induced pharmacologically by diamide. Interestingly, EPA prevented the alpha-tocopherol level from falling and the overall lipid peroxidation from increasing as it did during diamide treatment. In particular, incubation of diamide-treated platelets with EPA led to significantly lower amounts of 12-HETE. Conversely, preincubation of platelets with 100 nM EPA protected cells from oxidizing effects induced by diamide treatment, either on the level of lipid peroxides or on the antioxidant status. These results indicate that, in this particular model, EPA permitted platelets to have control levels of tocopherol, MDA and 12-HETE despite diamide treatment. Low concentrations of EPA might have prevented the increase of lipid hydroperoxides and especially the transient accumulation of 12-hydroperoxyeicosatetraenoic acid (12-HPETE).

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid

Age-related changes in arachidonic acid peroxidation and glutathione-peroxidase activity in human platelets.

Lipid peroxidation, vitamin E level and glutathione-peroxidase activity were determined in platelets from elderly (greater than 68 years) and young (21-43 years) people. To further assess the platelet lipid peroxidation, the metabolism of endogenous arachidonic acid in unstimulated platelets as well as that of the exogenous one were measured in the two groups. The oxygenated metabolites of arachidonic acid were enhanced in the elder population under both conditions tested. In addition, the platelet malondialdehyde content, a marker of the overall lipid peroxidation, was also found significantly increased in platelets from aged subjects. On the other hand, the platelet vitamin E level and the glutathione-peroxidase activity were significantly depressed in the elder group compared to the young one. These results suggest that the increased platelet activation observed with age could be linked to the accumulation of lipoxygenase-dependent peroxides associated with the decreased antioxidative defence of the cells, especially glutathione-peroxidase activity.

Adult

Decrease in platelet reduced glutathione increases lipoxygenase activity and decreases vitamin E.

Unstimulated normal human blood platelets were treated with azodicarboxylic acid bis(dimethylamide) (diamide), a thiol-oxidizing agent. Oxygenated arachidonic acid (AA) metabolites, malondialdehyde (MDA), and tocopherols were then quantified by high-performance liquid chromatography (HPLC). Diamide treatment partially decreased the amount of reduced glutathione (GSH) content and induced a subsequent decrease in peroxidase activity. However, formation of 12-hydroxy-eicosatetraenoic acid (12-HETE), the end-product of lipoxygenation of AA, increased. Formation of MDA, a marker of overall lipid peroxidation, was also enhanced. Furthermore, platelet alpha-tocopherol, but not gamma-tocopherol, significantly decreased. These results indicate that enhanced "basal" lipoxygenase activity, as a marker of specific AA oxygenation, may be linked to decreased platelet antioxidant status.

Antioxidants

[Effects of traditional cooking on antinutritional factors of the black beans (Phaseolus vulgaris) of Costa Rica].

Trypsin inhibitors, alfa amylase inhibitors and hemagglutinins were determined in black beans (P. vulgaris) produced in Costa Rica. The effect of the traditional cooking on such antinutritional factors was also studied. The antinutritional factors were analyzed spectrophotometrically in the raw beans, as well as after several cooking periods of time. The results showed that alfa-amylase inhibitors were the most thermoresistant. After 30 min of cooking time there was a 33% of activity left from the initial activity of the raw beans. Approximately 80% of the antitryptic activity was destroyed at 9 min of cooking time. After 10 min of cooking time, only 1% of hemagglutinin activity was present.

Amino Acids, Essential

Effects of small concentrations of eicosapentaenoic acid on platelets.

Increased platelet functions have been associated with enhanced arachidonic acid (AA) metabolism in diabetics and elderly people. We investigated these parameters in both groups after feeding low doses of pure eicosapentaenoic acid (EPA). After such an intake, platelet aggregation induced by various agonists was decreased whereas the oxygenated metabolism of endogenous AA was not substantially altered, and the fatty acid composition of plasma and platelet lipid pools did not change. In the most recent study, the measurement of vitamin E revealed that although its level in plasma was not modified, it was increased in platelets after EPA intake. It is concluded that small amounts of EPA intake do not reduce platelet aggregation in competing with AA metabolism but rather in depressing the peroxide tone of the cell.

Aged