Gender-specific inhibition of platelet aggregation following omega-3 fatty acid supplementation

Background and Aims : Increased platelet aggregation is a major risk factor for heart attacks, stroke and thrombosis. Long chain omega-3 polyunsaturated fatty acids (LCn-3PUFA; eicosapentaenoic acid, EPA; docosahexaenoic acid, DHA) reduce platelet aggregation; however studies in the published literature involving EPA and/or DHA supplementation have yielded equivocal results. Recent in vitro studies have demonstrated that inhibition of platelet aggregation by LCn-3PUFA is gender specific. We examined the acute effects of dietary supplementation with EPA or DHA rich oils on platelet aggregation in healthy male and females.

Methods and Results : A blinded placebo controlled trial involving 15 male and 15 female subjects. Platelet aggregation was measured at 0, 2, 5 and 24 h post-supplementation with a single dose of either a placebo or EPA or DHA rich oil capsules. The relationship between LCn-3PUFA and platelet activity at each time point was examined according to gender vs. treatment. EPA was significantly the most effective in reducing platelet aggregation in males at 2, 5 and 24 h post-supplementation (−11%, −10.6%, −20.5% respectively) whereas DHA was not effective relative to placebo. In contrast, in females, DHA significantly reduced platelet aggregation at 24 h (−13.7%) while EPA was not effective. An inverse relationship between testosterone levels and platelet aggregation following EPA supplementation was observed.

Conclusion : Interactions between sex hormones and omega-3 fatty acids exist to differentially reduce platelet aggregation. For healthy individuals, males may benefit more from EPA supplementation while females are more responsive to DHA.

The corrosion inhibition mechanism of new rare earth cinnamate compounds — electrochemical studies

A combination of linear polarisation resistance (LPR) and cyclic potentiodynamic polarisation (CPP) measurements demonstrated that the lanthanum-4 hydroxy cinnamate compound could inhibit both the cathodic and anodic corrosion reactions on mild steel surfaces exposed to 0.01 M NaCl solutions. However, the dominating response was shown to vary with inhibitor concentration. At the concentrations for which the highest level of protection was achieved, both REM-4 hydroxy cinnamate (REM being lanthanum and mischmetal) displayed a strong anodic behaviour for mild steel and their inhibition performance, including their resistance against localised attack, improved with time.

Electrochemical impedance spectroscopy (EIS) measurements and modelling were carried out so as to propose a simple electrical model and correlate the extracted parameters to the inhibition mechanism put forward for REM-cinnamate based compounds. The results supported the high corrosion inhibition performance of the compounds as well as the build-up of a protective film with time. Based on a two-layer model the results suggested that the upper layer of the inhibitor film seemed to offer less resistance to the diffusion of electrochemically active species than the highly resistive inner layer at the film/metal interface.

ATR characterisation of synergistic corrosion inhibition of mild steel surfaces by cerium salicylate

The nature of deposits on mild steel surfaces formed by exposure to corrosive and inhibiting solutions has been examined by attenuated total reflectance spectroscopy. For cerium-based inhibitors, e.g. CeCl₃ the formation of cerium-containing coatings was detected whilst the cerium carboxylate Ce(sal)₃ (sal=salicylate), which combines the Ce³⁺ with the known organic inhibitor sal⁻, was shown to involve substantial deposition of both cerium and a salicylate species. These results, combined with corrosion inhibition data for the respective inhibitor compounds clearly indicate a synergistic corrosion mechanism for Ce(sal)₃ which underpins the improved performance of this corrosion inhibitor in comparison to the individual components (i.e. Na(sal) or CeCl₃).

Influence of praseodymium - synergistic corrosion inhibition in mixed rare-earth diphenyl phosphate systems

Mixed rare-earth organophosphates have been investigated as potential corrosion inhibitors for AA2024-T3, and previously have shown synergistic inhibition behavior; however, the mechanism was not identified. In this paper, a key factor contributing to corrosion inhibition of AA2024-T3 with mischmetal diphenyl phosphate [Mm(dpp)3] is the unique stability of Pr(dpp)3 compared to other key rare earths in mischmetal. Although increasing pH causes precipitation of other components, the Pr compound is stable at higher pH. Electrochemically, a synergy is evident when Ce(dpp)3 and Pr(dpp)3 are combined. Raman mapping indicates the Pr(dpp)3 inhibitor leads to a more uniform coverage of the alloy.

Role of glutathione in schizophrenia? The effect of brain glutathione depletion on prepulse inhibition (PPI) in rats and mice

Reductions in brain glutathione (GSH) levels have been reported in schizophrenia. We investigated the effects of brain GSH depletion on prepulse inhibition (PPI), a model of sensorimotor gating which is disrupted in individuals with schizophrenia. It was hypothesized that GSH depletion would lead to disruption of PPI similar to that seen in schizophrenia and enhance the effect of increased dopamine release by amphetamine. Sprague-Dawley rats and C57Bl/6 mice were treated with saline or 2-cyclohexene-1-one (CHX, 75 mg/kg and 120 mg/kg respectively) to deplete brain GSH. 225 minutes later the animals were injected with amphetamine (2.5 mg/kg in rats and 25 mg/kg in mice). Total brain GSH levels were measured using an enzymatic recycling assay. Surprisingly, in rats CHX treatment prevented the disruption of PPI by amphetamine. Thus, while there was the expected disruption of PPI caused by amphetamine on its own (average %PPI reduced from 58 ± 5 to 44 ± 4), in combination with CHX, amphetamine had no significant effect (67 ± 4 vs. 63 ± 3, respectively). In contrast to rats, in mice CHX had no effect on PPI. Thus, amphetamine similarly disrupted PPI after saline (41 ± 5 vs. 28 ± 5) and CHX pretreatment (45 ± 6 vs. 26 ± 5). There were significant 40-63% depletions of GSH in frontal cortex and striatum of CHX-treated rats and mice. These data show that GSH depletion in the brain by CHX treatment did not induce the expected decrease in PPI. Because the levels of GSH depletion in this study were similar to those found in schizophrenia, these results cast doubt on a direct interaction between brain GSH levels and PPI disruption in this illness. In rats, CHX treatment prevented the disruption of PPI caused by amphetamine. We have observed that resting levels of GSH are lower in rats than in mice. It is plausible that some oxidative damage may occur after amphetamine treatment alone, which induces marked release of the electroactive species, dopamine. In mice with their higher levels of GSH (either with or without CHX treatment) and in control rats, this does not cause functional effects. However, in CHX-treated rats GSH levels are reduced to a point where amphetamine-induced dopamine release may cause increased metabolism and lipid peroxidation inducing a decrease in postsynaptic dopamine receptor function and consequently leading to an apparent inhibition of the disruption of PPI. In conclusion, while individuals with schizophrenia show disruption of PPI and reduced brain GSH levels, in rats and mice brain GSH depletion alone does not impact on PPI. In combination with a hyperdopaminergic state, functional effects on PPI regulation were found. These effects warrant further investigation.