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In the current public health framework, the importance of medication as a determinant of citizens’ health has emerged as a factor warranting special attention. Most studies investigating the relationship between medication and quality of life do so from the perspective of adherence. However, other medication-related factors identified at home visits may be associated with health-related quality of life.Methods and designObjective: To describe the relationship between medication-related factors and the health-related quality of life in patients older than 65 years who use multiple medications (polypharmacy).Design: Cross-sectional descriptive study.Setting: Primary care.Participants: Patients older than 65 years who use multiple medications (n = 375).Measurements: The main outcome measure was health-related quality of life according to the EuroQol-5D instrument. Sociodemographic, clinical and medication-related variables were recorded during home interviews.ResultsMean age was 74.72 ± 5.59 years, and 65.5% of our participants were women. The global level of health-related quality of life according to the EQ-5D visual analog scale was 59.25 ± 20.92. Of the five EuroQol dimensions, anxiety/depression and pain were the most frequently reported, while mobility and self-care were the dimensions with the greatest impact on self-reported quality of life. Multivariate analysis indicated that functional independence was the factor most strongly associated (β = 14.27 p < 0.001) with better health-related quality of life, while illiteracy (β = −13.58 p < 0.001), depression (β = −10.13 p < 0.001), social risk (β = −7.23 p = 0.004) and using more than 10 medicines (β = −4.85 p = 0.009) were strongly associated with a poorer health-related quality of life.ConclusionsFactors inherent within the patient such as functional incapacity, cognitive impairment and social and emotional problems were the main constraints to quality of life in our study population. The number of medicines taken was negatively related with quality of life.

We used an animal model of extrahepatic biliary obstruction of 7 days' duration to study the production of thiobarbituric acid reactive substances (TBARS), total glutathione (TG), reduced glutathione (GSH), and oxidized glutathione (GSSG), and the enzymatic activities of GSH-peroxidase, GSSG-reductase, and GSH-transferase. Four groups of six rats each were treated with saline, drug solvent, S-adenosyl-L-methionine (SAM) 5 mg/kg/d, subcutaneously, or SAM 10 mg/kg/d, subcutaneously. Extrahepatic biliary obstruction increased TBARS. SAM had the dose-dependent effects of inhibiting TBARS production and increasing TG content, mainly as a result of the increase in GSH. The activity of GSH-peroxidase and GSH-transferase was also significantly increased. In renal tissue these effects were statistically significant only in animals given the higher dose of SAM. In liver we found a reduction in biochemical values indicative of liver damage. We conclude that effect of SAM on hepatorenal function is strongly influenced by the drug's ability to reestablish equilibrium after oxidative tissue stress.

Virgin olive oil (VOO) contains the polyphenols hydroxytyrosol (HT) and hydroxytyrosol acetate (HT-AC). This study investigated the antiplatelet effect of HT and HT-AC in healthy rats and compared their effects to acetylsalicylic acid (ASA). All compounds were administered orally for 7 days. HT and HT-AC inhibited platelet aggregation in whole blood, with a 50% inhibitory dose (ID50) of 48.25 mg/kg per day for HT, 16.05 mg/kg per day for HT-AC, and 2.42 mg/kg per day for ASA. Platelet synthesis of thromboxane B2 was inhibited by up to 30% by HT and 37% by HT-AC; the ID50 of this effect for ASA was 1.09 mg/kg per day. Vascular prostacyclin production was inhibited by up to 27.5% by HT and 32% by HT-AC; the ID50 of this effect for ASA was 6.75 mg/kg per day. Vascular nitric oxide production was increased by up to 34.2% by HT, 66% by HT-AC, and 64% by ASA. We conclude that HT and HT-AC administered orally inhibited platelet aggregation in rats and that a decrease in thromboxane synthesis along with an increase in nitric oxide production contributed to this effect.

We investigated how virgin olive oil (VOO) affected platelet and hypoxic brain damage in rats. Rats were given VOO orally for 30 days at 0.25 or 0.5 mL kg(-1) per day (doses A and B, respectively). Platelet aggregation, thromboxane B2, 6-keto-PGF(1alpha), and nitrites + nitrates were measured, and hypoxic damage was evaluated in a hypoxia-reoxygenation assay with fresh brain slices. Oxidative stress, prostaglandin E2, nitric oxide pathway activity and lactate dehydrogenase (LDH) activity were also measured. Dose A inhibited platelet aggregation by 36% and thromboxane B2 by 19%; inhibition by dose B was 47 and 23%, respectively. Virgin olive oil inhibited the reoxygenation-induced increase in lipid peroxidation (57% in control rats vs. 2.5% (P < 0.05) in treated rats), and reduced the decrease in glutathione concentration from 67 to 24% (dose A) and 41% (dose B). Brain prostaglandin E2 after reoxygenation was 306% higher in control animals, but the increases in treated rats were only 53% (dose A) and 45% (dose B). The increases in nitric oxide production (213% in controls) and activity of the inducible isoform of nitric oxide synthase (175% in controls) were both smaller in animals given VOO (dose A 84%; dose B 12%). Lactate dehydrogenase activity was reduced by 17% (dose A) and 42% (dose B). In conclusion, VOO modified processes related to thrombogenesis and brain ischemia. It reduced oxidative stress and modulated the inducible isoform of nitric oxide synthase, diminishing platelet aggregation and protecting the brain from the effects of hypoxia-reoxygenation.

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A series of nitroderivatives has been synthesized from hydroxytyrosol, the natural olive oil phenol, to increase the assortment of compounds with putative effects against Parkinson’s disease. Nitrohydroxytyrosyl esters were obtained from nitrohydroxytyrosol using a chemoselective one-step, high-yield, transesterification procedure. The antioxidant activity of these new series of nitrocatechols was evaluated using FRAP, ABTS, and ORAC assays and compared to that of free hydroxytyrosol. The nitro functional group induced a significant increase in the antioxidant activity of nitrohydroxytyrosol compared to hydroxytyrosol. Regarding nitroester derivatives, variable antioxidant activity was observed depending on the acyl side-chain length; shorter chains maintained or even enhanced the antioxidant activity compared to nitrohydroxytyrosol, decreasing the activity with longer side chains in keeping with their lipophilic nature. Therefore, it may be concluded that nitroester derivatives of hydroxytyrosol, which may be obtained by a simple, high-yield reaction, have elevated antioxidant activity and thus present potential bioactivity.

The aim of the study was to analyze the possible neuroprotective effect of hydroxytyrosol (HT) in diabetic animals in a model of hypoxia-reoxygenation. Rats (10 animals/group) were distributed in five groups: nondiabetic rats, control diabetic rats (DR), and DR rats treated for 2 months with 1, 5, or 10 mg/kg/day po HT. At the end of follow-up, an experimental model of hypoxia-reoxygenation in brain slices was tested. The DR group showed increased cell death, oxidative and nitrosative stress, and an increase in brain inflammatory mediators. These alterations were significantly greater in DR than in normoglycemic animals. HT significantly reduced oxidative (38.5-52.4% lipid peroxidation) and nitrosative stress (48.0-51.0% nitric oxide and 43.9-75.2% peroxynitrite concentration) and brain inflammatory mediators (18.6-40.6% prostaglandin E and 17.0-65.0% interleukin 1β concentration). Cell death was reduced by 25.9, 37.5, and 41.0% after the administration of 1, 5, or 10 mg/kg/day. The administration of HT in rats with experimental diabetes thus had a neuroprotective effect.