Effects of Seed Roasting Temperature on Sesame Oil Fatty Acid Composition, Lignan, Sterol and Tocopherol Contents, Oxidative Stability and Antioxidant Potential for Food Applications.

Roasting is a key step for preparing sesame oil that leads to important changes in its organoleptic properties and quality. In this study, white sesame seeds were roasted for 20 min in an electric oven at different temperatures (120, 150, 180, 210, 250 and 300 °C). The oils extracted from unroasted and roasted seeds were compared for their chemical composition: fatty acids (including trans isomers), phytosterols, lignans (sesamin and sesamolin), tocopherols and total phenolic compounds, as well as their oxidative stability and antiradical capacity. There were no obvious differences in the oil densities, refractive indexes or iodine values, but the saponification values were affected by temperature. Relevant primary and secondary lipid oxidation were observed at T > 250 °C, resulting in a higher p-anisidine value and K232 as well as K268 values. Roasting improved oil yield (from 33.5 to 62.6%), increased its induction period (from 5.5 to 10.5 h) and enhanced the total phenolic content (from 152 to 194 mg/100 g) and antiradical activity of the extracted oil. Depending on roasting temperature, a gradual decline was recorded in total amounts of phytosterols (up to 17.4%), γ-tocopherol (up to 10.6%), sesamolin (maximum of 27.5%) and sesamin (maximum of 12.5%). All the investigated oils presented a low quantity in triglyceride polymers, clearly below the maximum tolerated quantity according to the European regulation. The optimal roasting temperature for obtaining high nutritional grade oil within the permissible values was 210 °C. The unsaponifiable components (including lignans and sterols) extracted from roasted seeds have been shown to be natural additives to fresh meatball products to extend shelf life. The results of this study may help to boost the nutritional content of plant-based diets by allowing for the use of roasted sesame seed oil and its components.

An innate contribution of human nicotinic receptor polymorphisms to COPD-like lesions.

Chronic Obstructive Pulmonary Disease is a generally smoking-linked major cause of morbidity and mortality. Genome-wide Association Studies identified a locus including a non-synonymous single nucleotide polymorphism in CHRNA5, rs16969968, encoding the nicotinic acetylcholine receptor α5 subunit, predisposing to both smoking and Chronic Obstructive Pulmonary Disease. Here we report that nasal polyps from rs16969968 non-smoking carriers exhibit airway epithelium remodeling and inflammation. These hallmarks of Chronic Obstructive Pulmonary Disease occur spontaneously in mice expressing human rs16969968. They are significantly amplified after exposure to porcine pancreatic elastase, an emphysema model, and to oxidative stress with a polymorphism-dependent alteration of lung function. Targeted rs16969968 expression in epithelial cells leads to airway remodeling in vivo, increased proliferation and production of pro-inflammatory cytokines through decreased calcium entry and increased adenylyl-cyclase activity. We show that rs16969968 directly contributes to Chronic Obstructive Pulmonary Disease-like lesions, sensitizing the lung to the action of oxidative stress and injury, and represents a therapeutic target.

Phenolic compounds from an Algerian medicinal plant (Pallenis spinosa): simulated gastrointestinal digestion, characterization, and biological and enzymatic activities.

Pallenis spinosa is a medicinal plant which is used in folk medicine as curative or preventive remedies for various diseases. Individual phenolic compounds from the methanolic extracts of its flowers, leaves and stem were determined by the high performance liquid chromatography method (HPLC) and total phenolic contents (TPC) were evaluated by Folin-Ciocalteu assay. The stability and bioactivity (antioxidant activity, micellar cholesterol solubility, α-amylase, and angiotensin converting enzymes (ACE) inhibitory effects) of these extracts in the gastrointestinal environment was determined before and after their protection in hydroxypropylmethylcellulose (HPMC) capsules. HPLC analysis revealed the presence of thirteen phenolic compounds with nine flavonoids and four phenolic acids. Except for kaempferol, the twelve other compounds have not been previously detected in the aerial part of the studied plant. Quantification of phenolics by HPLC and Folin Ciocalteu methods revealed that the highest TPC was detected in the flower extracts (104.31 ± 0.80 and 145.73 ± 0.48 mg EGA per g of extract, respectively). Leaf extracts displayed the best antioxidant capacity against the two tested radicals DPPH and ABTS (IC50 = 1.24 ± 0.03 and 0.94 ± 0.02 mg mL-1, respectively), FRAP assay (IC50 = 0.50 ± 0.02 mg mL-1), α-amylase inhibitory (IC50 = 1.25 ± 0.00 mg mL-1) and angiotensin activity with an inhibitory percent of 30.10 ± 0.12%. The best activity shown by stem extracts was against micellar cholesterol solubility (67.57 ± 0.00%). A strong decrease in TPC and their bioactivity was observed after the gastrointestinal digestion (GID) in non encapsulated extracts. These results showed that P. spinosa is a good source of phenolic compounds and GID affects significantly their composition, content and bioactivity.

Role of nicotinic acetylcholine receptors in cell proliferation and tumour invasion in broncho-pulmonary carcinomas.

OBJECTIVES: Nicotine and its associated nicotinic acetylcholine receptors (nAChRs) are believed to be involved in the progression of lung carcinomas. This study aimed at examining the localization of nAChRs in human lung tumours and, by using primary cultures of tumour cells derived from these tumours, determining the nAChR roles in cell proliferation and tumour invasion. MATERIALS AND METHODS: Immunohistochemistry was used to assess nAChR expression in non-small cell lung carcinomas (NSCLC). Primary cultures of tumour cells were established from NSCLC tissue samples and the effects of nicotine and nAChR antagonists on cell proliferation and invasion were assessed. RESULTS: α5, α7, ß2 and ß4 nAChR subunits were expressed in all adenocarcinomas (AC) and squamous cell carcinomas (SCC) tissue samples. In AC, all subunits were identified in glandular structures. In SCC, α5, ß2 and ß4 subunits were essentially identified in tumour cells at invasive fronts, whereas α7 subunit was mainly present in the most differentiated tumour cells and less frequently at invasive fronts. In AC and SCC, there was an inverse distribution of cell proliferation marker Ki-67 and α7 nAChR. Both α7 nAChR and heteromeric nAChRs positively regulated in vitro tumour invasion in NSCLC. Heteromeric nAChRs had a limited activity in regulating tumour cell proliferation in vitro. In contrast, α7 nAChR was a repressor of proliferation in tumour cells isolated from well differentiated NSCLC but mediated the pro-proliferative activity of nicotine in cells isolated from poorly differentiated NSCLC. CONCLUSION: α7 nAChR and heteromeric α5*ß2*ß4* nAChRs play a role in ex vivo tumour progression by stimulating invasion and, depending on the differentiation status of the tumour, by regulating proliferation. Our results suggest that the use of α7 nAChR antagonists to prevent lung cancer progression should be restricted to poorly differentiated tumours.

Heme oxygenase 1 is differentially involved in blood flow-dependent arterial remodeling: role of inflammation, oxidative stress, and nitric oxide.

Heme oxygenase 1 is induced by hemodynamic forces in vascular smooth muscle and endothelial cells. We investigated the involvement of heme oxygenase 1 in flow (shear stress)-dependent remodeling. Two or 14 days after ligation of mesenteric resistance arteries, vessels were isolated. In rats, at 14 days, diameter increased by 23% in high-flow arteries and decreased by 22% in low-flow arteries compared with normal flow vessels. Heme oxygenase activity inhibition using Tin-protoporphyrin abolished diameter enlargement in high-flow arteries and accentuated arterial narrowing in low-flow arteries (32% diameter decrease versus 22% in control). Two days after ligation, heme oxygenase 1 expression increased in high-flow and low-flow vessels, in association with a reduced mitochondrial aconitase activity (marker of oxidative stress) in high-flow arteries only. Inhibition of macrophage infiltration (clodronate) decreased heme oxygenase 1 induction in low-flow but not in high-flow arteries. Similarly, inhibition of NADPH oxidase activity (apocynin) decreased heme oxygenase 1 induction in low-flow but not high-flow arteries. However, dihydroethidium staining was higher in high-flow and low-flow compared with normal flow arteries. In arteries cannulated in an arteriograph, heme oxygenase 1 mRNA increased in a flow-dependent manner and was abolished by N(G)-nitro-l-arginine methyl ester, catalase, or mitochondrial electron transport chain inhibition. Furthermore, heme oxygenase 1 induction using cobalt-protoporphyrin restored altered high-flow remodeling in endothelial NO synthase knockout mice. Thus, in high-flow remodeling, heme oxygenase 1 induction depends on shear stress-generated NO and mitochondria-derived hydrogen peroxide. In low-flow remodeling, heme oxygenase 1 induction requires macrophage infiltration and is mediated by NADPH oxidase-derived superoxide.

Heme oxygenase-1 induction restores high-blood-flow-dependent remodeling and endothelial function in mesenteric arteries of old rats.

BACKGROUND: Aging is associated with reduced structural and functional adaptation to chronic changes in blood flow (shear stress) in small arteries. As heme oxygenase-1 (HO-1) is induced by hemodynamic forces in vascular smooth muscle and endothelial cells, we hypothesized that it might improve flow-dependent remodeling in aging. METHOD: First-order mesenteric arteries from 3 and 16-month-old rats were exposed to high, low, or normal flow by alternate ligation in vivo. Rats were treated with the HO-1 inducer, cobalt protoporphyrin (CoPP, 5 mg/kg) or vehicle. 14 days later, local blood flow was measured in vivo, and arteries were studied in vitro. RESULTS: Despite an equivalent change in blood flow, diameter enlargement in the high-flow arteries was blunted in old compared to young rats and was associated with decreased endothelium-dependent relaxation to acetylcholine. In old rats, HO-1 induction with CoPP restored outward remodeling, via a paradoxical reactive oxygen species-dependent mechanism, and was associated with a Mn-superoxide dismutase (SOD) overexpression, as well as a significant reduction of mitochondrial aconitase activity, used as a biomarker for oxidative stress. The heme oxygenase activity inhibitor, Sn-protoporphyrin, and the SOD-mimetic, TEMPOL, prevented the effect of CoPP on remodeling and oxidative status in old rats. Furthermore, HO-1 induction improved endothelial function, in association with increased endothelial nitric oxide synthase protein expression and phosphorylation (Ser-1177). In low-flow arteries, inward remodeling was unaffected by aging or by CoPP. Thus, in old rats, CoPP-induced up-regulation of HO-1 restored high-flow-dependent remodeling (diameter enlargement) and improved endothelial function in mesenteric arteries. CONCLUSION: This opens new perspectives in the treatment of ischemic diseases in aging.