Blackcurrant (Ribes nigrum L.) Seeds-A Valuable Byproduct for Further Processing.

The rational exploitation of byproducts is important from the point of view of their potential applicability in various fields. In this study, the possibility of further processing of blackcurrant seeds (BCs), which are a byproduct of fruit processing, was investigated. BCs were used as a material for the extraction of oil on a semi-industrial scale, and the residues were assessed in terms of their potential application in skin care products. Supercritical fluid extraction (SFE) using CO2 at pressures of 230 and 330 bar and extraction temperature of 40 °C was exploited for isolation of oil, and the products were characterised taking into account lipophilic constituents. After 120 min, the oil yields were 19.67% and 20.94% using CO2 at 230 and 330 bar, respectively, which showed that SFE was an effective method on a semi-industrial scale, taking into account the extraction yield. The oils had similar fatty acid compositions with a high percentage of linoleic acid (ca. 43%); however, tocopherols and carotenoids were most abundant in the oil obtained at 230 bar. It was also found that the composition of the SFE oils was comparable with that of cold-pressed oil, which shows that supercritical fluid extraction provides a high-quality product; therefore, it can be an alternative to cold pressing. Furthermore, the chemical compositions of the extracts from the oil isolation residues were established using UPLC-MS, and the impact of the extracts on human skin fibroblasts was assessed using the MTT and NR assays. The quantitative analysis revealed that the residues contained high amounts of polyphenolic acids, including gallic, protocatechuic, and hydroxybenzoic acid derivatives, as well as flavonoids, especially quercetin and kaempferol glucoside. Moreover, it was found that the extracts were nontoxic and exerted a stimulatory effect on cell metabolism. Therefore, they can be a valuable additive to natural plant-based cosmetics. Our results showed that blackcurrant seeds, regarded as a byproduct, can be a valuable material for further use.

Shotgun Lipidomic Analysis for Differentiation of Niche Cold Pressed Oils.

The fast-growing food industry is bringing significant number of new products to the market. To protect consumers' health and rights, it is crucial that food control laboratories are able to ensure reliable quality testing, including product authentication and detection of adulterations. In our study, we applied a fast and eco-friendly method based on shotgun-lipidomic mass spectrometry for the authentication of niche edible oils. Comprehensive lipid profiles of camelina (CA), flax (FL) and hemp (HP) seed oils were obtained. With the aid of principal component analysis (PCA), it was possible to detect and distinguish each of them based on their lipid profiles. Lipidomic markers characteristic ofthe oils were also identified, which can be used as targets and expedite development of new multiplexed testing methods.

Differential effects of statins on endogenous H2S formation in perivascular adipose tissue.

Hydrogen sulfide (H(2)S) is a new gasotransmitter synthesized enzymatically from l-cysteine in cytosol and is oxidized in mitochondria. In the cardiovascular system, H(2)S regulates vascular tone, inhibits atherogenesis, and protects against myocardial ischemia-reperfusion injury. We examined the effect of statins on vascular H(2)S production. Male Wistar rats received pravastatin (40mg/kg/day) or atorvastatin (20mg/kg/day) for 3 weeks and then H(2)S formation was measured in aortic media, periaortic adipose tissue (PAAT) and the liver. Only atorvastatin increased H(2)S production in PAAT whereas both statins stimulated its formation in the liver. Neither statin affected H(2)S production in aortic media. H(2)S formation in post-mitochondrial supernatant was higher than in mitochondria-containing supernatant and was not influenced by statins in any tissue. In addition, oxidation of exogenous H(2)S in isolated liver mitochondria was slower in statin-treated than in control rats. These data indicate that statins increase net H(2)S production by inhibiting its mitochondrial oxidation. Statins had no effect on the activity of H(2)S-metabolizing enzyme, sulfide:quinone oxidoreductase, measured at saturating coenzyme Q concentration. Both statins reduced CoQ(9) concentration in plasma and liver, but only atorvastatin decreased CoQ(9) in PAAT. Atorvastatin attenuated phenylephrine-induced contraction of PAAT+ but not of PAAT- aortic rings. Effects of atorvastatin on net H(2)S production, mitochondrial H(2)S oxidation and aortic contractility were abolished by supplementation of exogenous CoQ(9). In conclusion, lipophilic atorvastatin, but not hydrophilic pravastatin, increases net H(2)S production in perivascular adipose tissue by inhibiting its mitochondrial oxidation. This effect is mediated by statin-induced CoQ(9) deficiency and results in the augmentation of anticontractile effect of perivascular adipose tissue.