烃氧化产物皂化后活性组分在油、水相的分配

用强酸酸化后测定乙醚抽出物酸量和酯量、溴甲酚绿两相滴定测定羧酸盐等方法研究了烃氧化产物皂化后活性组分在油、水相的分配。结果表明,在现行的用NaOH皂化烃氧化产物以制备水溶性石油磺酸盐的过程中有相当多的活性组分分配到油相;在水相和油相中均有大量羧酸酯存在,羧酸酯量远远超过羧酸盐量。     

氧化蜡乳液的研制

采用自制氧化蜡研制氧化蜡乳液,考察了乳化剂的质量分数、乳化温度、搅拌速率、乳化时间等因素对乳液性能的影响,确定了制备氧化蜡乳液的复合乳化剂质量分数以及乳化工艺。实验结果表明,当氧化蜡质量分数15%、乳化剂质量分数3%、乳化剂的亲水亲油平衡值约为12.0、乳化温度85℃、搅拌速率800r/min、乳化时间35min时,可得到稳定性好、分散性为一级的乳白色的氧化蜡乳液。     

乙酰化磷脂的制备及性能研究

本文以乙酰氯为酰化试剂合成了乙酰化磷脂。通过实验确定了适宜的反应条件，利用红外光谱法确定了改性磷脂的结构。对改性磷脂及磷脂的分散性和乳化性进行了测试比较，实验表明：乙酰化磷脂的分散性有了显著提高；在0／W型乳状液中，乙酰化磷脂的乳化性有了一定的提高。     

Roasting effects on the distribution of tocopherols and phospholipids within each structural part and section of soybeans

To clarify the effects of microwave roasting on the distribution of tocopherols and FA of phospholipids within soybeans, whole soybeans (Glycine max) were treated by microwave and further evaluted as compared to a raw sample. Tocopherol homologs, measured using HPLC, and phospholipid profiles, quantified with GC, were determined in the seed coat, the embryonic axis, and selections of cotyledons separated from three cultivars. The tocopherols were predominantly detected in the axis, followed by the cotyledons, and then very little in the coat. As much as 25% of the individual tocopherols originally present in the coat were lost at 12 min of roasting, whereas <25% was lost in the cotyledons and the axis after 20 min of roasting. The greatest rate of phospholipid loss (P<0.05) was observed in PE, followed by PC and PI, and their changing patterns were more pronounced in the coat than in the cotyledons or the axis. Thus, tocopherol content and phospholipid profiles change with microwave roasting according to tissue.     

Antioxidant effect of soy lecithins on vegetable oil stability and their synergism with tocopherols

The antioxidant effect of lecithins was tested on several oils and fats varying in FA composition and tocopherol content. Standard lecithins, when added at a level of 1% w/w, exhibited a good protective effect against oxidation. This effect was observed to depend on the phospholipid content of the tested lecithins and the FA composition of the tested oils. Better results were obtained with lecithin samples containing high proportions of PC and PE. Indeed, the main antioxidant mechanism of lecithins was due to a synergistic effect between amino-alcohol phospholipids and γ- and δ-tocopherols. No synergism was observed with α-tocopherols, especially when the tested oil was rich in linoleic acid. Therefore, the antioxidant protection of lecithins was not effective for sunflower oil. Finally, the use of fractionated or enriched lecithins was not clearly advantageous compared to standard oil lecithins.     

A 1D High Performance Thin Layer Chromatography Method Validated to Quantify Phospholipids Including Cardiolipin and Monolysocardiolipin from Biological Samples

The aim of this study is to identify high performance thin layer chromatography (HPTLC) conditions allowing the separation and quantification of mammalian cellular phospholipids (PLs) (sphingomyelin, phosphatidylcholine, phosphatidylserine, phosphatidylinositol, phosphatidylethanolamine, and especially phosphatidic acid, cardiolipin, and monolysocardiolipin, these latter two being specifically located in mitochondria membranes). In order to make this method faster and easier, a 1D HPTLC method is chosen, testing several eluents as well as several staining methods. A pre‐conditioning of HPTLC plates with boric acid and a copper staining reagent followed by carbonization are selected for the quality of PL separation and homogeneity of staining. The selected conditions are discussed and the method validation is performed according to the International Conference on Harmonization guidelines. Linearity is effective between 1 and 8 µg and limit of quantification is between 0.5 and 2.3 µg depending on PL classes. Precision measurements show coefficients of variation <6%, and when amounts are close to the detection limit, <12%. Lipid extracts of tumor cell lines or isolated mitochondria are used to assess PL profiles. This shows that the HPTLC method can be used routinely to follow level variations of PLs. Practical Applications: The changes in PL composition play a crucial role in tumor processes and regulate cellular functions modulating cellular signaling or mitochondrial metabolism. The simple and cost‐effective 1D HPTLC method that is developed is applied to lipid extracts of whole tumor cells or hepatocyte‐isolated mitochondria. It is sensitive as well as precise to detect variations of phosphatidic acid or cardiolipin levels linked to physio‐pathological conditions. It can also be used to investigate the composition changes of other membrane PLs. Moreover, with a simultaneous analysis of 14 samples/standards on the same plate (six plates per day), this method is adapted for large series of samples.     

Hydroxyoctadecadienoic Acids Regulate Apoptosis in Human THP‐1 Cells in a PPARγ‐Dependent Manner

Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, including hydroxyoctadecadienoic acids (HODEs). These stable oxidation products of linoleic acid (LA) are abundant in atherosclerotic plaque and activate PPARγ and GPR132. We investigated the mechanisms through which HODEs regulate apoptosis. The effect of HODEs on THP‐1 monocytes and adherent THP‐1 cells were compared with other C18 fatty acids, LA and α‐linolenic acid (ALA). The number of cells was reduced within 24 hours following treatment with 9‐HODE (p < 0.01, 30 μM) and 13 HODE (p < 0.01, 30 μM), and the equivalent cell viability was also decreased (p < 0.001). Both 9‐HODE and 13‐HODE (but not LA or ALA) markedly increased caspase‐3/7 activity (p < 0.001) in both monocytes and adherent THP‐1 cells, with 9‐HODE the more potent. In addition, 9‐HODE and 13‐HODE both increased Annexin‐V labelling of cells (p < 0.001). There was no effect of LA, ALA, or the PPARγ agonist rosiglitazone (1μM), but the effect of HODEs was replicated with apoptosis‐inducer camptothecin (10μM). Only 9‐HODE increased DNA fragmentation. The pro‐apoptotic effect of HODEs was blocked by the caspase inhibitor DEVD‐CHO. The PPARγ antagonist T0070907 further increased apoptosis, suggestive of the PPARγ‐regulated apoptotic effects induced by 9‐HODE. The use of siRNA for GPR132 showed no evidence that the effect of HODEs was mediated through this receptor. 9‐HODE and 13‐HODE are potent—and specific—regulators of apoptosis in THP‐1 cells. Their action is PPARγ‐dependent and independent of GPR132. Further studies to identify the signalling pathways through which HODEs increase apoptosis in macrophages may reveal novel therapeutic targets for atherosclerosis.     

Changes in Phospholipid/Ceramide Profiles and Eicosanoid Levels in the Plasma of Rats Irradiated with UV Rays and Treated Topically with Cannabidiol

Chronic UV radiation causes oxidative stress and inflammation of skin and blood cells. Therefore, in this study, we assessed the effects of cannabidiol (CBD), a natural phytocannabinoid with antioxidant and anti-inflammatory properties, on the phospholipid (PL) and ceramide (CER) profiles in the plasma of nude rats irradiated with UVA/UVB and treated topically with CBD. The results obtained showed that UVA/UVB radiation increased the levels of phosphatidylcholines, lysophospholipids, and eicosanoids (PGE2, TxB2), while downregulation of sphingomyelins led to an increase in CER[NS] and CER[NDS]. Topical application of CBD to the skin of control rats significantly upregulated plasma ether-linked phosphatidylethanolamines (PEo) and ceramides. However, CBD administered to rats irradiated with UVA/UVB promoted further upregulation of CER and PEo and led to significant downregulation of lysophospholipids. This was accompanied by the anti-inflammatory effect of CBD, manifested by a reduction in the levels of proinflammatory PGE2 and TxB2 and a dramatic increase in the level of anti-inflammatory LPXA4. It can therefore be suggested that topical application of CBD to the skin of rats exposed to UVA/UVB radiation prevents changes in plasma phospholipid profile resulting in a reduction of inflammation by reducing the level of LPE and LPC species and increasing antioxidant capacity due to upregulation of PEo species.