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Masthead: Lipid Technology 7/2016 报头:脂质技术7/2016
Pub Date : 2016-07-03 DOI: 10.1002/lite.201670072
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引用次数: 0
India 印度
Pub Date : 2016-07-03 DOI: 10.1002/lite.201600035
Gary List
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引用次数: 0
Contents: Lipid Technology 7/2016 内容:脂质技术7/2016
Pub Date : 2016-07-03 DOI: 10.1002/lite.201670071
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引用次数: 0
Research Highlights 研究突出了
Pub Date : 2016-07-03 DOI: 10.1002/lite.201600033
Prof. Michael Eskin, Mr. Peter Clough, Dr. Gary List
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引用次数: 0
Toxic contaminants of thermo-oxidatively processed edible oils/fats 热氧化处理的食用油/脂肪的有毒污染物
Pub Date : 2016-07-03 DOI: 10.1002/lite.201600032
Felix Aladedunye

Processing of edible oils during refining of the crude oil, or when used in frying, often exposes the oils to thermal and oxidative stresses. However, because of weaknesses inherent in their chemical structure, oils subsequently undergo structural decomposition and transformation in response to thermooxidative stresses. Whereas some of the decomposition products from the processed oils confer some value additions to the oils and the foods prepared in them (e.g. flavor, color, texture, and even stability), a number of edible oils' degradation products are known to be potentially toxic, and at reasonably high quantity, can compromise the health and wellbeing of consumers. This article describes the sources and updated knowledge on major toxic compounds that are generated during high temperature processing and usage of vegetable oils.

食用油的加工过程中,在提炼原油或用于油炸时,经常使油暴露在热应激和氧化应激下。然而,由于其化学结构固有的弱点,油随后在热氧化应激下发生结构分解和转化。虽然加工油中的一些分解产物给油和用它们制备的食品带来了一些附加价值(例如风味、颜色、质地甚至稳定性),但已知一些食用油的降解产物具有潜在毒性,并且在相当高的数量下,可能危及消费者的健康和福祉。本文介绍了植物油在高温加工和使用过程中产生的主要有毒化合物的来源和最新知识。
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引用次数: 3
Oilseeds and Vegetable Oil 油籽和植物油
Pub Date : 2016-07-03 DOI: 10.1002/lite.201600031
Gary List
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引用次数: 0
Fat‐soluble arsenic – new lipids with a sting in their tail 脂溶性砷——尾巴上有刺的新型脂质
Pub Date : 2016-06-01 DOI: 10.1002/LITE.201600024
K. Francesconi, T. Schwerdtle
Lipids encompass a myriad of natural compounds with many essential biological functions and applications across the areas of food and nutrition, health and medicine, and modern nanotechnologies. Arsenic has long been known as a highly toxic element. What happens when the two come together?
脂类包含了无数的天然化合物,它们具有许多基本的生物功能,并在食品和营养、健康和医学以及现代纳米技术等领域得到了应用。砷一直被认为是一种剧毒元素。当两者结合在一起会发生什么?
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引用次数: 5
Targeted delivery of mitochondrial protectors prevents cardiolipin oxidation and cell degeneration following brain trauma or radiation injury 线粒体保护剂的靶向递送可防止脑外伤或辐射损伤后的心磷脂氧化和细胞变性
Pub Date : 2016-06-01 DOI: 10.1002/LITE.201600023
M. Rabinovich
Reactive oxygen species (ROS) produced by injured cell powerhouses, mitochondria may lead to the development of heavy neuronal disorders of both chronic (Alzheimer disease, Parkinson disease, etc.) and acute brain injury followed by a secondary neuronal damage and death over time. Once a mitochondrion is injured, a phospholipid constituent of its inner membrane, cardiolipin (CL) undergoes externalization triggering a sequence of events which may lead to either natural elimination of injured mitochondria without the host cell injury or programmed host cell suicide, apoptosis. Mitochondria-induced apoptosis is, among other, also responsible for radiation-induced damage of radiosensitive organs like bone marrow and the small intestine. In order to prevent cell suicide, (per)oxygenation of externalized CL at the outer side of the inner mitochondrial membrane catalyzed by the cytochrome c/CL complex should be suppressed. Here some approaches that lead to the targeted suppression of ROS and inhibition of cyt c/CL complex (per)oxygenative activity within mitochondria are discussed, which provide the basis for the development of new anti-apoptotic drugs defending the neuronal and other tissues from degeneration by ROS. The positive effects of these drugs were demonstrated in the laboratory animals developing secondary neuronal damage over time following traumatic brain injury or suffering from radiation-induced disorders.
活性氧(ROS)由受损的细胞动力,线粒体产生,可能导致慢性(阿尔茨海默病,帕金森病等)和急性脑损伤的严重神经元疾病的发展,随后继发性神经元损伤和死亡。一旦线粒体受损,其内膜磷脂成分心磷脂(CL)发生外化,引发一系列事件,可能导致受损线粒体自然消除而不损伤宿主细胞或程序性宿主细胞自杀,凋亡。线粒体诱导的细胞凋亡,除其他外,还会导致放射性敏感器官(如骨髓和小肠)的辐射损伤。为了防止细胞自杀,应抑制由细胞色素c/CL复合物催化的线粒体内膜外侧外化CL的氧合作用。本文讨论了靶向抑制ROS和抑制线粒体内cyt c/CL复合物(per)氧化活性的一些方法,为开发新的抗凋亡药物保护神经元和其他组织免受ROS的退化提供了基础。这些药物的积极作用在实验室动物身上得到了证明,这些动物在创伤性脑损伤或遭受辐射引起的疾病后,随着时间的推移出现了继发性神经元损伤。
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引用次数: 0
Lipid autoxidation in ozone‐processed crustacea under cold storage: A treatise 冷藏条件下臭氧处理甲壳类动物脂质自氧化的研究
Pub Date : 2016-06-01 DOI: 10.1002/LITE.201600026
C. Okpala
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引用次数: 11
Detecting the modest signals of omega‐3 fatty acids' antidepressant effects by homogenizing depressed patient groups 通过均质化抑郁患者组来检测omega - 3脂肪酸抗抑郁作用的适度信号
Pub Date : 2016-06-01 DOI: 10.1002/LITE.201600028
S. Kumaran, Y. Shih, K. Su
Major depressive disorder (MDD) is predicted to become the top leading cause of disability worldwide by 2020, with a high lifetime prevalence rate of up to one-tenth or possibly even one-fifth [1]. The current psychopharmacologic interventions have had fairly limited success and the development of novel antidepressant medications has had mixed results with several unfortunate failures due to limited efficacy and adverse side effects. With such challenges of prevailing pharmacotherapies towards MDD, a new therapeutic strategy in treatment with omega-3 polyunsaturated fatty acids (omega-3 or n-3 PUFAs) supplementation has shown promising outcomes in lowering the risk of depression.
据预测,到2020年,重度抑郁症(MDD)将成为全球致残的头号原因,其终生患病率高达十分之一,甚至可能达到五分之一[1]。目前的精神药理学干预措施取得了相当有限的成功,新型抗抑郁药物的开发结果好坏参半,由于疗效有限和不良副作用,一些不幸的失败。面对当前MDD药物治疗的挑战,补充omega-3多不饱和脂肪酸(omega-3或n-3 PUFAs)治疗的新治疗策略在降低抑郁症风险方面显示出有希望的结果。
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引用次数: 3
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Lipid Technology
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