Anthocyanins extract from bilberry enhances the therapeutic effect of pollen of Brassica napus L. on stress-provoked benign prostatic hyperplasia in restrained mice

Clinical research has revealed that stressed men are susceptible to develop benign prostatic hyperplasia (BPH). In this study, restraint-stress mice model was employed to mimic the physiological conditions of the population that was susceptible to develop BPH. Male mice were subjected to restraint stress after being subcutaneously injected with testosterone propionate (TP) for 14 d. Results demonstrated that TP-induced BPH was significantly aggravated by restraint stress, as manifested by increases of prostate index, serum testosterone level, and prostate 5α-reductase (5AR) and serum acid phosphatase (ACP) activities. These findings were further supported by results of prostate pathological examination. However, we found that anthocyanins extract (AE) from bilberry (Vaccinium myrtillus L.) had additive effect with pollen of Brassica napus L. (PBN), a widely used folk remedy for BPH in traditional Chinese medicine, on stress-provoked BPH in mice. The mechanism was associated with the protective effects of AE against stress-induced oxidative damage, as indicated by decreased lipid peroxidation level, increased oxygen radical absorbance capacity (ORAC) and glutathione (GSH) content, along with elevated superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Our results proved that stress-induced oxidative damage promoted the development and aggravation of BPH, while antioxidative defense contributed to the amelioration of BPH.     

Dietary Monascus adlay supplements facilitate suppression of cigarette smoke-induced pulmonary endoplasmic reticulum stress,autophagy, apoptosis and emphysema-related PLGF in the rat

Cigarette smoke (CS) exposure may cause oxidative stress in the lung, leading to cell death and long-term injury. Monascus adlay (MA) with antioxidant components produced by inoculating adlay (Cois lachrymal-jobi L. var. ma-yuen Stapf) with Monascus purpureus may protect lung against CS-induced lung injuries in rats. MA and lovastatin had higher antioxidant activities than either M. purpureus or adlay. CS exposure caused significant lung damage, as evidenced by higher levels of reactive oxygen species (ROS), neutrophil infiltration, dityrosine and 4-HNE, as well as lower levels of Mn-superoxide dismutase and catalase expression. Lung tissues with CS exposure had higher levels of ER stress, apoptosis, autophagy and emphysema-related placenta growth factor (PlGF) expressions. All CS-induced injuries were significantly suppressed by MA supplements. MA would be a beneficial nutritional therapy to ameliorate CS-induced lung injury via preserving antioxidant defense mechanisms, decreasing oxidative stress and inhibiting ER stress, autophagy, apoptosis and emphysema-related risk factor.     

In vivo protective effects of quercetin against sodium fluoride-induced oxidative stress in the hepatic tissue

The protective effects of quercetin against sodium fluoride induced oxidative stress were examined in rat’s liver. Rats were divided into five groups. The first group served as normal group that was treated with standard diet. The second group was intoxicated with sodium fluoride (600 ppm) through drinking water for 1 week. The third, fourth and fifth groups were treated with quercetin at a dose of 10 and 20 mg/kg and vitamin C (as the positive control) at a dose of 10 mg/kg intraperitoneally for 1 week before sodium fluoride intoxication, respectively. After 1 week, activities of superoxide dismutase and catalase, level of reduced glutathione and lipid peroxidation end product were determined in the homogenates of rat liver. The results of the present study suggested that quercetin protects rat liver from sodium fluoride induced oxidative stress, probably via its antioxidant activity.     

Cocoa-rich diet prevents azoxymethane-induced colonic preneoplastic lesions in rats by restraining oxidative stress and cell proliferation and inducing apoptosis

Cocoa is a rich source of bioactive compounds with potential chemopreventive ability but up to date its effectiveness in animal models of colon carcinogenesis has not been addressed. Herein, we investigated the in vivo effect of a cocoa-rich diet in the prevention of azoxymethane (AOM)-induced colon cancer and the mechanisms involved. Our results showed that cocoa feeding significantly reduced AOM-induced colonic aberrant crypt foci formation and crypt multiplicity. Oxidative imbalance in colon tissues seems to be prevented by cocoa as indicated by reduced oxidation markers levels and increased enzymatic and non-enzymatic endogenous defences. Cocoa-rich diet also exhibited antiproliferative effects by decreasing the levels of extracellular regulated kinases, protein kinase B and cyclin D1 together with pro-apoptotic effects evidenced by reduced Bcl-x(L) levels and increased Bax levels and caspase-3 activity. Our findings provide the first in vivo evidence that a cocoa-rich diet may inhibit the early stage of colon carcinogenesis probably by preventing oxidative stress and cell proliferation and by inducing apoptosis.     

Thymoquinone effects on DMH-induced erythrocyte oxidative stress and haematological alterations during colon cancer promotion in rats

The effect of thymoquinone (TQ), the abundant component of black cumin seed (Nigella sativa) oil extract, was evaluated on 1,2-dimethylhydrazine (DMH)-induced erythrocyte oxidative stress and haematological perturbations during colon cancer promotion in rats. Two TQ approaches, the pre- and post-treatment, were used. DMH promoted erythrocyte oxidative damage in rats by enhancing lipid peroxidation (30%) and decreasing antioxidant enzymes activities (20–35%). This was associated with the decline of erythrocyte count, haemoglobin concentration and haematocrit (20%) and the count increase of white blood cell (60%) and platelet (180%). TQ pre-treatment repaired DMH-induced erythrocyte oxidative stress, anaemia, leukocytosis, and thrombocytosis and allowed a 60% of tumour incidence decline. TQ post-treatment exerted a slight effect on erythrocyte oxidative stress and reduced colon cancer incidence by 30% only. Thus, TQ efficacy in preventing DMH-induced colon cancer promotion was related to its virtue antioxidant effect on erythrocyte oxidative stress.     

Protective effects of sweet orange (Citrus sinensis) peel and their bioactive compounds on oxidative stress

Protective effects of sweet orange (Citrus sinensis) peel and their bioactive compounds on oxidative stress were investigated. According to HPLC-DAD and HPLC-MS/MS analysis, hesperidin (HD), hesperetin (HT), nobiletin (NT), and tangeretin (TT) were present in water extracts of sweet orange peel (WESP). The cytotoxic effect in 0.2 mM t-BHP-induced HepG2 cells was inhibited by WESP and their bioactive compounds. The protective effect of WESP and their bioactive compounds in 0.2 mM t-BHP-induced HepG2 cells may be associated with positive regulation of GSH levels and antioxidant enzymes, decrease in ROS formation and TBARS generation, increase in the mitochondria membrane potential and Bcl-2/Bax ratio, as well as decrease in caspase-3 activation. Overall, WESP displayed a significant cytoprotective effect against oxidative stress, which may be most likely because of the phenolics-related bioactive compounds in WESP, leading to maintenance of the normal redox status of cells.     

Oxidative stress and DNA interactions are not involved in Enniatin‐ and Beauvericin‐mediated apoptosis induction

The fusariotoxins beauvericin (BEA) and the structurally related enniatins (ENN) are frequent contaminants of grain‐based food and feed. They exert potent cytotoxic activities based on apoptosis induction. Since it is known, that reactive oxygen species (ROS) and DNA damage lead to apoptotic cell death, this study aimed to clarify whether oxidative stress and DNA interactions are involved in ENN‐ and BEA‐induced cytotoxicity. Diverse cellular and molecular assays indicated that oxidative stress does not contribute to ENN‐ and BEA‐induced cytotoxicity. In contrast, both fusariotoxins were shown to exert moderate antioxidative activities. Moreover, only at high concentrations (>100 μM) both mycotoxins were found to intercalate substantially into dsDNA and to inhibit the catalytic activity of topoisomerase I and II. Furthermore, the potent cytotoxic activity of ENN and BEA was shown to be widely independent of cellular mismatch‐ and nucleotide excision repair pathways. Also the ataxia‐telangiectasia mutated (ATM) protein kinase, a well known DNA damage sensor, did not affect BEAs cytotoxic potential while in ENN‐induced cytotoxicity ATM had a detectable but not a major modulating influence. Together, our data suggest that ROS and DNA damage are not key factors in ENN‐ and BEA‐mediated cytotoxicity.     

Protective effect of selenium-polysaccharides from the mycelia of Coprinus comatus on alloxan-induced oxidative stress in mice

We investigated the effect of selenium-polysaccharide (SPS) isolated from selenium-enriched mycelia of Coprinus comatus on hypoglycaemic, hypolipidemic and antioxidant activities in diabetic mice. Compared with untreated diabetic mice, the administration of SPS for 20 days caused a significant decrease (p < 0.05) in blood glucose levels. Simultaneously, the alteration in lipid metabolism was partially attenuated as evidenced by decreased serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL) levels and by increased high-density lipoprotein cholesterol (HDL) concentration in diabetic mice (p < 0.05). In addition, the SPS caused a significant decrease (p < 0.05) in the level of malondialdehyde (MDA) and a significant increase (p < 0.05) in the activities of enzymic antioxidants and the levels of non-enzymic antioxidants in liver and kidney of diabetic mice. Furthermore, the effects of SPS was more potent than that of polysaccharide (PS) from mycelia of C. comatus at the same dose.     

甘蓝型油菜幼苗对光氧化胁迫的生理响应

研究油菜光氧化胁迫的生理响应对明确其抗性机理具有重要意义.以甘蓝型油菜中双11号为植物材料,对盆栽幼苗叶片进行光氧化剂甲基紫精（MV）处理,分析测定24h内叶片生理指标的变化.油菜叶片受光氧化胁迫后,抗氧化酶活性、超氧自由基合成速率和丙二醛（MDA）的含量有所提高,并随着处理时间的增加呈现先升高后降低的变化趋势,其中SOD（超氧化物歧化酶）活性在4h达到最大值485.16U· g-1FW,较对照高72.74％;POD（过氧化物酶）活性、CAT（过氧化氢酶）活性、超氧自由基合成速率以及MDA含量均在6h时达到最大值,分别比对照高69.48％,62.81％,98.65％和79.17％;同时,光氧化胁迫降低了可溶性蛋白和可溶性糖含量.回归分析表明短期光氧化胁迫影响油菜高光效的生理因素主要有SOD、POD、CAT和可溶性蛋白含量,其中最重要的效应因子是CAT.     

Hydroxytyrosyl acetate contributes to the protective effects against oxidative stress of virgin olive oil

The effects of virgin olive oil phenols, hydroxytyrosyl acetate (HTy-Ac) and hydroxytyrosol (HTy), on cell integrity and steady-state values of cellular redox status were assessed in HepG2 cells, as well as their potential protective effects against oxidative stress induced by tert-butyl hydroperoxide (t-BOOH). Direct treatment for 20 h with 0.5-10 μM HTy or HTy-Ac reduced ROS generation and increased glutathione peroxidase activity at the higher concentrations. Furthermore, after t-BOOH exposure, pretreatment with HTy-Ac and HTy for 2 or 20 h counteracted cell viability damage from 1 μM, counterbalanced reduced glutathione levels from 0.5 μM, protected against lipid peroxidation from 0.5 μM, decreased ROS generation from 1 μM as well as antioxidant enzyme activities from 1 μM. All these changes were statistically significant.HTy-Ac presents antioxidative stress protective effects at physiological concentrations similar to or even slightly higher than that of HTy, thus contributing to the protective role of virgin olive oil.     

枸杞子多糖通过改善氧化应激延缓疲劳作用的研究

本文研究枸杞子多糖（LBP）对小鼠疲劳的延缓作用及机制。将昆明种小鼠分为空白对照组（给予生理盐水）和高、中、低剂量枸杞子多糖处理组（剂量分别为100、50和25 mg/kg/day）,灌胃给药2周,通过跑步、疲劳转棒和负重游泳实验考察枸杞子多糖对小鼠的抗疲劳作用,并对运动后小鼠体内肝糖原、肌糖原以及血清、肝脏和肌肉中抗氧化指标进行检测。实验结果表明,LBP可以明显延长小鼠的运动时间,增加小鼠肝糖原和肌糖原含量,同时明显提高血清、肝脏和肌肉中超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性,显著降低肝脏和肌肉中丙二醛（MDA）和活性氧（ROS）含量及血清中MDA含量。LBP具有延缓疲劳的作用,其机制可能是减弱氧化应激和提高糖原含量。      

葡萄采后紫外线(UV)处理对白藜芦醇的诱导作用

采用不同剂量的紫外线(254nm)照射处理采后赤霞珠、玫瑰香葡萄,室温避光贮藏24小时后检测葡萄果皮中白藜芦醇的含量变化,以及葡萄可溶性固形物、总酸、总酚和花色素的含量,结果发现:1)在赤霞珠、玫瑰香葡萄果皮中检测到反式白藜芦醇,但未检测到顺式白藜芦醇;2)UV照射处理显著影响了葡萄的花色素、可溶性固形物含量;3)低剂量的UV照射对葡萄果皮中白藜芦醇具有诱导作用,明显提高了白藜芦醇含量,而高剂量UV处理后白藜芦醇含量呈降低趋势.     

Review of recent data on the metabolism,biological effects,and toxicity of resveratrol in humans

Several recently published clinical trials have extended our knowledge on the use of resveratrol (RVT) to treat several human pathological and metabolic disorders. Herein, we present insights into the metabolism, biological effects, and toxicity of RVT in humans. Recent data show that RVT exhibits antioxidant and anti‐inflammatory activities. It can also improve glucose and lipid metabolism, it acts on cardiovascular parameters, and can modify some pathways involved in carcinogenesis. However, these effects are mostly tiny and the results are sometimes controversial as they depend on the protocols (i.e. dose, form of administration, patients’ characteristics, adjuvant therapy, etc.). Toxicological data confirm that RVT is well tolerated. Any adverse effects (mainly concerning the abdomen), at doses of ≥0.5 g/day for long periods, remain moderate and reversible. Nevertheless, the efficacy and safety of RVT need to be further investigated.     

Impact of apoE genotype on oxidative stress, inflammation and disease risk

Although in developing countries an apolipoprotein E4 (apoE4) genotype may offer an evolutionary advantage, as it has been shown to offer protection against certain infectious disease, in Westernised societies it is associated with increased morbidity and mortality, and represents a significant risk factor for cardiovascular disease, late-onset Alzheimer's disease and other chronic disorders. ApoE is an important modulator of many stages of lipoprotein metabolism and traditionally the increased risk was attributed to higher lipid levels in E4 carriers. However, more recent evidence demonstrates the multifunctional nature of the apoE protein and the fact that the impact of genotype on disease risk may be in large part due to an impact on oxidative status or the immunomodulatory/anti-inflammatory properties of apoE. An increasing number of studies in cell lines, targeted replacement rodents and human volunteers indicate higher oxidative stress and a more pro-inflammatory state associated with the epsilon4 allele. The impact of genotype on the antioxidant and immunomodulatory/anti-inflammatory properties of apoE is the focus of the current review. Furthermore, current information on the impact of environment (diet, exercise, smoking status, alcohol) on apoE genotype-phenotype associations are discussed with a view to identifying particular lifestyle strategies that could be adapted to counteract the 'at-risk' E4 genotype.     

Molecular mechanisms of the chemopreventive effects of resveratrol and its analogs in carcinogenesis

Resveratrol (3,4',5-trihydroxy-trans-stilbene), a phytoalexin found in grape skins, peanuts, and red wine, has been reported to exhibit a wide range of biological and pharmacological properties. It has been speculated that dietary resveratrol could be an explanation for the so-called 'French paradox' as it may act as an antioxidant, promote nitric oxide production, inhibit platelet aggregation, and increase high-density lipoprotein cholesterol, and thereby serve as a cardioprotective agent. Recently, it has been demonstrated that resveratrol can function as a cancer chemopreventive agent, and there has been a great deal of experimental effort directed toward defining this effect. It has been shown that resveratrol and some of its analogs interfere with signal transduction pathways, modulate cell cycle-regulating proteins, and is a potent inducer of apoptosis in multiple carcinoma cell lines. This review summarizes the recent advances that have provided new insights into the molecular mechanisms underlying the promising properties of resveratrol.     

氧化应激参与丙烯酰胺致神经细胞凋亡及炎症反应的研究进展

丙烯酰胺（acrylamide,AA）是一种重要的工业原料,具有神经毒性、生殖毒性、遗传毒性及潜在致癌性。2002年,AA首次被报道作为美拉德反应的副产物之一,在油炸和焙烤等热加工高淀粉食品中广泛存在。氧化应激（oxidative stress, OS）是机体内氧化与抗氧化系统之间的平衡被破坏而造成的应激状态,可被多种环境因素激活,并与细胞凋亡及炎症反应的发生密切相关。大量研究发现,OS常伴随着AA诱导的中枢神经系统细胞凋亡及炎症反应发生,也是AA与神经退行性疾病相关性的重要连接纽带。本文就OS在AA诱导的凋亡及炎症反应中的作用进行综述,为AA神经毒性机制的深入研究及其毒性干预提供参考。