In vitro cytotoxicity to human cells in culture of some phenolics from olive oil

The neutral red in vitro cytotoxicity assay was used to evaluate the comparative responses of human cells isolated from tissues of the oral cavity to olive oil phenolics. The cell lines used included normal gingival fibroblasts, immortalized, nontumorigenic gingival epithelial cells, and carcinoma cells from the salivary gland. No differences in the relative sensitivities to the phenolics amongst the three cell types were noted. In general, for all cell types, the sequence of increasing cytotoxicity was: oleuropein aglycone>oleuropein glycoside, caffeic acid>o-coumaric acid>cinnamic acid>tyrosol, syringic acid, protocatechuic acid, vanillic acid. Cytotoxicity was noted only at phenolic concentrations far exceeding those attainable after habitual consumption, thus indicating that consumption of phenol-rich olive oil is safe.     

Protective role of flax lignans against lead acetate induced oxidative damage and hyperlipidemia in rats

The results showed that the lead concentration was higher than Cr, Ni and Cd in roadside soil samples. Also, the present study was conducted to investigate the protective role of flax lignans against the effects of lead acetate on oxidative stress, antioxidant enzymes and lipid profile. Animals were divided into three groups; the first group was used as control. While, groups 2, and 3 were orally treated with 200 mg/L lead acetate in drinking water and the combination of lead acetate (200 mg/L) plus flax lignans (30 mg/100 g BW), respectively. Rats were administered their respective doses daily for 3 weeks. Results showed that lead acetate increased TBARS, and decreased the activities of GST, SOD, GR and CAT, and the contents of glutathione in liver extracts, compared to control. The present data indicated that total lipids, cholesterol, triglycerides and LDL-c were significantly increased by lead acetate treatment, while HDL-c levels were decreased in the serum and liver extracts. Animals treated with flax lignans in combination with lead acetate alleviated its toxic effects in the tested parameters. Also, the morph metric analysis of the dorsal aorta revealed that, the histological alterations induced after lead acetate treatments were markedly reduced.     

Nitroderivatives of olive oil phenols protect HepG2 cells against oxidative stress

A series of nitroderivatives has been synthetized from natural and synthetic olive oil phenols to increase the assortment of compounds with a putative effect against Parkinson disease. Before considering the potential therapeutical and nutraceutical applications of the new compounds it was critical to assess any cytotoxic effects in the liver. The precursor compounds of the nitroderivatives have shown oxidative stress protective effects, therefore we also assessed if the new compounds counteracted oxidative stress. The antioxidant activity of nitrohydroxytyrosol (NO-HTy), nitrohydroxytyrosyl-acetate (NO-HTy-A) and ethyl-nitrohydroxytyrosyl-ether (NO-HTy-E) at 5–20 μM for 20 h, as well as the protective effects of the nitroderivatives after 20 h against oxidative stress induced by tert-butylhydroperoxide (t-BOOH), were assessed in HepG2 cells. Direct treatment with the three nitroderivatives decreased ROS generation compared to the control and NO-HTy at 20 μM also increased glutathione peroxidase (GPx) activity (p < 0.001). Pretreatment with the three nitroderivatives at 5–20 μM counteracted t-BOOH cell damage by decreasing ROS generation (p < 0.001) and malondialdehyde (MDA) levels (p < 0.001), increasing reduced glutathione (p < 0.001) and disminishing GPx (p < 0.05) activity. NO-HTy, NO-HTy-A and NO-HTy-E decreased glutathione reductase activity (p < 0.05). Conclusion: the nitroderivatives do not present cytotoxic effects in the liver and in addition may protect against the oxidative stress involved in degenerative diseases.     

Protective effect of extract of Crataegus pinnatifida pollen on DNA damage response to oxidative stress

The protective effect of extract of Crataegus pinnatifida (Rosaceae) pollen (ECPP) on the DNA damage response to oxidative stress was investigated and assessed with an alkaline single-cell gel electrophoresis (SCGE) assay and pBR322 plasmid DNA breaks in site-specific and non-site-specific systems. Total phenolic content, total flavonoid content, individual phenolic compounds, antioxidant activities (1,1-diphenyl-2-picrylhydrazyl (DPPH), radical scavenging activity, FRAP, and chelating activity) were also determined. The results showed that ECPP possessed a strong ability to protect DNA from being damaged by hydroxyl radicals in both the site-specific system and the non-site-specific system. It also exhibited a cytoprotection effect in mouse lymphocytes against H₂O₂-induced DNA damage. These protective effects may be related to its high total phenolic content (17.65 ± 0.97 mg GAE/g), total flavonoid content (8.04 ± 0.97 mg rutin/g), strong free radical scavenging activity and considerable ferrous ion chelating ability (14.48 ± 0.21 mg Na₂EDTA/g).     

Protective effect of olive oil and colocynth oil against cadmium-induced oxidative stress in the liver of Wistar rats

Cadmium (Cd) is one of the most common heavy metal pollutants. It is accumulated particularly in liver and kidney. The present study examined the possible protective effect of olive oil and colocynth oil consumption against Cd-induced damage on plasma lipids and stress biochemical parameters of rats. Male albino Wistar rats were randomly divided into 6 groups of 5 animals each and treated orally with Cd (50 mg/l), olive oil and colocynth oil (4%) alone or in combination with cadmium for 8 weeks. It was shown that Cd exposure induced significant increases in the activities of serum alanine aminotransferase, aspartate aminotransferase, lipid peroxidation levels (MDA) and protein carbonyl contents in exposed groups of rats compared to control group while the antioxidant enzymes, reduced glutathione and vitamins (C, A and E) were significantly decreased. Co-treatment with olive oil or colocynth oil significantly improved the oxidative damage induced by Cd. The antioxidant potential in plasma and liver were markedly restored with a significant decline in MDA levels and activity of transaminases.In conclusion, these results suggest that olive oil or colocynth oil consumption could protect the rat liver against Cd-induced injury by increasing the activities of antioxidant enzymes and reducing oxidative stress.     

锌金属硫蛋白对镉中毒小鼠肾损伤的修复作用

目的：研究锌金属硫蛋白（Zn-MT）对镉中毒小鼠肾损伤的修复作用。方法：以昆明种小鼠作为研究对象，染镉14d建立亚急性镉中毒模型，随后经口给予Zn-MT。收集24h尿液，测定尿N－乙酰－β－D－氨基葡萄糖苷酶（NAG酶）活性作为衡量肾脏损伤程度的一项指标，同时电镜观察肾组织形态学变化；测定并分析肾组织上清液中脂质过氧化代谢产物一丙二醛（MDA）水平、超氧化物歧化酶（SOD）、谷胱甘肽过氧化酶（GSH－Px)活性。结果：Zn-MT可明显降低肾组织中MDA水平，使肾组织中SOD、GSH－Px活力有一定程度的恢复，此时尿NAG酶活性降低表明肾损伤程度减轻，且上述作用呈明显的剂量－反应关系；电镜下观察到给予Zn-MT后肾组织形态学病变有所减轻。结论：Zn-MT可对镉中毒小鼠肾组织脂质过氧化损伤起到一定的修复作用。     

Bioactive effects of olive oil phenolic compounds in humans: reduction of heart disease factors and oxidative damage

Oxidative stress is defined as an imbalance between the oxidant and antioxidant systems of the body, in favour of the oxidants. Oxidative stress produced by free radicals has been linked to the development of several diseases such as cardiovascular, cancer, and neurodegenerative diseases. Olive oil is the main source of fat of the Mediterranean diet which has been shown to be effective against oxidative stress associated diseases and also with the ageing. Besides its richness in monounsaturated fatty acid, the oleic acid, olive oil contains minor components with antioxidant properties. Here, we update the state of the art, and degree of evidence, of the body of knowledge concerning the protective role on lipids and lipid oxidative damage in humans of the olive oil phenolic compounds.     

Phenols of virgin olive oil protects nuclear DNA against oxidative damage in HeLa cells

Oxidative DNA damage is an inescapable consequence for cells constantly exposed to oxidative stress derived from normal metabolic processes and from environmental factors. Phenolic compounds, which have strong antioxidant activity, prevent DNA damage by protecting the cells against harmful effects of oxidative stress. In this study, the effect of virgin olive oil phenolic extract (OOPE) was investigated on H₂O₂-induced mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) damage in HeLa cells. DNA damage was assessed in mitochondria and two nuclear regions by using quantitative PCR (QPCR) assay. The cells were pre-treated with non-cytotoxic doses of OOPE for 4 h, and DNA damage was determined. OOPE alone does not change the steady-state level of DNA damage. The oxidative stress generated with 750 μM H₂O₂ caused two times greater damages in mtDNA compared to nDNA, which included the nonexpressed β-globin region (1.507 ± 0.110 lesions/10 kb) and the expressed APEX1 gene (1.623 ± 0.243 lesions/10 kb) with respect to the control region. When cells were preincubated with OOPE for 4 h, nDNA damage under stress condition was completely inhibited; however, mtDNA damage was not affected by this procedure. These results suggest that OOPE has a protective effect against nDNA damage in HeLa cells.     

Protective role of selenium against renal toxicity induced by cadmium in rats

Cadmium is an environmental toxic metal implicated in human diseases. The mechanism of its toxicity is not fully understood. Therefore, the role of cadmium in renal toxicity, and the protective role of selenium against this toxicity were investigated. Forty-five male rats were used through out the study and divided into three groups of 15. The first group received saline solution daily for 10 days. The second group, received cadmium chloride (CdCl₂) (2 mg/kg body weight) intraperitoneally daily for a period of 10 days. The third group, received sodium selenite (1 mg/kg body weight, twice a day) and CdCl₂ (once a day) for a period of 10 days. The results showed that cadmium treatment increased renal lipid peroxidation (measured as malondialdehyde, MDA) which was associated with a significant decrease in the antioxidant systems such as reduced glutathione levels and the activities of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR). On the other hand, pretreatment of rats with selenium and cadmium led to a significant decrease in MDA concentration, and increased levels of GSH and the activities of GPx and TrxR when compared with those of cadmium-treated group. The total levels of phospholipid, triglyceride, and cholesterolester classes were decreased, while free fatty acids levels were markedly increased after cadmium treatment. In addition, the total levels of both mono- and poly-unsaturated fatty acids of different lipid classes were significantly decreased, while the total saturated fatty acids was significantly increased by cadmium treatment. Pretreatment of rats with selenium, was found to protect kidney tissues of rats against the biochemical changes resulting from cadmium administration. These results suggest that cadmium causes renal toxicity by inducing lipid peroxidation, decreasing antioxidant systems, and also by altering lipid metabolism. In addition, selenium treatment could protect the kidney tissues against the toxicity of cadmium since it reduced MDA levels and increased the activities of antioxidant enzymes in these tissues. These results could be important for the further understanding of the complex mechanisms of cadmium toxicity in kidney tissues and in the development of better treatments for people and/or animals exposed to the heavy metal.     

Ginkgo biloba extract protects against mercury(II)-induced oxidative tissue damage in rats.

Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5mg/kg mercuric chloride (HgCl(2); Hg group) either saline or EGb (150mg/kg) was administered for 5days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl(2) induced oxidative damage caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects.     

Protective effects of sesame oil on 4-NQO-induced oxidative DNA damage and lipid peroxidation in rats

Sesame oil could be considered as a potent antioxidant and dietary supplement. It possesses antimutagenic, anti-inflammatory and anti-cardiac toxicity. In the view of available findings, the current study focused on determining the protective effects of sesame oil on 4-Nitroquinoline-1-oxide (4-NQO) -induced oxidative DNA damage and lipid peroxidation (LPO) in rats. Seven groups of Wistar albino rats each with 6 either sex were used. Groups were given vehicle control and sesame oil alone orally and 4-NQO (30?mg/kg) by intraperitoneal injection. Following the four dose levels (1, 2, 4, and 8?ml/kg orally), sesame oil plus 4-NQO were also tested. After 24 hours of 4-NQO injection, blood samples were drawn by venipuncture. DNA damage (8-hydroxy-2-deoxy guanosine; 8-OHdG) and LPO were estimated. LPO from the 4-NQO-treated group was 2.5-fold higher than that of the control LPO. Pretreatment with sesame oil reduced this by 16–61%. 8-OHdG DNA damage from 4-NQO was found to be 3-fold higher than that of controls. Pretreatment with sesame oil effectively protected against DNA damage in a dose-dependent fashion. This study indicates that the antioxidant, sesame oil, effectively protected DNA damage and LPO induced by 4-NQO.     

Characterization and quantification of phenolic compounds of extra-virgin olive oils with anticancer properties by a rapid and resolutive LC-ESI-TOF MS method

The characterization and quantification of extra-virgin olive oil (EVOO) phenolic compounds by a rapid resolution liquid chromatography (RRLC) method coupled to diode-array and time of flight mass spectrometry (TOF) detection systems was developed. The RRLC method transferred from a conventional HPLC one achieved better performance with shorter analysis times. The phenolic compounds were separated with a C18 column (150 mm × 4.6 mm, 1.8 μm) using water with 0.5% acetic acid and acetonitrile as mobile phases. Good peak resolution was obtained and 19 different phenols were identified in less than 20 min providing a new level of information about the samples in shorter time. The applicability of this analytical approach was confirmed by the successful analysis of three different EVOO varieties (Picual, Hojiblanca, and Arbequina) obtained from different trademarks. Besides identification of the most important phenolic compounds and their quantification in three different ways (RRLC-UV, RRLC-MS and a new approach using the total polyphenol content obtained with Folin Ciocalteau, the relative areas and the response factors), we also described the occurrence of correlations between the phenolic composition of EVOO-derived crude phenolic extracts and their anti-proliferative abilities toward human breast cancer-derived cell lines. When compared with lignans-rich EVOO varieties, secoiridoids-rich EVOO had a significantly strong ability to alter cell viability in four different types of human breast carcinoma cells.     

Protective effect of dietary flaxseed oil on arsenic-induced nephrotoxicity and oxidative damage in rat kidney

Arsenic, a naturally occurring metalloid, is capable of causing acute renal failure as well as chronic renal insufficiency. Arsenic is known to exert its toxicity through oxidative stress by generating reactive oxygen species (ROS). Flaxseed, richest plant based dietary source of ω-3 polyunsaturated fatty acids (PUFAs) and lignans have shown numerous health benefits. Present study investigates the protective effect of flaxseed oil (FXO) on sodium arsenate (NaAs) induced renal damage. Rats prefed with experimental diets (Normal/FXO diet) for 14 days, were administered NaAs (20 mg/kg body weight i.p.) once daily for 4 days while still on the experimental diets. NaAs nephrotoxicity was characterized by increased serum creatinine and blood urea nitrogen. Administration of NaAs led to a significant decline in the specific activities of brush border membrane (BBM) enzymes both in kidney tissue homogenates and in the isolated membrane vesicles. Lipid peroxidation and total sulfhydryl groups were altered upon NaAs treatment, indicating the generation of oxidative stress. NaAs also decreased the activities of metabolic enzymes and antioxidant defence system. Histopathological studies supported the biochemical findings showing extensive damage to the kidney by NaAs. In contrast, dietary supplementation of FXO prior to and alongwith NaAs treatment significantly attenuated the NaAs-induced changes.     

Protective effect of N-acetyl-L-cysteine against maneb induced oxidative and apoptotic injury in Chinese hamster V79 cells

The role of antioxidant N-acetyl-L-cysteine (NAC) in protection against cellular changes triggered by maneb during in vitro exposure was investigated in cultured Chinese hamster V79 cells. We observed high apoptotic activity and high oxidative stress induced by exposure to maneb evidenced by a statistically significant increase in lipid peroxidation (measured as TBARS - thiobarbituric acid reactive substances) as well as a decrease of glutathione (GSH) and glutathione disulfide (GSSG) ratio (GSH/GSSG). Maneb did not exhibit any effect on protein oxidation (measured by protein carbonyls content). NAC suppressed cellular changes induced by maneb in V79 cells. NAC pre-treatment prevented TBARS production and significantly decreased the number of apoptotic cells. However, protective effect of NAC on GSH and GSSG levels has been shown only in cells exposed to lower concentration of maneb (100 μM).     

The protective effect of fish oil against cisplatin induced eye damage in rats

Ocular toxicity induced by anticancer chemotherapy is not uncommon, but underestimated and under-reported. Visual changes have been attributed to a number of chemotherapeutic agents in humans. Cisplatin (CP), a heavy metal compound, is used in the treatment of many types of tumours. CP is known to produce nonspecific blurred vision, papilledema, and optic neuritis for high doses as well as cumulative dose regimens. The aim of this study was to investigate the possible beneficial effects of fish oil (FO) on eye tissue oxidative status and histological alterations against CP-induced in the rats. The animals were randomly divided into the following four groups: the control, CP, FO, and CP?+?FO groups. CP was intraperitoneally administered at the dose of 7?mg/kg and FO was orally given at 1 softgel per day for 14 days. The eye injury was assessed by biochemical and histological examinations. The levels of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were evaluated in the eye tissue. TBARS levels were significantly higher, the activities of the antioxidant enzyme and GSH levels were significantly lower in the CP group than in the control group. The histopathological evaluation also confirmed the foregoing findings. On the other hand, treatment of FO ameliorated the biochemical and histological alterations caused by CP. The results showed that treatment with FO may protect against the negative ocular effects of CP.     

Efficacy of royal jelly against the oxidative stress of fumonisin in rats.

Fumonisins (FB) are mycotoxins produced by Fusarium verticillioides, frequently associated with corn. It produces toxicity, including teratogenicity, equine leukoencephalomalacia, porcine pulmonary edema, hepatic or renal damage in most animal species and perturb sphingolipid metabolism. The aim of the present study was to evaluate the protective effects of royal jelly (RJ) against FB toxicity. Sixty male Sprague-Dawley rats were divided into six treatment groups including the control group; group fed FB-contaminated diet (200mg/kg diet) and the groups treated orally with RJ (100 or 150mg/kg body weight) with or without FB for 3 weeks. FB alone decreased body weight gain, feed intake, GPX and SOD. Whereas it increased in ALT, AST, triglycerides, cholesterol, HDL, LDL, createnine and uric acid levels. Animals received FB showed severe histological and histochemical changes in liver and kidney tissues. Cotreatment with FB plus RJ resulted in a significant improvement in all the tested parameters and the histological and histochemical pictures of the liver and kidney. These improvements were pronounced in animals fed FB-contaminated diet plus the high dose of RJ. It could be concluded that RJ have a protective effects against FB toxicity and this protection was dose dependent.     

Protective effect of icariin on DNA against radical-induced oxidative damage

Icariin (2-(4'-methoxylphenyl)-3-rhamnosido-5-hydroxyl-7-glucosido-8-(3'-methyl-2-butylenyl)-4-chromanone) is a flavonoid with a rhamnose as ligand. It is the major component in Herba epimedii, widely used for the treatment of atherosclerosis and neuropathy in Chinese traditional medicine, and its antioxidative property has attracted much scientific interest. The major objective of this work is to determine the antioxidative effect of icariin against oxidative DNA damage induced by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH). The oxidative damage of DNA was followed by measuring the formation of carbonyl compounds that can react with thiobarbituric acid (TBA) to form thiobarbituric acid reactive substance (TBARS). We found that icariin protects DNA against AAPH-induced oxidative damage in a concentration-dependent manner, although it does not affect the rate of AAPH-induced DNA damage. This result indicates that icariin is a concentration-dependent chemopreventor in protecting DNA against radical-induced damage.     

Protective effect of quince (Cydonia oblonga Miller) fruit against oxidative hemolysis of human erythrocytes

The aim of this study was to determine the phenolic content and evaluate the antioxidant activity of quince (Cydonia oblonga) fruit. For this purpose, fruits were separated into pulps, peels and seeds and methanolic extracts were prepared. The phenolic profiles were determined by HPLC/UV and antioxidant properties were studied for their ability to quench the stable free radical 2,2′-diphenyl-1-picrylhydrazyl (DPPH) and to inhibit the 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced oxidative hemolysis of human erythrocytes.     

GC-MS法分析橄榄油与沙棘油中的脂肪酸

目的 采用GC-MS分析沙棘油和橄榄油中的脂肪酸,并比较两种植物油中主要脂肪酸的分布.方法 采用DB-23色谱柱(60 m×0.25 mm,0.15 μm),进样器和FID检测器温度为250 ℃,进样量1μL,分流比10:1,程序升温:起始温度为50℃、保持1 min,以20℃·min-1升至175℃后,以3℃·min-升至190℃、保持3 min,再以5℃·min-1升至230℃、保持2 min.结果 橄榄油和沙棘油中分别含有13和16种脂肪酸,其中,不饱和脂肪酸的含量分别为85.04％、80.09％,饱和脂肪酸的含量分别为14.96％、19.91％.结论 橄榄油中不饱和脂肪酸的总含量更高,而沙棘油中不饱和脂肪酸的种类更多,且多不饱和脂肪酸的含量更高.