共查询到20条相似文献,搜索用时 8 毫秒
1.
Aflatoxin B 1 (AFB 1)-mediated hepatic damage is involved in production of AFB 1-8,9-epoxide-bound DNA adducts and this is also affected by a pro-oxidant potential of the toxin. In this study we investigated the effects of quercetin on AFB 1-treated HepG2 cells. We also examined the biochemical mechanisms associated with the effects of quercetin on AFB 1-mediated liver damage in mice. Our results revealed that quercetin and isorhamnetin inhibit production of reactive oxygen species and cytotoxicity, and block the decrease of reduced glutathione (GSH) levels in AFB 1-treated HepG2 cells. Isorhamnetin have inhibitory ability on lipid peroxidation stronger than quercetin in the cells. Oral supplementation with quercetin decreased serum lactate dehydrogenase levels, increased hepatic GSH levels and superoxide dismutase activity, and reduced lipid peroxidation in both the liver and kidney in AFB 1-treated mice. However, quercetin did not show a significant reduction on serum levels of alkaline phosphate, alanine aminotransferase and aspartate aminotransferase that were increased in AFB 1-treated mice. HPLC analysis revealed that quercetin in plasma is mainly present as glucoronides and/or sulfates of quercetin. Collectively, it is suggested that quercetin does not directly protect against AFB 1-mediated liver damage in vivo, but exerts a partial role in promoting antioxidative defense systems and inhibiting lipid peroxidation. 相似文献
3.
The current study was conducted to evaluate the chemoprevention effects of ginseng extract (GE) against pre-cancerous lesions in female Sprague–Dawley rats treated with aflatoxin B 1 (AFB 1) and fumonisin (FB). Six experimental groups treated for 12 weeks and included: the control group; the GE alone-treated group (150 mg/kg b.w); the group treated orally with AFB 1 (17 μg/kg b.w) during the first 2 weeks and fed FB-contaminated diet (250 mg/kg diet) during the 6th to 8th weeks; the group treated with GE during the mycotoxin protocol and continued till week 10; the group treated with GE 2 weeks before AFB 1 administration and continued till the end of FB treatment and the group treated with GE for 4 weeks after the toxin protocol stopped. The sequential mycotoxins treatment induced significant changes in serum biochemical parameters accompanied by severe histological and histochemical changes of the liver tissue. Treatment with GE during, before or after the treatment with the mycotoxins improved all biochemical parameters and histological picture of the liver. Moreover, treatment with GE after the administration of the mycotoxins was found to be more effective. It could be concluded that GE has a protective effects as pre-cancerous lesions and therapeutic effects as well. 相似文献
4.
The potential of Saccharomyces cerevisiae (Sc) was evaluated for reducing the micronucleated normochromatic erythrocytes (MNNE) rate in mice fed AFB 1 contaminated corn. The study included two groups fed AFB 1 contaminated corn (0.4 and 0.8 mg/kg), a control fed uncontaminated corn, another group fed uncontaminated corn and 0.3% of Sc (1 × 10 8 live cells/g), and two groups fed AFB 1 contaminated corn (0.4 and 0.8 mg/kg) plus 0.3% Sc. Weight and MNNE were determined weekly for six weeks. Subsequently, the same determinations were made for another three-week period, but in mice receiving only a normal diet, without AFB 1 and Sc. Results in the first period revealed the following: control and Sc fed mice had similar constant weight increase, and low MNNE rate; mice fed only AFB 1 showed weight decrease and significant MNNE increase; finally, Sc improved weight gain and reduced MNNE produced by AFB 1. In the second period, results exhibited a tendency similar to that of the previous phase in the control and Sc fed mice; the weight and MNNE values improved in the other groups. We also determined the capacity of Sc for adsorbing and modifying the mycotoxin structure. The mixture was filtered to obtain two phases, and AFB 1 content was measured. Sc revealed a potent adsorbent capacity; however, chromatographic determination suggested no structural modification. 相似文献
5.
目的:建立HPLC法同时测定燕泰胶囊中维生素B1和维生素B6的含量.方法:C18柱,1%的冰醋酸为流动相,检测波长为276nm.结果:在本法条件下维生素B1与维生素B6均能与其它组分达到基线分离;维生素B1在62.22~165.92μg/ml范围内峰面积与浓度具有良好线性关系,维生素B6在65.34~174.24μg/ml范围内峰面积与浓度具有良好线性关系;维生素B1的回收率为99.61%,RSD%为1.53%(n=6),维生素B6的回收率为102.5%,RSD%为1.41%(n=6).结论:方法专属性强、精密度好、操作简便,适用于燕泰胶囊中所含组分维生素B1与维生素B6的含量控制. 相似文献
6.
The effect of esterified glucomannan on aflatoxin B 1 toxicity in ducklings was studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA) in hepatic cells on formalin-fixed paraffin-embedded liver samples. Cherry Valley ducklings were divided into five groups, 20 birds in each. One of the groups was fed with conventional feed, and the other groups were fed with diet containing 100 ppb aflatoxin B 1, that containing 0.05% esterified glucomannan, or that containing 100 ppb aflatoxin B 1 supplemented with 0.05 or 0.1% esterified glucomannan, from five days of age for one month, and subsequently all the groups were fed with conventional feed for 20 days. Four birds of each group were sacrificed on the 30th, 35th, 40th, 45th and 50th day of feeding, and PCNA on the liver tissue sections was quantitatively analyzed by immunohistochemical staining. The percentage of PCNA-positive hepatocytes was significantly higher in the group given diet containing aflatoxin B 1 than in the other groups, which were not significantly different from each other. The results demonstrate that supplementation of feed with esterified glucomannan is effective in reduction of aflatoxin B 1-induced hepatic injury in ducklings. 相似文献
7.
The effects of repeated intraperitoneal administration of aflatoxin B 1 on the peripheral and central nervous systems of rats were investigated. Biochemical markers of neurotoxicity were monitored in nervous tissues following aflatoxin B 1 dosage and after the cessation of aflatoxin B 1 administration. Aflatoxin B 1 increased the activities of β-glucoronidase and β-galactosidase in the central and peripheral nervous systems. Repeated exposure of rats to aflatoxin B 1 also activated Na + K +-ATPase and inhibited Mg 2+-ATPase. Nervous tissue levels of DNA and total protein increased while the concentrations of RNA and phospholipid were depressed by aflatoxin B 1. The alterations in these parameters were specific for each of the tissues examined during the recovery of the rats. The findings indicate that the repeated administration of aflatoxin B 1 to rats results in degeneration in the central and peripheral nervous systems that may be related to the overt toxicity observed following aflatoxin administration. 相似文献
8.
Aflatoxin B 1 (AFB 1) is one of the most active hepatotoxic and hepatocarcinogenic compounds known for rats. In order to evaluate the mechanism of action of the toxin on the liver, the effects of aflatoxin B 1 on the enzymes involved in its transformation, such as the monooxygenase-cytochromes P-450-dependent and conjugating enzymes, were studied. At the same time, liver damage was determined by measuring the activities of plasma γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) as well as the concentration of bilirubin.Male Sprague-Dawley rats received a single ip dose of AFB 1 (1 or 3 mg/kg). The effects of the toxic compound on the activity of drug-metabolizing enzymes were followed 20 days after this single exposure. Mortality (18%) within 7 days following administration was produced only by the higher dose. The same dose also significantly decreased the total level of hepatic proteins and impaired the activity of aminopyrine N-demethylase. AFB 1 lowered the content of cytochromes P-450 by 32 and 69% at the 1 and 3 mg/kg dose levels, respectively. Epoxide hydrase activity was increased by 121 and 170% at 1 and 3 mg/kg, respectively, whereas UDP-glucuronyltransferase activity was increased (44%) at 1 mg/kg, but also decreased at the same extent for the higher dose. The activity of GSH S-epoxide transferase was decreased by a maximum of 53% by 3 mg/kg AFB 1. Results obtained by the 3rd day following the administration of 3 mg/kg AFB 1 showed that blood levels of all the factors studied in this experiment were increased above control values, while at lower dose of AFB 1 (1 mg/kg), only the activities of AST and ALT were significantly increased. The activities of these enzymes were 27 to 42 times greater in rats treated with 3 mg/kg AFB 1 than in rats given 1 mg/kg AFB 1. Most of the biological features studied tended to return to control values between the 9th and 20th day after AFB 1 treatment. This study makes it possible to compare changes in tissue levels of drug-metabolizing enzymes at two doses of AFB 1. It can also be used to demonstrate any time lag or differing behavior of the serum enzymes, notably the sensibility of transaminases. 相似文献
9.
Aflatoxin M 1 (AFM 1) is an important mycotoxin frequently found in milk and dairy products. AFM 1 is a major metabolic product of Aflatoxin B 1 and is usually excreted in the milk and urine of dairy cattle that have consumed aflatoxin-contaminated feed. The aim of this study was to determine the AFM1 concentration in curd and whey of Iranian white cheese. The cheese milk samples were artificially contaminated with AFM1 in six levels (0.25, 0.5, 0.75, 1, 1.25, and 1.75 μg L−1). Cheese was produced according to Iranian traditional recipe. AFM1 distribution between curd, whey and cheese was determined by high performance liquid chromatography (HPLC) using immunoaffinity column clean up and florescence detection. AFM1 was recovered in whey, curd and cheese in the concentrations of 0.43, 1.47 and 1.57 μg L−1,respectively. The level of Aflatoxin M1 in curd and cheese obtained 3.12- and 3.65-fold more than that in whey that shows the affinity of Aflatoxin M1 to the protein fraction of milk. 相似文献
10.
The extreme sensitivity of turkeys to aflatoxin B 1 (AFB 1) is associated with efficient hepatic cytochrome P-450 (P450)-mediated bioactivation, and deficient glutathione S-transferase (GST) mediated detoxification. Butylated hydroxytoluene (BHT) protects against AFB 1 toxicity in turkeys through mechanisms that include competitive inhibition of P450-mediated AFB 1 bioactivation. To test whether dietary BHT alters hepatic AFB 1–DNA adduct formation, excretion, and bioavailability of AFB 1 in vivo, turkeys were given diets with BHT (4000 ppm) for 10 days, given a single oral dose of [ 3H]-AFB 1 (0.05 μg/g; 0.02 μCi/g), then sampled at intervals up to 24 h. Radiolabel in serum, red blood cells, liver, and breast meat was frequently lower in BHT-treated compared to control. Hepatic AFB 1–DNA adducts in BHT-treated turkeys were significantly lower at 12 and 24 h. BHT-fed birds had significant higher bile efflux, though biliary radiolabel excretion was not different from control. The amount of aflatoxin M 1 (AFM 1) excreted in the bile was lower than in control, but BHT had no effect on the biliary excretion of AFB 1, aflatoxin Q 1 or glucuronide and sulfate conjugates. Thus, the chemopreventive properties of BHT may also occur through a reduction in AFB 1 bioavailability in addition to inhibition of bioactivation. 相似文献
11.
Mycotoxins are secondary metabolites having a high cytotoxic potential. They are produced by molds and released in food and feed. To date, the mechanisms underlying the mycotoxin-induced cytotoxicity have not been fully clarified. The induction of oxidative stress, as a possible mechanism, has been postulated. This in vitro study was focused on the effect of two widely occurring mycotoxins, aflatoxin B 1 (AFB 1) and fumonisin B 1 (FB 1), on the oxidative status of bovine peripheral blood mononuclear cells (PBMC) incubated for 2 and 7 days at different levels of AFB 1 (0, 5 and 20 μg/ml) and FB 1 (0, 35 and 70 μg/ml). Reactive oxygen metabolites (ROM), intracellular thiols (SH), malondialdehyde (MDA) and gene expression of cytoplasmic superoxide dismutase (SOD) and glutathione peroxidase (GSHPX-1) were measured on PBMC after incubation. The highest concentration of AFB 1 and all concentrations of FB 1 caused an increase ( p < 0.05) of intracellular ROM without any time dependent effect. Intracellular SH decreased with 20 μgAFB 1/ml ( p < 0.05) and the effect was particularly marked after 7 days of exposure. Intracellular SH were not affected by FB 1 even though a lower ( p < 0.05) SH level after 2 days exposure than after 7 days was observed. MDA increased ( p < 0.05) in AFB 1 or FB 1 treated PBMC. The exposure to FB 1 for 7 days increased MDA ( p < 0.05) only in cells treated with 70 μg/ml. Exposure of PBMC to AFB 1 reduced SOD mRNA while FB 1 decreased both SOD and GSHPX-1 mRNA abundance. These results demonstrate that, even though by different mechanisms, AFB 1 and FB 1 may induce cytotoxicity through an impairment of the oxidative status of PBMC. 相似文献
12.
A subacute dose of aflatoxin B 1 (3 mg/kg body weight) increases liver putrescine levels within 1 hr after administration, with high levels persisting over 24 hr. Higher doses of the carcinogen elicited larger increases in liver polyamine levels. A marked elevation of putrescine, spermidine and spermine were noted in aflatoxin B 1-induced preneoplastic liver. Pretreatment of rats with phenobarbital prior to aflatoxin B 1 administration resulted in no synergistic or additive effects. 相似文献
13.
The effects of chronic intra-peritoneal administration of aflatoxin B 1 on the activity of alkaline and acid phosphatases; glutamic oxaloacetate (GOT) and pyruvaate transaminases (GPT); 5′-nucleotidase and lactic dehydrogenase enzymes were monitored in the testis and kidney opf adult albino rats. Results showed that aflatoxin B 1 depressed the activity of alkaline phosphatase in both tissues, but increased that of acid phosphatase in only the testis. While GOT and 5′-nucleotidase were inhibited, GPT and lactic dehydrogenase activity was enhanced by this carcinogen. These responses were similar for the testis and kidney.The above findings coupled with the microscopical observation of the testis tissue seem to indicate that the essential lesion of this toxin on the testis may be a modification of the enzymes of germinal cells resulting from a gradual depletion of the latter. Furthermore, the results appear to show that by and large, aflatoxin B 1 exerts only slightly different effects on the testis and kidney at the enzyme level. 相似文献
14.
Aflatoxin B 1 (AFB 1) is biotransformed in vivo into an epoxide metabolite that forms DNA adducts that may induce cancer if not repaired. p53 is a tumor suppressor gene implicated in the regulation of global nucleotide excision repair (NER). Male heterozygous p53 knockout (B6.129- Trp53tm1BrdN5, Taconic) and wild-type mice were exposed to 0, 0.2 or 1.0 ppm AFB 1 for 26 weeks. NER activity was assessed with an in vitro assay, using AFB 1-epoxide adducted plasmid DNA as a substrate. For wild-type mice, repair of AFB 1–N7-Gua adducts was 124% and 96% greater in lung extracts from mice exposed to 0.2 ppm and 1.0 ppm AFB 1 respectively, and 224% greater in liver extracts from mice exposed to 0.2 ppm AFB 1 (p < 0.05). In heterozygous p53 knockout mice, repair of AFB 1–N7-Gua was only 45% greater in lung extracts from mice exposed to 0.2 ppm AFB 1 (p < 0.05), and no effect was observed in lung extracts from mice treated with 1.0 ppm AFB 1 or in liver extracts from mice treated with either AFB 1 concentration. p53 genotype did not affect basal levels of repair. AFB 1 exposure did not alter repair of AFB 1-derived formamidopyrimidine adducts in lung or liver extracts of either mouse genotype nor did it affect XPA or XPB protein levels. In summary, chronic exposure to AFB 1 increased NER activity in wild-type mice, and this response was diminished in heterozygous p53 knockout mice, indicating that loss of one allele of p53 limits the ability of NER to be up-regulated in response to DNA damage. 相似文献
15.
Aflatoxin B 1 (AFB 1) is a severe threat to human and animal health. The aflatoxin B 1 aldehyde reductase (AFAR) family specifically catalyzes AFB 1-dialdehyde, a toxic metabolic intermediate of AFB 1, producing a nontoxic dialcohol. Although several AFARs have been found and characterized, the binding specificity of the family for AFB 1-dialdehyde remains unclear. Herein, according to the published sequence, we cloned a porcine AFAR gene. Recombinant porcine AFAR was expressed and purified from Escherichia coli as hexa-histidine tagged fusion protein. Using the cloned porcine AFAR as a model, site-directed mutagenesis combined with high performance liquid chromatography studies revealed that the substitution of Trp266 with Ala resulted in almost complete loss of catalytic activity for AFB 1-dialdehyde. Interestingly, the substitution of Met86 with Ala exhibited an obviously increased activity to the dialdehyde. Based on these results and by using molecular docking simulations, this work provides a structural explanation for why the AFAR family exhibits high specificity for AFB 1-dialdehyde. The Trp266 residue in porcine AFAR plays a critical role in stabilizing the binding of AFB 1-dialdehyde in the active pocket through the hydrophobic interaction of the side-chain indole ring of Trp266 with the fused coumarin rings of the dialdehyde molecule. The enhanced activity of M86A may be attributed to the formed π–π stacking interaction between Trp266 and the dialdehyde. In addition, other hydrophobic residues ( e.g. Phe and Trp) around the dialdehyde molecule also stabilize the substrate binding. The findings may contribute to understanding the substrate specificity of the AFAR family for AFB 1-dialdehyde. 相似文献
16.
Sprague-Dawley rats were given either ten daily doses of aflatoxin B 1 (AFB 1) or the solvent tricaprylin intragastrically over a 2-wk period and were fed diets containing either 1.6 or 20% corn oil throughout the study. Hepatic lipid composition was analysed in groups of five rats both 3 and 13 wk after the start of treatment, in order to determine short-term and longer-term alterations. Total lipid and cholesterols (total, free and esterified) increased on the high-fat diet at wk 3. At wk 13 only total and esterified cholesterol were increased by 20% corn oil. AFB 1 treatment resulted in large intra-group variations in total lipid and cholesterol at wk 3, but these were no longer apparent by wk 13. AFB 1 produced various alterations in the fatty acid composition of hepatic phosphatidylcholine (PC) and phosphatidylethanolamine (PE), apparent at wk 3 but not at wk 13. The unsaturation index decreased but no changes were seen in the saturated fatty acids. Only in animals fed 20% corn oil did AFB 1 result in significant changes in 18:2, 20:3 and 22:6 fatty acids, while 20:4 and 22:5 tended to decrease and 18:1 to increase in response to AFB 1 treatment with both diets in both phospholipids. The high-corn oil diet was found to increase 18:2, 22:6, and total unsaturation in PC and PE, while the ratio of 20:4 to 18:2 tended to decrease in these phospholipids, γ-Glutamyltranspeptidase, an indicator of liver damage, was significantly increased in AFB 1-treated animals, with the greatest increase over controls in those fed the high-fat diet. 相似文献
17.
Aflatoxin B1 (AFB1) is a carcinogenic metabolite produced by certain Aspergillus species. Ochratoxin A (OTA) is a metabolite of Aspergillus ochraceus and Penicillium verrucosum. AFB1 and OTA are amongst the most frequent combinations of mycotoxins found in plant products. Thus, synergistic effects or interactions between the two mycotoxins could be taking place. The aim of the present study was to investigate the effect of OTA on Aspergillus parasiticus growth and AFB1 production in yeast extract sucrose (YES) medium at concentrations of 0.16, 1.6 and 16 ng OTA flask(-1). The AFB1 extracted from cultures and purified with immunoaffinity columns was then quantitated by HPLC. The recovery and detection limit of the method were 95.3% and 0.02 ng AFB1 mL(-1), respectively. Maximum AFB1 productions in cultures with OTA were observed from 9 to 12 days (76.09-82.52 ng AFB1 flask(-1)) while in control cultures (without OTA) maximum production (197.2 ng AFB1 flask(-1)) was observed on 14th day. Maximum AFB1 levels in cultures with OTA were reduced by a percentage of 58-61% compared to control cultures. Furthermore AFB1 levels in cultures with OTA were practically (92%) degraded after 18 days of incubation. Conclusively when OTA is present the production of AFB1 by A. parasiticus in YES medium is inhibited. 相似文献
18.
目的建立高效液相色谱–光化学衍生–荧光检测法测定沉香药材中黄曲霉毒素B1、B2、G1、G2。方法采用高效液相色谱法,通过免疫亲和柱提取和净化,荧光检测器检测。Agilent Zorbax Ecilpse Plus C18色谱柱(250 mm×4.6 mm,5μm);流动相:甲醇–水(45∶55);体积流量:0.8 m L/min;柱温:30℃;进样盘温度:4℃;荧光激发波长为360 nm,发射波长为450 nm。结果黄曲霉毒素B1、B2、G1、G2分别在9.3~74.4、3.0~24.0、9.3~74.4、3.5~28.0 pg线性关系良好,r均大于0.998 0;检测限分别为1.86、0.60、1.86、0.70 pg,定量限分别为7.44、2.40、7.44、2.80 pg。平均回收率分别为78%、92%、82%、99%,RSD值分别为4.4%、3.0%、4.3%、2.8%。结论所建立的方法结果准确、重复性、稳定性均良好,可用于沉香药材中黄曲霉毒素的质量控制。 相似文献
19.
In this study, the effectiveness of gaseous ozone and ozonated water on microbial flora and aflatoxin B(1) content of dried figs were investigated. After dried figs were exposed to13.8mgL(-1) ozone gas and 1.7mgL(-1) ozonated water for 7.5, 15 and 30min, variation of aerobic mesophilic bacteria (AMB), E. coli, coliform, yeast and mold counts were determined. Before and after ozone treatments molds on dried figs were also isolated and identified. In both ozone treatments, AMB was not exactly inactivated whereas E. coli was completely destroyed at 7.5min. Coliform, and yeast were also destroyed at 7.5 and 15min in ozonated water, respectively. Ozone applications at 15min were sufficient for inactivation of all molds. Aspergillus flavus and Aspergillus parasiticus which cause aflatoxin formation were isolated from dried figs. Artificially contaminated with aflatoxin B(1) samples were also treated with gaseous ozone and ozonated water for 30, 60 and 180min, respectively. In both of treatments, degradation of aflatoxin B(1) was increased due to increasing of ozonation time. Results indicated that gaseous ozone was more effective than ozonated water for reduction of aflatoxin B(1), whereas ozonated water was affected for decreasing microbial counts. 相似文献
20.
Mycotoxicosis has been produced in the rat by daily oral administrations of ochratoxin A (1.5 mg/kg/day) or aflatoxin B1 (1 mg/kg/day). Hepatic microsomal cytochrome P-450 and b5 contents and many phase I and II biotransformation systems have been measured in the course of ochratoxicosis (4 to 15 dosings) and aflatoxicosis (1 to 8 dosings). In case of ochratoxicosis, decreases in cytochrome P-450 level, aminopyrine demethylase and aniline hydroxylase activities were observed in rats receiving 15 administrations of the toxin. Aflatoxicosis induced more severe decreases in cytochrome P-450, aminopyrine demethylase and ethoxycoumarin deethylase following 8 daily gavages. In the two studies, there was no significant change in activities of liver phase II biotransformation enzymes. 相似文献
|