No changes in lymphocyte muscarinic receptors and platelet monoamine oxidase-B examined as surrogate central nervous system biomarkers in a Faroese children cohort prenatally exposed to methylmercury and polychlorinated biphenyls

Experimental evidence suggests that monoamine oxidase B (MAO-B) and muscarinic cholinergic receptors (mAChRs) are involved in the pathogenesis of neurotoxicity caused by methylmercury and polychlorinated biphenyls (PCBs). Blood samples from 7-year-old exposed children were analyzed for platelet MAO-B and lymphocyte mAChRs as potential markers of exposure to these neurotoxicants. The blood neurotoxicity biomarkers were compared with prenatal and current exposures and with neuropsychological test results. Both biomarkers showed homogeneous distributions within this cohort (mAChR, range 0.04–36.78?fmol/million cells; MAO-B, 0.95–14.95?nmol mg^?1 protein h^?1). No correlation was found between the two biomarkers and either blood neurotoxicant concentrations or clinical findings. MAO-B and mAChR sensitivity may not be sufficiently high to assess early, subclinical responses to low/moderate methylmercury and/or PCB exposure, whereas these markers are significantly altered in sustained exposure scenarios, as shown by clinical studies in drug addicts or patients treated with psychopharmacological agents.     

Isolation and Characterization of Acidic Peptides in Soy Sauce

A soy sauce sample was fractionated by gel filtration on a Sephadex G–15 column, then the fractions were subfractionated on the basis of acidity by ion exchange chromatography on a QAE-Sephadex A–25 column. The acidic subfractions with various acidities were further fractionated, using a preparative amino acid analyzer and by paper chromatography to separate the acidic peptide components.

Four dipeptides and sugar derivatives of ten dipeptides and two tripeptides were isolated and characterized as the major acidic peptides in soy sauce. However, it was difficult to anticipate any direct contribution of these peptides to the flavor construction in soy sauce on the basis of their contents and taste intensities.     

Interaction of estrogen and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in immature male chickens (Gallus domesticus)

The interaction of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and estrogen was studied in chickens to more clearly define this relationship in an avian species and its role in the enhanced sensitivity of female chickens to TCDD-induced wasting syndrome. Twenty male chickens (7-9 weeks old) were divided evenly into four groups: control (CTL, received the same volume of vehicle); estrogen-treated (E2, 1 mg/kg estradiol cypionate injections on days 1, 2 and 3); TCDD-treated (TCDD, single 50 microg/kg injection on day 4); and estrogen plus TCDD (E2+TCDD, as above), with measurements taken on day 14. The E2 group compared with the CTL group had decreased comb height (24%), comb length (26%) and adipose tissue (AT) lipoprotein lipase (LPL) activity relative to AT mass (51%), while liver mass and body weight gain were each increased by 28%. The TCDD group had increased liver mass (62%), reduced comb length (17%), and reduced AT LPL activity indexed to AT mass (70%) compared with the CTL group. Finally, the E2+TCDD group had 37% lower body weight gain and 30% larger livers relative to body mass compared with the E2 group, but were not significantly different from the TCDD group. These data show that TCDD antagonized several effects of exogenous estrogen in male chickens, while estrogen enhanced TCDD toxicity in a tissue-specific manner.     

Degradation of chlorobiphenyls catalyzed by the bph-encoded biphenyl-2,3-dioxygenase and biphenyl-2,3-dihydrodiol-2,3-dehydrogenase of Pseudomonas sp. LB400

Abstract In order to characterize the metabolites produced in vivo by biphenyl-2,3-dioxygenase and biphenyl-2,3-dihydrodiol-2,3-dehydrogenase, the first two enzymes of the (polychloro)biphenyl catabolic pathway encoded by the bph locus of Pseudomonas sp. LB400, recombinant E. coli strains expressing the respective genes were constructed. Biphenyl-2,3-dioxygenase attack on 2,2'- or 2,4'-dichlorobiphenyl was shown to give rise to virtually quantitative ortho -dechlorination of these congeners by hydroxylation at the chlorinated carbon 2 and its unsubstituted neighbour. Elimination of hydrochloric acid directly leads to 2,3-dihydroxy-chlorobiphenyls and obviates the need for biphenyl-2,3-dihydrodiol-2,3-dehydrogenase for the catabolism of such congeners.     

Association between exudates of brown algae and polychlorinated biphenyls

Exudates from the brown algaeCaepidium antarcticum andDesmarestia sp. were investigated for their ability to associate with hydrophobic pollutants such as polychlorinated biphenyls (PCB s). The percentage of PCB associated with algal exudates ranged from 79% for decachlorobiphenyl to 23% for the pentachlorobiphenyl congener No. 95. Exudates from the tested brown algae may therefore alter the bioavailability of PCBs in natural or artificial ecosystems.     

Direct evidence that an arene oxide is a metabolic intermediate of 2,2',5,5'-tetrachlorobiphenyl.

Radiolabeled arene oxide was recovered from incubations containing [³H]-2,2′,5,5′-tetrachlorobiphenyl (³H-TCB), unlabeled 2,2′,5,5′-tetrachlorobiphenyl-3,4-oxide (TCBAO), 3,3,3-trichloropropene-1,2-oxide (TCPO), NADPH, and liver microsomes from phenobarbital-induced rats. No labeled arene oxide was generated in the absence of NADPH, nor during the metabolism of unlabeled TCB in the presence of [³H]-H₂O. The recovered oxide (radiolabeled and carrier) was characterized by mobility on silica gel and by conversion to 3- and 4-hydroxy-TCB. Formation of a dihydrodiol metabolite was apparently blocked by inhibition of epoxide hydrase. These data provide the first direct evidence that arene oxides are intermediates of halogenated biphenyl metabolism.     

Computational identification and analysis of functional polymorphisms involved in the activation and detoxification genes implicated in endometriosis

Endometriosis is a complex disorder of the female reproductive system where endometrial tissue embeds and grows at extrauterine location leading to inflammation and pain. Hundreds of polymorphisms in several genes have been studied as probable risk factors of this debilitating disease. Bioinformatics tools have come a long way in augmenting the search for putative functional polymorphisms in human diseases. In this study we have explored 16 genes involved in the detoxification of xenobiotic chemicals that are implicated in endometriosis by utilising publically available programs like SIFT, Polyphen, Panther, FastSNP, SNPeffect and PhosSNP. The variations among different ethnic populations of the SNPs were studied. We then calculated the extent to which bioinformatics based predictions are concurrent with real world epidemiological, genotyping studies using a set of SNPs that have been studied in endometriosis case–control studies. Our study shows that there is a significant positive correlation (r = 0.569, p < 0.005) between the summary of the predicted scores taken from 4 different servers and the odds ratio found from epidemiological studies. This report has identified and catalogued various deleterious SNPs that could be important in endometriosis and could aid in further analysis by in vitro and in vivo methods for the better understanding of the disease pathophysiology.     

多氯联苯对剑尾鱼超氧化物岐化酶活性的影响

目的　研究多氯联苯 (PCBs)暴露对剑尾鱼 (Xiphophorushelleri)超氧化物歧化酶 (SOD)活性的影响 ,探讨剑尾鱼器官组织内SOD活性变化作为环境风险评价 (ERA)的有效生物学标记的可行性。方法　测定了PCBs对剑尾鱼 30d的半致死浓度 (LC50 ) ;使用浸浴法以 0、2、5 0 μg L三个PCBs浓度为剑尾鱼染毒 ,定量测定了 72h内肝、鳃及卵巢组织中的SOD的活性变化。结果　PCBs对剑尾鱼的 30dLC50 为 1 0 5 80 μg L ;PCBs对剑尾鱼肝脏和卵巢的SOD活性有明显 (P <0 0 1 )的影响。在最初染毒的 1 2h内 ,SOD活性略有上升 ,但随暴露时间延长 ,浓度增加 ,肝和卵巢的SOD活性均呈下降趋势。此外 ,结果还显示肝组织的SOD活性较高于卵巢的SOD活性 ,表明不同器官组织的SOD活性对PCBs胁迫的敏感性存在一定的差异。实验中鳃组织SOD活性在PCBs暴露后其变化不明显 (P >0 0 5 )。结论　表明剑尾鱼肝细胞SOD活性可作为环境风险评价 (ERA)的有效生物学标记     

On the isolation of polychlorinated dibenzo-p-dioxins and furans from serum samples using immunoaffinity chromatography prior to high-resolution gas chromatography–mass spectrometry

Immunoaffinity chromatography (IAC) for the purification of polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs) from biological samples was explored as a means to simplify the cleanup procedure and thereby decrease the time and cost of dioxin analysis. A monoclonal antibody (DD3) was used to produce IAC columns and to isolate the PCDD/Fs from serum. Native and ¹³C-labeled PCDD/Fs were spiked at the ppq to ppt range into serum. Quantitation of the PCDD/Fs was performed by a standard dioxin analytical method, i.e. high-resolution gas chromatography–mass spectrometry (GC–MS), which was easily compatible with IAC. Five of the most toxic PCDD/Fs consistently showed acceptable recoveries (>25%) and were reliably quantitated. The congeners specifically recovered by this method represent almost 80% of the toxic equivalency of dioxins and furans present in the serum samples. Dioxin-like polychlorinated biphenyls (PCBs) were not recognized by this antibody column. Compared to conventional dioxin cleanup methods, IAC decreased solvent usage by 1.5 l/sample and took only 2 h to process a sample for analysis.     

多氯联苯对鸡胚的毒性作用

The toxic effects of polychlorinated biphenlys (PCB) on embryonic chickens, especially on liver morphology, were studied. PCB (Aroclor 1 254) was injected into yolk of Hyline fertilized eggs, with doses of 0, 1, 10 and 100 μg/egg, respectively. The survival rate of chicken embryos in each PCB treatment group was significantly lower than that of the control group. The hatching rate of 1 μg/egg group was only 40%. Subcutaneous edema and hydrocephally were found in dead embryos and newly hatched chicks of all treatment groups. Livers of newly hatched chickens were removed for examination of histological structures. After PCB treatment, severe liver injury was apparent. The hepatic structures were damaged and steatosis was observed, together with necrosis and cell vacuolation and pyknosis. There were more Kupffers cells in the hepatic sinusoid. No PAS positive staining was found in the hepatic cytoplasm, indicating that glycogen was exhausted in the hepatic cells. The higher death rate in PCB treated groups may be related to glycogen exhaustion. These findings indicate that PCBs reduced the hatching rate by causing severe subcutaneous edema and liver injury in chicken embryos.