RÉSUMÉ
Background Formaldehyde and benzene homologues are common environmental pollutants, and their neurotoxicity has aroused widespread concern. Objective To investigate the effect of taurine on cognitive impairment after exposure to formaldehyde and benzene analogues in young rats. Methods Twenty four-week old SD rats were randomly divided into four groups, with six rats in each group: control group (clean air), model group (5 mg·m−3 formaldehyde + 5 mg·m−3 benzene + 10 mg·m−3 toluene + 10 mg·m−3 xylene), low-dose taurine intervention group (5 g·L−1 taurine + mixture of formaldehyde and benzene analogues), and high-dose taurine intervention group (10 g·L−1 taurine + formaldehyde and mixture of benzene analogues), and the exposure was administered by oral and nasal aerosol inhalation for 28 d. At the end of exposure, the learning and memory ability of rats in each group was measured by Morris water maze test. After the behavioral test, the rats were anesthetized and neutralized, and the brain tissue was harvested for histopathological and molecular biological tests. The apoptosis rate of neurons in hippocampal CA1 area was detected by Tunel assay, and the expression levels of apoptosis-related proteins such as caspase 3, bax, and bcl-2 in hippocampal tissue were detected by Western blotting. Results The growth and development of rats in each group were good during inhalation. During the Morris water maze experiment, the escape latencies of rats in the taurine intervention groups were not different from that in the control group (P>0.05) from day 3 to day 5 of training, while the escape latency of rats in the model group was significantly higher than that in the control group (P <0.05). The number of crossing platform and the target quadrant residence time in the high-dose taurine intervention group were not different from those in the control group (P>0.05), while the two variables in the model group and low-dose taurine intervention group were significantly lower than those in the control group (P <0.05). The apoptotic rates of neurons in the hippocampal CA1 area of rats in the control group, model group, and low-dose and high-dose taurine intervention groups were 5.11%, 18.87%, 9.39%, and 4.63%, respectively. The apoptotic rate in the model group was higher than those in the control group and low-dose and high-dose taurine intervention groups (P<0.05). The expression levels of caspase 3, bax, and bcl-2 in the hippocampus of rats in the low-dose and high-dose taurine intervention groups showed no difference compared with the control group (P>0.05). The expression levels of caspase 3 and bax in the model group were higher than those in the control group and low-dose or high-dose taurine intervention groups (P<0.05), and the expression levels of bcl-2 was lower (P<0.05). Conclusion The mixed exposure to formaldehyde and benzene analogues can damage the learning and memory ability of young rats, and increase the apoptosis of neurons in hippocampal CA1 region. Taurine can reverse the damage induced by formaldehyde and benzene analogues.
RÉSUMÉ
RESUMO: Avaliou-se a degradação anaeróbia do alquilbenzeno linear sulfonato (LAS) e seus homólogos em experimento em escala de laboratório. Foi usado lodo disperso para minimizar o efeito da adsorção. Em primeiro lugar, determinaram-se a maior concentração de LAS (substrato) e a menor concentração de etanol (cossubstrato) que manteriam os micro-organismos ativos, resultando em 25 e 200 mg.L-1, nessa ordem. Posteriormente, o experimento (90 dias) foi realizado em um reator somente com etanol (controle) e outro (reator teste, triplicata) com ambos os substratos nas concentrações anteriores. Os micro-organismos apresentaram crescimento exponencial em 48 h para os 2 reatores; não ocorreu toxicidade pelo LAS no reator teste durante esse período inicial, quando o etanol foi todo consumido. Após então, houve decréscimo de micro-organismos, indicando possível toxicidade por LAS ou intermediários. Observou-se também a diminuição ou ausência da produção de ácidos graxos voláteis e de metano. Portanto, com lodo disperso, a maior parcela da remoção foi por conta da biodegradação, porém, com formação de intermediários que não o acetato nem o metano, apontando a inibição à acidogênese e à metanogênese. Ao final, a remoção do LAS foi de 35% por biodegradação e apenas 0,35% por adsorção ao lodo. A ordem preferencial de biodegradação para os homólogos foi de C13 para C12, C11 e C10, com percentual de degradação em relação à massa inicial de 49, 31, 24 e 17%, respectivamente. A mesma ordem deu-se para a adsorção, da maior para a menor cadeia alquílica, sendo a remoção por adsorção de 0,85; 0,32; 0,13 e 0,01%, respectivamente.
ABSTRACT: The anaerobic degradation of linear alquibenzene sulfonate (LAS) and its homologues was evaluated in batch experiment. Dispersed sludge was used to minimize the effect of adsorption. Initially, the highest concentration of LAS (substrate) and the lowest concentration of ethanol (co-substrate) were determined to maintain the microorganisms active; the results were 25 and 200 mg.L-1, respectively. Afterwards, a 90-day period experiment was conducted with one reactor with only the addition of ethanol (control) and the other (test reactor in triplicate) with both substrates and the previous concentrations found. The microorganisms showed exponential growth in the first 48 h for both reactors; LAS toxicity has not occurred in the test reactor during the first 4 days, during which ethanol was consumed. After that, the microorganisms decreased, indicating possible toxicity due to LAS or intermediates; a decrease or absence of volatile organic acids and methane production was also observed. Therefore, with dispersed sludge the largest removal was due to biodegradation, but with formation of intermediates other than acetate or methane, indicating inhibition of acidogenesis and methanogenesis. At the end, the removal was 35% by biodegradation and only 0.35% by adsorption to the biomass. The preferential order of the biodegradation for the homologues was from C13 to C12, C11 and C10; and the removal in relation to the initial mass of each was 49, 31, 24 and 17%, respectively. The same order occurred to adsorption, from the higher to the lower alkyl chain, with removal of 0.86, 0.32, 0.13 and 0.01%, respectively.
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To study the antagonistic effect of ginkgolide homologues on platelet-activating factor (PAF)-induced platelet aggregation and investigate its neuroprotective effect. PAF was used as a coagulant, and ginkgolides were added to the rabbit blood samples respectively. The inhibitory effect of each compound on platelet aggregation was detected by turbidimetry. In L-glutamate induced primary cortical neuron cell injury model, MTT assay was used to detect cell viability. Intracellular free Ca2+ concentration in neurons was measured by using the fluorescent Ca2+ indicator Fura-2 AM. Morphological observation and Hoechst 33258 staining were used to detect the inhibitory effect of ginkgolide on neuronal apoptosis. The results showed that the inhibitory effect on PAF-induced platelet aggregation activity in ginkgolide homologues was ginkgolide K (GK), ginkgolide B (GB), ginkgolide A (GA), ginkgolide C (GC), ginkgolide M (GM), ginkgolide J (GJ) and ginkgolide (GL) from high to low. GB and GK (1-100 μmol•L ⁻¹) could significantly reduce the cell damage caused by L-glutamate, with survival rate increasing, intracellular calcium concentration reducing and cell morphology restoring. This paper has identified the activities and characteristics of various compounds of ginkgolide homologues on PAF-induced platelet aggregation as well as its neuroprotective effect.
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For many years, prokaryotic cells were distinguished from eukaryotic cells based on the simplicity of their cytoplasm, in which the presence of organelles and cytoskeletal structures had not been discovered. Based on current knowledge, this review describes the complex components of the prokaryotic cell cytoskeleton, including (i) tubulin homologues composed of FtsZ, BtuA, BtuB and several associated proteins, which play a fundamental role in cell division, (ii) actin-like homologues, such as MreB and Mb1, which are involved in controlling cell width and cell length, and (iii) intermediate filament homologues, including crescentin and CfpA, which localise on the concave side of a bacterium and along its inner curvature and associate with its membrane. Some prokaryotes exhibit specialised membrane-bound organelles in the cytoplasm, such as magnetosomes and acidocalcisomes, as well as protein complexes, such as carboxysomes. This review also examines recent data on the presence of nanotubes, which are structures that are well characterised in mammalian cells that allow direct contact and communication between cells.
Sujet(s)
Bactéries/ultrastructure , Cytosquelette/ultrastructure , Nanotubes/ultrastructure , Organites/ultrastructure , Cellules procaryotes/ultrastructure , Cytosquelette/physiologie , Microscopie électronique à transmission , Protéines membranaires/physiologie , Organites/physiologie , Cellules procaryotes/physiologieRÉSUMÉ
8-alkylberberine homologues (Ber-C8-n, where n indicates carbon atom number of gaseous normal alkyl at 8 position, n =0, 2, 4, 6, 8, 10, 12, or 16) were synthesized and their effects on the hemolysis of rabbit erythrocyte, the fluidity of membrane and the fluorescence of membrane protein were investigated by fluorescence analysis technique. Ber-C8-n with mediate length alkyl (4<n<10) exhibited obvious hemolysis effect on rabbit erythrocyte when their concentration exceed 1.25×10-4 mol/L, and Ber-C8-8 displayed the highest hemolysis effect among all tested homologues. All of Ber-C8-n influenced the fluidity of erythrocyte membrane to different extents, which exhibited an obvious dose-effect relationship. The effect of Ber-C8-n on fluidity increased as the length of alkyl chain was elongated and decreased gradually when the alkyl carbon atoms exceeded 8. The fluorescence of erythrocyte membrane protein was quenched by Ber-C8-n, which showed a similar changing tendency on membrane fluidity. Experiments in vitro suggested that disturbing effects of Ber-C8-n on the conformation and function of membrane protein leaded to the changes of membrane fluidity and stability, and then the membrane was broken down.
RÉSUMÉ
FabB(?-ketoacyl-acyl carrier protein synthase Ⅰ)and FabF(?-ketoacyl-acyl carrier protein synthase Ⅱ)are two key enzymes of fatty acid biosynthesis in E.coli.The Gram-positive pathogenic bacterium Enterococcus faecalis has a fatty acid composition very similar to that of E.coli.Bioinformatic analysis reveals that though E.faecalis has two fabF homologues,there is no recognizable fabB homologue in the genome of E.faecalis.Two fabF homologues(fabF1 and fabF2)were amplified by using E.faecalis V583 genomitic DNA as template,and two plasmids,pHW13(fabF1)and pHW14(fabF2),were constructed.The results of experiments in vivo and in vitro have shown that fabF1 gene could complement E.coli fabB mutation and FabF1 possessed ?-ketoacyl-acyl carrier protein synthase Ⅰ(FabB)activity,while fabF2 gene could complement E.coli fabF mutation and FabF2 had ?-ketoacyl-acyl carrier protein synthase Ⅱ(FabF)activity.Meanwhile the data also shown that FabF2 possessed partial function of ?-ketoacyl-acyl carrier protein synthase Ⅰ(FabB),and it could make E.coli fabB mutation synthesized low amount of unsaturated fatty acid.From these data it is clear that FabF species enzymes could have activity of ?-ketoacyl-acyl carrier protein synthase Ⅰ(FabB).