滇杠柳扦插繁殖及生根相关理化特性的动态分析

目的:探索不同生长素类调节剂对滇杠柳扦插繁殖的影响,以及其生根过程中内源激素、氧化酶活性的动态变化规律。方法:采用不同浓度的吲哚丁酸(IBA)、生根粉1号(ABT1)和萘乙酸(NAA)处理滇杠柳插穗,检测生根效果及生根过程中内源激素吲哚乙酸(IAA)、玉米素核苷类(ZR s)、脱落酸(ABA)含量及吲哚乙酸氧化酶(IAAO)、多酚氧化酶(PPO)、过氧化物酶(POD)活性的变化。结果:150 mg/L IBA处理滇杠柳插穗生根率达到80%,150 mg/L ABT1和NAA处理的插穗生根率为70%和68%,而对照只有23%生根。滇杠柳扦插生根过程可分为不定根诱导期、露白期和生长期3个阶段。不定根诱导期需要低含量的内源激素IAA、ZR s、ABA、较高活性的IAAO;不定根形成露白期需要高含量内源激素IAA、较高活性的PPO、低含量的ZR s、ABA和低活性的IAAO和POD;不定根生长期需要一定含量的IAA、ZR s、ABA和较高活性的PPO、POD、IAAO,在生根后期三种氧化酶活性下降。生根过程中,150 mg/L IBA的处理增加了插穗内IAA含量和PPO活性,降低了插穗内ABA、ZR s含量和IAAO...     

Metabolism of trichloroethylene in man

Volunteers inhaled a constant concentration of 50 ppm trichloroethylene (Tri) for 6 hrs per day on 5 consecutive days. Simultaneous ethanol (EtOH) ingestion (blood level 0.6 %.) inhibits the metabolization of Tri to triehloroethanol (TCE) and trichloroacetic acid (TCA) by 40 % on the average. Oxidation of Tri to TCA does not occur as long as EtOH is present. During this time period the blood Tri-concentration increases 21/2-fold, that in the expired air rising 4-fold, as compared to Tri inhalation without EtOH. TCE glucuronidation is not subject to inhibition. On concurrent inhalation of Tri, the EtOH and acetaldehyde levels are slightly increased over the control values without Tri.The mechanisms underlying the alternate inhibition of mixed-function oxygenases and aldehyde dehydrogenase on simultaneous intake of Tri and EtOH are discussed. The intolerance reaction occurring on combined exposure to Tri and EtOH can be interpreted as an accumulation of Tri in the CNS resulting from the complete depression of Tri oxidation.We are grateful to Miss J. Ahamer and Mrs. R. Kraus for their skilled technical assistance.     

Epithelial TLR4 Signaling Activates DUOX2 to Induce Microbiota-Driven Tumorigenesis

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Pterostilbeno Reduz o Estresse Oxidativo no Pulmão e no Ventrículo Direito Induzido por Infarto do Miocárdio Experimental

BackgroundPterostilbene (PS), a natural and antioxidant polyphenolic compound emerges as a promising intervention in improving the myocardial infarction (MI) damages.ObjetivesThis study aimed to evaluate PS actions in promoting redox homeostasis in lungs and right ventricle (RV) of infarcted animals.MethodsMale Wistar rats (60 day-old) were randomized into three groups: SHAM, MI (infarcted), and MI+PS (MI+pterostilbene). Seven days after MI procedure, rats were treated with PS (100 mg/kg/day) via gavage for eight days. Animals were euthanized and the lungs and RV were harvested for analyses of redox balance (Differences were considered significant when p<0.05).ResultsOur results show that MI triggers a redox disruption scenario in RV and lungs, which can contribute to MI-induced damage on these organs. Consistently, PS mitigated oxidative stress and restored antioxidant defenses (GSH in lungs: SHAM= 0.79±0.07; MI=0.67±0.05; MI+PS=0.86±0.14; p<0.05), indicating its protective role in this scenario.ConclusionsOur work evidences the PS potential use as an adjuvant therapeutic approach after MI focusing on protecting pulmonary and right-sided heart tissues.     

Microsomal aspects of carcinogenesis and neoplasia.

Neither immunologic nor genetic concepts of carcinogenesis have yet been decisively confirmed, and epigenetic theories, as formulated so far, are either non-predictive or insufficiently consistent with morphologic and experimental evidence. Computing data, concerned with carcinogenic mechanisms and neoplastic changes at the level of the endoplasmic reticulum, may lead to a new coherent understanding of tumor pathogenesis. Carcinogenic agents initiate biophysical perturbations, chemical alterations and conformational transitions in the membrane lattice of the endoplasmic reticulum. Foremost among the resulting neoplastic changes is an increased, irreversible separation of polyribosomes from membranes of the ergastoplasm. The carcinogenic process, apparently, deletes a protein required for polysome attachment. Since microsomal cytochromes can be synthesized by membrane-bound polysomes only, the translation of genetic information for their biosynthesis is irreversibly restricted. A similar, self-perpetuating deficiency may be postulated for the polysome attachment protein. Activities, depending on cytochromes P-450 and b5, are hampered, e.g. those of the monoxygenase system. Cholesterogenesis is derepressed. Ratios of phospholipids/cholesterol are decreased, and lipid-protein complexes, altered both in structure and function. Another distinct effect of the membrane-polysome separation is the unmasking of thiol-disulfide exchange enzymes which, in turn, stimulate the biosyntehsis of proteins and of deoxyribonucleotides involved in cell replication.