Modulation of the mitotic action of ethylene dibromide

Refeeding rats treated with a single high dose of ethylene dibromide (1,2-dibromoethane, EDB) induced liver DNA synthesis. The peak of DNA synthesis, as measured by [methyl-3H]thymidine incorporation was attained after 24 h in refed rats and at 48 h in fasted ones. Fasting enhances the EDB action leading to liver cell necrosis, as shown by elevation of serum enzymes' activities, glutamic pyruvic transaminase (GPT) and sorbital dehydrogenase (SDH). A low dose of EDB administered during 2 and 3 weeks slightly enhanced the liver DNA synthesis and elevated the activity of serum enzymes. Phenobarbitone (PB) treatment of rats together with low dose of EDB during 2 weeks prevented the enzyme activity elevation and attenuated the DNA synthesis. Diethyldithiocarbamate (DDC) pretreatment potentiated the DNA synthesis in fed rats after both a small dose of EDB for 2 weeks and after a single high-dose treatment. In DDC pretreated rats, the high single dose of EDB caused biochemical perturbations in serum and liver representative of liver cell necrosis; changes in serum enzymes' activities also were noticed as early as 2 h after EDB toxication. The possible function of modulators on the mitogenic or the necrogenic action of EDB is discussed.     

Respiratory chain components involved in the glycerophosphate dehydrogenase-dependent ROS production by brown adipose tissue mitochondria

Involvement of mammalian mitochondrial glycerophosphate dehydrogenase (mGPDH, EC 1.1.99.5) in reactive oxygen species (ROS) generation was studied in brown adipose tissue mitochondria by different spectroscopic techniques. Spectrofluorometry using ROS-sensitive probes CM-H₂DCFDA and Amplex Red was used to determine the glycerophosphate- or succinate-dependent ROS production in mitochondria supplemented with respiratory chain inhibitors antimycin A and myxothiazol. In case of glycerophosphate oxidation, most of the ROS originated directly from mGPDH and coenzyme Q while complex III was a typical site of ROS production in succinate oxidation. Glycerophosphate-dependent ROS production monitored by KCN-insensitive oxygen consumption was highly activated by one-electron acceptor ferricyanide, whereas succinate-dependent ROS production was unaffected. In addition, superoxide anion radical was detected as a mGPDH-related primary ROS species by fluorescent probe dihydroethidium, as well as by electron paramagnetic resonance (EPR) spectroscopy with DMPO spin trap. Altogether, the data obtained demonstrate pronounced differences in the mechanism of ROS production originating from oxidation of glycerophosphate and succinate indicating that electron transfer from mGPDH to coenzyme Q is highly prone to electron leak and superoxide generation.     

类黄酮对AM真菌及宿主植物的影响研究

类黄酮[apigenin(4,5,7-trihydroxyflavone,4,5,7-三羟基黄酮)和hesperitin(3?5,7trihydroxy4?methoxyflavanone,3?5,7-三羟-4-甲氧基黄烷酮)]对接种AM真菌的紫云英的生物量、AM真菌侵染率、菌丝ALP(碱性磷酸酶)和SDH(琥珀酸脱氢酶)活性都有显著影响。对于Glomusintraradices侵染的紫云英的生物量,4,5,7-三羟基黄酮处理组第6周有显著差异(生物量分别为6.3g、5.7g和6.5g,而对照为3.0g),3?5,7-三羟-4-甲氧基黄烷酮处理组三次取样都有显著差异;对于Endo-1(一个商业菌剂,由Glomusintraradices和Glomusmosseae组成)侵染的紫云英的生物量,4?5,7-三羟基黄酮处理组第6周1.5mmol/L组和第9周150nmol/L组都有显著差异(生物量分别为7.2g和16.8g,而对照为4.1g和8.1g),3?5,7-三羟-4?甲氧基黄烷酮处理组第6、9周都有显著差异,尤以第9周150nmol/L组差异更大(生物量为14.4g,而对照为8.1g)。对于G.intraradices的侵染率,与对照相比,4?5,7-三羟基黄酮处理组三次取样都有显著差异(第9周对照为36.6%,而处理组分别为71.5%、80.8%和75.9%);3?5,7-三羟-4?甲氧基黄烷酮处理组三次取样也有显著差异,尤以150nmol/L组效果最好(第9周AM真菌侵染率为94.8%,而对照为36.6%);对于Endo-1的侵染率,与对照相比,4,5,7-三羟基黄酮处理组三次取?     

In vitro kinetics of the rat brain succinate dehydrogenase inhibition by hexachlorophene.

Brain succinate dehydrogenase (SDH) activity was inhibited by in vitro hexachlorophene (HCP) with a half inhibitory concentration (IC50) of 0.65 x 10(-3) M. The HCP exerted noncompetitive inhibition at 0.5 mM (IC50) on SDH activity. The brain SDH demands more energy of activation (deltaE) in the presence of HCP. The ionizable groups of SDH such as the sulfhydral group of cysteine and alpha-amino groups of cysteine were not altered qualitatively in the presence of HCP.     

Characterization of synaptosomes from the central nervous system of insects

Nerve terminals from the head ganglia of Locusta migratoria were isolated by means of a modified microscale flotation technique. Enzymatic, ultrastructural and chemical analysis revealed that the synaptosomal fraction was highly enriched in well-preserved nerve endings containing almost no free mitochondria. Cholinergic activities (choline acetyltransferase, acetylcholinesterase, acetylcholine receptors) were found to be concentrated in the synaptosomal fraction. The cholinergic nature and the functional integrity of nerve endings isolated from locusts were further supported by the existence of a high affinity choline uptake system, which is abolished by hemicholinium-3 as well as by low temperature, is essentially sodium dependent and inhibited by elevated potassium concentrations. After slight modifications of the gradient densities, synaptosomes could also be isolated from other insect species.     

Membranes of Rhodopseudomonas sphaeroides. VI. Isolation of a fraction enriched in newly synthesized bacteriochlorophyll a-protein complexes

Radioactivity eventually destined for the chromatophore membrane of Rhodopseudomonas sphaeroides was shown in pulse-chase studies to appear first in a distinct pigmented fraction. This material formed an upper pigmented band which sedimented more slowly than chromatophores when cell-free extracts were subjected directly to rate-zone sedimentation on sucrose density gradients. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated that the purified fraction contained polypeptide bands of the same mobility as light-harvesting bacteriochlorophyll a and reaction center-associated protein components of chromatophores; these were superimposed upon cytoplasmic membrane polypeptides. The pulse-chase relation was confined mainly to the polypeptide components of these pigment-protein complexes. It is suggested that the isolated fraction may be derived from sites at which new membrane invagination is initiated.     

Mitochondrial potassium channels and reactive oxygen species

Pretreatment of tissues with potassium channel openers (KCO’s) has been observed to be cytoprotective in a broad variety of insults. This phenomenon has been proposed to be intimately linked to activation of mitochondrial potassium channels which apparently modulate the mitochondrial production of reactive oxygen species (ROS). This critical review summarizes literature findings about the mitochondrial production of ROS, the action of KCO’s on mitochondrial ROS production and the putative link to the cytoprotective action of these drugs.