• Journal of Environmental Science International
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• v.1 no.1
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• pp.1.1-11
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• 1992

To find heavy metal-specific effects on the photosynthetic apparatus of higher plants, we investigated effects of $CuCl_2$, HgCl_2$ and $ZnCl_2$ on electron transport activity and chlorophyll fluorescence induction kinetics of chloroplasts isolated from barley seedlings. Effects on some related processes such as germination, growth and photosynthetic pigments of the test plants were also studied. Germination and growth rate were inhibited in a concentration-dependent manner by these metals. Mercury was shown to be the most potent inhibitor of germination, growth and biosynthesis of photosynthetic pigments of barley plants. In the inhibition of electron transport activity, quantum yield of PS II, and chlorophyll fluorescence induction kinetics of chloroplasts isolated from barley seedlings, mercury chloride showed more pronounced effects than other two metals. Contrary to the effects of other two metals, mercury chloride increased variable fluorescence significantly and abolished qE in the fluorescence induction kinetics from broken chloroplasts of barley seedlings. This increase in variable fluorescence is due to the inhibition of the electron transport chain after PS ll and the following dark reactions. The inhibition of qE could be attributed to the interruption of pH formation and do-epoxidation of violaxathin to zeaxanthin in thylakoids by mercury. This unique effect of mercury on chlorophyll fluorescence induction pattern could be used as a good indicator for testing the presence and/or the concentration of mercury in the samples contaminated with heavy metals.

• YAKHAK HOEJI
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• v.31 no.6
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• pp.361-369
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• 1987

The four azo dyes such as Amaranth (FD & C Red No. 2), Tartrazine (FD & C Yellow No. 4), sunset Yellow (FD & C Yellow No. 5) and Allura red (FD & C Red No. 40) are currently employed as a food additives in Korea. In this study, the effects of these azo dyes on the hepatic microsomal mixed function oxidase systems in Rats. (i.e., Cyt. P-450, Cyt. b$_5$, NADPH cyt. c-reductase and azo reductase) were investigated. Furthermore, to determine the relationship among the electron transport systems, each level of azo reductase, Cyt. P-450 and NADPH cyt. c-reductase was measured upon the administration of phenobarbital (known as an inducer of Cyt. P-450), 3-methylcholanthrene (Known as an inducer of Cyt. P-448), CoCl$_2$ (inhibitor on Cyt. P-450) or $CCl_4$ (inhibitor on Cyt. P-450). The results of these studies are as follows; (1) The levels of Cyt. P-450 and Cyt. b$_5$ were decreased upon the administration of these azo dyes. (2) When the level of Cyt. P-450 was decreased, the azo reductase activity was also decreased. (3) These azo dyes did not show any significant effect on the level of NADPH cyt. c-reductase. (4) The administration of 3-methylcholanthrene resulted in the elevation of azo reductase activity. The 3-methylcholanthrene may be responsible for the induction of CO-insensitive electron transport system.

• Journal of Ginseng Research
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• v.14 no.1
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• pp.57-62
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• 1990

In order to Investigate the mechanism of the leaf-burning disease of ginseng (Panax ginseng C.A. Meyer), studies on the generation of singlet oxygen (1O2) and the photooxidation of the pigments were carried out in comparison with the ones of soybean (G1ycine max L). The studies were mainly focalized on the effects of light intensity, light intensity, inhibitor and electron donor/acceptor of the Photosynthetic electron transport system. When we measured the amounts of 1O2 generated in the thylakoids of ginseng and soybean by the irradiation of light (300 w/m2) as a function its time. It was identified that a higher amount of 1O2 was formed in the ginseng thylakoid than the case of soybean. A generation ratio of lO2 between ginseng and soybean sltbstantially identical in the range of light intensities 50∼150w/m2 However much higher amount of 1O2 was generated in ginseng by irradiation of strong intensity of light (200 500w/m2). Wave length dependency on the generation of 1O2 and the pigment photooxidation was observed on ginseng thylakoids; red light (600-700 nm) gave a maximum effect in the contrast with blur green light (400-60 nm). When the ginseng thylalioid was treated with the electron donor (Mn2+) and acceptors (DCPIP, FeCy) of the photosynthetic electron transport system. a drastic inhibition of 1O2 generation was observed. However, treatment with its inhibitors (DCMU, KCW) activated 1O2 generation. An interesting fact that an electron donor or acceptor of the photosystem II(P680) Inhibited 1O2 generation, suggests an intimate relationship between 1O2 generation and photosystem II.

• Journal of Ginseng Research
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• v.23 no.4
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• pp.205-210
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• 1999

The growth of hairy roots were increased $69\%$ by 0.1 mM DCPIP under light conditions. In these conditions, the contents of seven ginsenosides were none significant variation. The influence of electron inhibitors on growth and ginsenoside contents in ginseng hairy roots was tested. The growth was inhibited $71\%\;and\;22\%$ respectively by CCCP and methylamine. The ginsenoside contents were as decreased above $45\%$ in all treatment tested except triazine treatment. In antioxidants treatment, the growth of hairy roots was increased about $68\%$ by propylgallic acid, about $23\~25\%$ by ascorbic acid or 2,5-dimethylfuran, while the contents of seven ginsenosides were none significant variation. The ginsenoside productivity was high when hairy roots were cultured in $\circledR^{\wedge}MS$ medium for 4 weeks and then transferred to 1/2MS medium with ascorbic acid or 2,5-dimethylfuran for 1 weeks in light conditions. It is suggested that ginsenoside productivity could be accelerated by some antioxidants in hairy root cultures of ginseng.

• International Journal of Oral Biology
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• v.37 no.1
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• pp.17-23
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• 2012

Recent studies indicate that reactive oxygen species (ROS) are critically involved in persistent pain primarily through spinal mechanisms, and that mitochondria are the main source of ROS in the spinal dorsal horn. To investigate whether mitochondrial ROS can induce changes in membrane excitability on spinal substantia gelatonosa (SG) neurons, we examined the effects of mitochondrial electron transport complex (ETC) substrates and inhibitors on the membrane potential of SG neurons in spinal slices. Application of ETC inhibitors, rotenone or antimycin A, resulted in a slowly developing and slight membrane depolarization in SG neurons. Also, application of both malate, a complex I substrate, and succinate, a complex II substrate, caused reversible membrane depolarization and enhanced firing activity. Changes in membrane potential after malate exposure were more prominent than succinate exposure. When slices were pretreated with ROS scavengers such as phenyl-N-tert-buthylnitrone (PBN), catalase and 4- hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPOL), malate-induced depolarization was significantly decreased. Intracellular calcium above $100{\mu}M$ increased malateinduced depolarization, witch was suppressed by cyclosporin A, a mitochondrial permeability transition (MPT) inhibitor. These results suggest that enhanced production of spinal mitochondrial ROS can induce nociception through central sensitization.

• Microbiology and Biotechnology Letters
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• v.31 no.1
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• pp.1-12
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• 2003

Myxobacteria are soil bacteria that move by gliding and have a complicated life cycle. In the research over the 25 years the myxobacteria have been shown to be a rich source of potentially useful bioactive substances. So far about 80 different basic compounds and 450 structural variants have been characterized. It is remarkable that myxobacteria produce the substance has special mechanisms. 26 new electron transport inhibitors,5 inhibitors of nucleic acid polymerases, 10 substances that act on the cytoskeleton, and 1 inhibitor of fungal acetyl-CoA carboxylase have been found. Presently, large-scale technical process was not fully established. But one of the compounds from myxobacteria is able to pass the many thresholds, which are on the road to application.

• BMB Reports
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• v.43 no.9
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• pp.614-621
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• 2010

Propamidine, an aromatic diamidine compound, is widely used as an antimicrobial agent. To uncover its mechanism on pathogenetic fungi, Botrytis cinerea as an object was used to investigate effects of propamidine in this paper. The transmission electron microscope results showed that the mitochondrial membranes were collapsed after propamidine treatment, followed that mitochondria were disrupted. Inhibition of whole-cell and mitochondrial respiration by propamidine suggested that Propamidine is most likely an inhibitor of electron transport within Botrytis cinerea mitochondria. Furthermore, the mitochondrial complex III activity were inhibited by propamidine.

• Biomedical Science Letters
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• v.11 no.4
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• pp.441-446
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• 2005

The molecular mechanism of ischemia/reperfusion injury remains unclear. Reactive oxygen species (ROS) are implicated in cell death caused by ischemia/reperfusion in vivo or hypoxia in vitro. Poly (ADP-ribose) polymerase (PARP) activation has been reported to be involved in hydrogen peroxide-induced cell death in renal epithelial cells. This study was therefore undertaken to evaluate the role of P ARP activation in chemical hypoxia in opossum kidney (OK) cells. Chemical hypoxia was induced by incubating cells with antimycin A, an inhibitor of mitochondrial electron transport. Exposure of OK cells to chemical hypoxia resulted in a time-dependent cell death. In OK cells subjected to chemical hypoxia, the generation of ROS was increased, and this increase was prevented by the $H_2O_2$ scavenger catalase. Chemical hypoxia increased P ARP activity and chemical hypoxia-induced cell death was prevented by the inhibitor of PARP activation 3-aminobenzamide. Catalase prevented OK cell death induced by chemical hypoxia. $H_2O_2$ caused PARP activation and $H_2O_2-induced$ cell death was prevented by 3-aminobenzamide. Taken together, these results indicate that chemical hypoxia-induced cell injury is mediated by PARP activation through H202 generation in renal epithelial cells.

• Journal of Korean Society for Atmospheric Environment
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• v.12 no.3
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• pp.307-314
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• 1996

The rate of evolution of ethylent by tomato plants was rapidly increased by ozone fumigation. In the present study, the mechanism of ethylent evolution by ozone was investigated in experiments with aminoethoxyvinylglycine (AVG) and tiron, which inhibit the formation of ethylene and peroxidation of lipids, respectively. Pretreatment with AVG significantly inhibited the ozone-induced ethylent evolution, but the treatment of plants with tiron did not inhibit. These results indicate that the induction of the evolution of ethylene by ozone involves the pathway via aminocyclopropane-1-carboxylate (ACC), while not released as a result of the peroxidation of lipids. Ozone-induced ethylent evolution was greater in dar- than light-incubated, intact tomato plants. The difference between dark- and light-ethylene evolution was examined with diuron, an inhibitor of photosynthetic electron transport. The inhibitor treatment promoted ethylent evolution. These results suggest that ethylent retention and metabolism in plants were regulated by internal $CO_2$ levels which, in turn, were controlled in large part by photosynthesis. Thus, ethylene was retained in illuminated leaf tissue under low intenal $CO_2$ concentration which may develop in a sealed container without exogenously supplied $CO_2$.

• International Journal of Oral Biology
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• v.42 no.2
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• pp.55-61
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• 2017

Recent studies indicate that mitochondria are an important source of reactive oxygen species (ROS) in the spinal dorsal horn. In our previous study, application of malate, a mitochondrial electron transport complex I substrate, induced a membrane depolarization, which was inhibited by pretreatment with ROS scavengers. In the present study, we used patch clamp recording in the substantia geletinosa (SG) neurons of spinal slices, to investigate the cellular mechanism of mitochondrial ROS on neuronal excitability. DNQX (an AMPA receptor antagonist) and AP5 (an NMDA receptor antagonist) decreased the malate-induced depolarization. In an external calcium free solution and addition of tetrodotoxin (TTX) for blockade of synaptic transmission, the malate-induced depolarization remained unchanged. In the presence of DNQX, AP5 and AP3 (a group I metabotropic glutamate receptor (mGluR) antagonist), glutamate depolarized the membrane potential, which was suppressed by PBN. However, oligomycin (a mitochondrial ATP synthase inhibitor) or PPADS (a P2 receptor inhibitor) did not affect the substrates-induced depolarization. These results suggest that mitochondrial substrate-induced ROS in SG neuron directly acts on the postsynaptic neuron, therefore increasing the ion influx via glutamate receptors.