Electron transport, decreased

In erythrocytes, external oxidants such as ferricyanide increase glycolysis (Harrison et al., 1991). Since these cells have no mitochondria, the increase in glycolysis could increase lactate or pyruvate formation, and excretion of these acids could be a basis for proton movement across the plasma membrane. In cells with mitochondria, the transmembrane electron transport decreases available NADH, so lactate formation would be decreased with consequent accumulation of pyruvate. The pyruvate... 

The electron transport through PS-I seems to be influenced by the pH of the medium as shown at Fig. 4. In order to verify how coupled was the membrane ADP 2 mM was added. This resulted in a 12% stimulation of the electron transport velocity at each pH value. When gramicidine D (4 ug/ml) was utilized instead of ADP, it was noted that the stimulation of the electron transport decreased progressively with the increase of the external pH. 

The steady state level of tightly bound nucleotides is inverse to the rate of phosphorylation as a function of light intensity and uncoupler concentration (Strotmann et al. 1981). An inverse relationship between these two parameters is also observed when Mg " as a cofactor in phosphorylation is replaced by other divalent cations (Table I). With the employed metal ions the steady state level of tightly bound nucleotides increases in the order Mg2+< Mn2+< Co2+< Ca < Cu2+, while the rates of photophosphorylation and concomitant electron transport decrease in the same order. 

Light and photosynthetic electron transport convert DPEs into free radicals of undetermined stmcture. The radicals produced in the presence of the bipyridinium and DPE herbicides decrease leaf chlorophyll and carotenoid content and initiate general destmction of chloroplasts with concomitant formation of short-chain hydrocarbons from polyunsaturated fatty acids (37,97). 

From an analysis of data for polypyrrole, Albery and Mount concluded that the high-frequency semicircle was indeed due to the electron-transfer resistance.203 We have confirmed this using a polystyrene sulfonate-doped polypyrrole with known ion and electron-transport resistances.145 The charge-transfer resistance was found to decrease exponentially with increasing potential, in parallel with the decreasing electronic resistance. The slope of 60 mV/decade indicates a Nemstian response at low doping levels. 

In resting muscle the high concentration of ADP does not decrease the proton gradient effectively and the high membrane potential slows electron transport. ADP, formed when ATP is hydrolyzed by myosin ATPase during contraction, may stimulate electron transport. However, the concentration of ATP (largely as its Mg salt) is buffered by its readily reversible formation from creatine phosphate catalyzed in the intermembrane space, and in other cell compartments, by the various isoenzymes of creatine kinase (reviewed by Walliman et al., 1992). 

In rat liver mitochondria, in state 4, the AP was estimated to be about 220 mV, with the membrane potential representing about 90% of this (Nicholls, 1974 Appendix 3). Similar values have been reported for human and rat skeletal muscle mitochondria in state 4 (Stumpf et al., 1982). The control of the rate of electron transport is not only determined by the availability of ADP, but also of Pj oxidizable substrates, and oxygen. There is evidence for futile cycling of protons in intact normal rat hepatocytes (Brand et al., 1993). Recently, Porter and Brand (1993) found a correlation between the proton permeability of the inner membrane of liver mitochondria and body size in animals from the mouse (20 g) to horses (150 kg) with a decrease in permeability with increasing weight of several-fold at a constant... 

Allelopathic inhibition of mineral uptake results from alteration of cellular membrane functions in plant roots. Evidence that allelochemicals alter mineral absorption comes from studies showing changes in mineral concentration in plants that were grown in association with other plants, with debris from other plants, with leachates from other plants, or with specific allelochemicals. More conclusive experiments have shown that specific allelochemicals (phenolic acids and flavonoids) inhibit mineral absorption by excised plant roots. The physiological mechanism of action of these allelochemicals involves the disruption of normal membrane functions in plant cells. These allelochemicals can depolarize the electrical potential difference across membranes, a primary driving force for active absorption of mineral ions. Allelochemicals can also decrease the ATP content of cells by inhibiting electron transport and oxidative phosphorylation, which are two functions of mitochondrial membranes. In addition, allelochemicals can alter the permeability of membranes to mineral ions. Thus, lipophilic allelochemicals can alter mineral absorption by several mechanisms as the chemicals partition into or move through cellular membranes. Which mechanism predominates may depend upon the particular allelochemical, its concentration, and environmental conditions (especially pH). 

These results were interpreted using the electron pool hypothesis There is an electron pool situated in the linear photosynthetic electron transport chain between photosystems II and I (Fig. 9). A phobic response is triggered by a decrease in the flow rate through the pool. This can be accomplished in two ways ... 

It is important that mitochondrial oxygen radical production depends on the type of mitochondria. Recently, Michelakis et al. [78] demonstrated that hypoxia and the proximal inhibitors of electron transport chain (rotenone and antimycin) decreased mitochondrial oxygen radical production by pulmonary arteries and enhanced it in renal arteries. This difference is probably explained by a lower expression of the proximal components of electron transport chain and a greater expression of mitochondrial MnSOD in pulmonary arteries compared to renal arteries. 

Excellent electron-transporting properties of quinoxaline (also demonstrated for noncon-jugated quinoxaline-containing polymer 588 [684] and quinoxaline-based polyether 589 [685]) resulted in a substantially decreased turn-on voltage of PPV/590 PLED (3.6 V), which is much lower than that of pure PPV in the same conditions (7 V). These diodes showed a maximum luminance of 710 cd/m2 (ca. 40 times brighter than the PPV diode at the same current density and voltage) [686]. 

If electron transport is fast, the system passes from zone R to zone S+R and then to zone SR. In the latter case there is a mutual compensation of diffusion and chemical reaction, making the substrate concentration profile decrease within a thin reaction layer adjacent to the film-solution interface. This situation is similar to what we have termed pure kinetic conditions in the analysis of an EC reaction scheme adjacent to the electrode solution interface developed in Section 2.2.1. From there, if electron transport starts to interfere, one passes from zone SR to zone SR+E and ultimately to zone E, where the response is controlled entirely by electron transport. 

Pretreatment with the Type I substrate, ethylmorphine, resulted in 100% mortality in both rats and mice, and aminopyrine pretreatment resulted in 100% and 64% mortality in rats and mice, respectively, exposed to disulfoton (Pawar and Fawade 1978). Nickel chloride, cobalt chloride, or cycloheximide decreased the levels of cytochrome bs, cytochrome c reductase, and total heme in rats (Fawade and Pawar 1983). These electron transport components were further decreased in rats pretreated with these inhibitors and given a single dose of disulfoton. Data from this study suggests an additive effect, since disulfoton also decreases the activities of these components. Evidence of an additive effect between disulfoton and these metabolic inhibitors was suggested by the decrease in ethylmorphine N-demethylase and acetanilide hydroxylase activities when rats were given an inhibitor followed by disulfoton. In another experiment, these inhibitors decreased the activity of delta-aminolevulinic acid synthetase, but this decrease was reversed when disulfoton was administered. 

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