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PubMed2003

Delta sleep inducing peptide (DSIP): effect on respiration activity in rat brain mitochondria and stress protective potency under experimental hypoxia.

Neuromodulatory delta sleep inducing peptide (DSIP) seems to be implicated in the attenuation of stress-induced pathological metabolic disturbances in various animal species and human beings. Mitochondria, as cell organelles, are considered especially sensitive to stress conditions. In this work, the influence of DSIP and Deltaran((R))-a recently developed product based upon DSIP-on processes of oxidative phosphorylation and ATP production in rat brain mitochondria and rat brain homogenates was studied. A polarographic measurement of oxygen consumption was applied to evaluate the impact of DSIP on maximal rates of mitochondrial respiration and coupling of respiration to ATP production. We provide evidence that DSIP affected the efficiency of oxidative phosphorylation on isolated rat brain mitochondria. This peptide significantly increased the rate of phosphorylated respiration V3, while the rate of uncoupled respiration V(DNP) remaining unchanged. It enhanced the respiratory control ratio RCR and the rate of ADP phosphorylation. DSIP and Deltaran exhibited the same action in rat brain homogenates. We also examined the influence of DSIP under hypoxia when mitochondrial respiratory activity is altered. In rats subjected to hypoxia, we detected a significant stress-mediated reduction of V3 and ADP/t values. Pretreatment of rats with DSIP at the dose of 120 microgram/kg (i.p.) prior to their subjection to hypoxia completely inhibited hypoxia-induced reduction of mitochondrial respiratory activity. The revealed capacity of DSIP to enhance the efficiency of oxidative phosphorylation found in vitro experiments could contribute to understanding pronounced stress protective and antioxidant action of this peptide in vivo.

Animals↗
PubMed1999

Antioxidants and mitochondrial respiration in lung, diaphragm, and locomotor muscles: effect of exercise.

Previous studies have shown that exhaustive exercise may increase reactive oxygen species (ROS) generation in oxidative muscles that may in turn impair mitochondrial respiration. Locomotor muscles have been extensively examined, but there is few report about diaphragm or lung. The later is a privileged site for oxygen transit. To compare the antioxidant defense system and mitochondrial function in lung, diaphragm and locomotor muscles after exercise, 24 young adult male rats were randomly assigned to a control (C) or exercise (E) group. E group rats performed an exhaustive running test on a motorized treadmill at 80-85% VO2max Mean exercise duration was 66+/-2.7 min. Lung, costal diaphragm, mixed gastrocnemius, and oxidative muscles (red gastrocnemius and soleus: RG/SOL homogenate) were sampled. Mitochondrial respiration was assessed in tissue homogenates by respiratory control index (RCI: rate of uncoupled respiration/rate of basal respiration) measurement. Lipid peroxidation was evaluated by malondialdehyde concentration (MDA) and we determined the activity of two antioxidant enzymes: superoxide dismutase (SOD) and glutathione peroxidase (GPX). We found elevated basal (C group data) SOD and GPX activities in both lung and diaphragm compared to locomotor muscles (p<.001). Exercise led to a rise in GPX activity in red locomotor muscles homogenate (GR/SOL; C = 10.3+/-0.29 and E = 14.4+/-1.51 micromol x min(-1) x gww(-1); p<.05), whereas there was no significant change in lung and diaphragm. MDA concentration and mitochondrial RCI values were not significantly changed after exercise. We conclude that lung and diaphragm had higher antioxidant protection than locomotor muscles. The exercise test did not lead to significant oxidative stress or alteration in mitochondrial respiration, suggesting that antioxidant function was adequate in both lung and diaphragm in the experimental condition.

Animals↗
PubMed2000

Interactions between photosynthesis and 'light-enhanced dark respiration' (LEDR) in the flagellate Euglena gracilis after irradiation with ultraviolet radiation.

The effects of ultraviolet radiation (UV-A, 315-400 nm plus UV-B, 280-315 nm) on photosynthesis and 'light-enhanced dark respiration' (LEDR) in Euglena gracilis have been investigated by using light pulses (80 s) with increasing photon fluence rates of 59, 163, 600, 1180, 2080 and 3340 micromol m(-2) s(-1) and dark periods between the light pulses. LEDR is estimated as the maximum rate of oxygen consumption after a period of light minus the rate of oxygen consumption 30 s after the maximum rate. Without any exposure to UV radiation, the photosynthetic rate and LEDR increase with increasing photon fluence rate. After 20 and 40 min exposures to UV radiation, the photosynthetic rate and LEDR as functions of photon fluence rate are reduced. After a 20 min UV treatment respiration is greater than photosynthesis after the first light pulse of 59 micromol m(-2) s(-1) radiation, and especially at higher photon fluence rates photosynthesis is lower than the control values. The inhibitory effects of UV radiation on photosynthetic rate and LEDR are greater after a 40 min UV exposure than after a 20 min exposure. Only at 600 micromol m(-2) s(-1) is the rate of oxygen evolution greater than that of oxygen consumption after a 40 min UV treatment. Both photosynthetic rate and LEDR are inhibited by the photosynthetic inhibitor DCMU (10(-5) M) in a similar way, which indicates close regulatory interactions between photosynthesis and LEDR. Potassium cyanide (KCN) inhibits dark respiration more than it inhibits LEDR. Dark respiration is not affected to the same degree by UV radiation as are photosynthesis and LEDR.

Animals↗
PubMed1977

Inhibition of Escherichia coli growth and respiration by polymyxin B covalently attached to agarose beads.

Polymyxin B was attached to agarose beads by stable covalent bonds and the antimicrobial activity of the immobilized peptide was examined. Polymyxin-agarose inhibited the growth of Escherichia coli and Pseudomonas aeruginosa, but not Bacillus subtilis. In addition, the respiration of E. coli, E. coli spheroplasts, and B. subtilis protoplasts was inhibited by immobilized polymyxin, whereas the respiration of B. subtilis was unaffected by polymyxin-agarose. The activity of polymyxin-agarose was not due to the release of free peptide from the derivative. These data indicate that polymyxin can inhibit the growth and respiration of gram-negative bacteria by interacting with the outer surface of these cells. It is proposed that perturbation of outer membrane structure by polymyxin-agarose indirectly affected the selective permeability of the inner membrane and inhibited respiration. The results of this study emphasize the importance of outer membrane structural integrity for the normal functions of gram-negative bacteria.

Bacillus subtilis↗
PubMed2006

Inhibition of cellular respiration by doxorubicin.

Doxorubicin executes apoptosis, a process known to produce leakage of cytochrome c and opening of the mitochondrial permeability transition pores. To define the loss of mitochondrial function by apoptosis, we monitored cellular respiration during continuous exposure to doxorubicin. A phosphorescence analyzer capable of stable measurements over at least 5 h was used to measure [O(2)]. In solutions containing glucose and cells, [O(2)] declined linearly with time, showing that the kinetics of oxygen consumption was zero order. Complete inhibition of oxygen consumption by cyanide indicated that oxidations occurred in the respiratory chain. A decline in the rate of respiration was evident in Jurkat and HL-60 cells exposed to doxorubicin. The decline was abrupt, occurring after about 2 h of incubation. The inhibition was concentration-dependent and was completely blocked by the pan-caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone. Respiration in resistant HL-60/MX2 cells, characterized by an altered topoisomerase II activity, was not inhibited by doxorubicin. A decline in cellular ATP was measured in Jurkat cells after 2-4 h of incubation with 20 microM doxorubicin, paralleling the decline in respiration rate. Thus, cells incubated with doxorubicin exhibit caspase-mediated inhibition of oxidative phosphorylation.

Adenosine Triphosphate↗
PubMed1997

Similar nature of inhibition of mitochondrial respiration of heart tissue and malignant cells by methylglyoxal. A vital clue to understand the biochemical basis of malignancy.

The effect of methylglyoxal on the oxygen consumption of mitochondria of heart and of several other organs of normal animals of different species has been tested. The results indicate that methylglyoxal (3.5 mM) strongly inhibits ADP-stimulated alpha-oxoglutarate and malate plus pyruvate-dependent respiration of exclusively heart mitochondria of normal animals of different species. Whereas, with the same substrates, but at a higher concentration of methylglyoxal (7.5 mM), the respiration of mitochondria of other organs of normal animals is not inhibited. Methylglyoxal also inhibits the respiration of slices of rat and toad hearts. But this inhibition is less pronounced. However, methylglyoxal (15 mM) fails to have any effect on perfused toad heart. Using rat heart mitochondria as a model, the effect of methylglyoxal on the oxygen consumption was also tested with different respiratory substrates, electron donors at different segments of the mitochondrial respiratory chain and site-specific inhibitors to identify the specific respiratory complex which might be involved in the inhibitory effect of methylglyoxal. The results strongly suggest that methylglyoxal inhibits the electron flow through complex I of rat heart mitochondrial respiratory chain. Moreover, lactaldehyde (0.6 mM), a catabolite of methylglyoxal, can exert a protective effect on the inhibition of rat heart mitochondrial respiration by methylglyoxal (2.5 mM). The effect of methylglyoxal on heart mitochondria as described in the present paper is strikingly similar to the results of our previous work with mitochondria of Ehrlich ascites carcinoma cells and leukemic leukocytes. We have recently proposed a new hypothesis on cancer which suggests that excessive ATP formation in cells may lead to malignancy. The above mentioned similarity apparently provides a solid experimental foundation for the proposed hypothesis which has been discussed.

Animals↗
PubMed2002

A flow cytometric approach to assess phytoplankton respiration.

Microbial respiration in the ocean is considered as the major process representative of the organic matter biological oxidation. The corresponding metabolic CO2 production was estimated to be about 22 Pg C y(-1). However, the in situ respiration rate is generally too low (by several orders of magnitude) to be accessible to the available direct measurement methods. Some fluorescent probes, such as DiOC6(3) (Molecular Probes, USA) have been shown to be very sensitive to changes in the proton electrochemical potential difference (DeltamuH+), characterising mitochondrial and plasmic membranes bearing the cell respiratory system in eukaryotic and prokaryotic cells respectively. In mitochondria, DeltamuH+ is linked to the flux of oxygen uptake by a linear relationship. To our knowledge, no such relationship has been established in the case of whole marine cells. In the present work, we addressed the dark respiration rate of the Chlorophyceae Dunaliella tertiolecta (Butcher) in axenic cultures, both directly by using a highly sensitive oxygraph (Oroboros) and by staining cells with DiOC6(3). We found and standardized a linear relationship between oxygen uptake by D. tertiolecta and its green fluorescence induced by DiOC6(3), enabling the determination by flow cytometry of the respiration rate of D. tertiolecta.

Animals↗
PubMedDate not supplied

IgG from patients with liver diseases inhibit mitochondrial respiration in permeabilized oxidative muscle cells: impaired function of intracellular energetic units?

The effect of IgG purified from the sera of healthy persons and patients with primary biliary cirrhosis (PBC) and chronic hepatitis (CH) on ADP dependent respiration (oxidative phosphorylation) in skinned muscle fibers from rat oxidative muscles (heart and M. soleus) and glycolytic skeletal muscle (M. gastrocnemius) was studied. The results show that IgG from three different sources inhibited the rate of respiration by 13, 44 and 42%, respectively, these effects being equally expressed in both types of oxidative muscles, whereas no inhibition was observed in glycolytic muscle. The following washout of unbound IgG did not abolish the inhibition of respiration suggesting that the specific interaction of IgG with antigens had taken place. Laser confocal analysis revealed binding of IgG predominantly to the sarcomeric structures such as Z-disk and M-lines in the cardiomyocytes. The staining of IgG within Z-disks and intermitochondrial space coincided throughout the muscle cells so that transversally serial spaces, each containing mitochondria and adjacent sarcomere, became clearly visible. When the IgG from a CH patient was incubated with the skinned myocardial fibers of the desmin knockout mice, its binding to Z-disks and the sarcomeric area was found to be similar to that in normal cardiac muscle. However, the transversal staining pattern was disintegrated, because of the slippage of the myofibrils in relation to each other and accumulation of mitochondria between them. These observations support the recent hypothesis that in oxidative muscles the mitochondria and adjacent sarcomeres form complexes, termed as the intracellular energetic units, ICEUs. Moreover, they indicate that human autoantibodies can be useful tools for localizing the proteins responsible for formation of ICEUs and modulation of their function. Thus, it appears that the proteins associated with the Z-disks and M-lines may participate in formation of ICEUs and that binding of IgG to these proteins decreases the access of exogenous adenine nucleotides to mitochondria, which manifests as decreased rate of ADP-dependent respiration.

Animals↗
PubMed2003

Stem respiration of Populus species in the third year of free-air CO2 enrichment.

Carbon cycling in ecosystems, and especially in forests, is intensively studied to predict the effects of global climate change, and the role which forests may play in 'changing climate change'. One of the questions is whether the carbon balance of forests will be affected by increasing atmospheric CO2 concentrations. Regarding this question, effects of elevated [CO2] on woody-tissue respiration have frequently been neglected. Stem respiration of three Populus species (P. alba L. (Clone 2AS-11), P. nigra L. (Clone Jean Pourtet), and P. x euramericana (Clone I-214)) was measured in a managed, high-density forest plantation exposed to free-air CO2 enrichment (POPFACE). During the period of measurements, in May of the third year, stem respiration rates were not affected by the FACE treatment. Moreover, FACE did not influence the relationships between respiration rate and both stem temperature and relative growth rate. The results were supported by the reported absence of a FACE-effect on growth and stem wood density.

Journal Article↗
PubMed1984

Mitochondrial calcium accumulation and respiration in ischemic acute renal failure in the rat.

Changes in mitochondrial (Mito) calcium (Ca++) and Mito respiration have been demonstrated 24 hr after a renal ischemic insult. The Ca++ accumulation has been suggested to contribute to impaired Mito function; alternatively, the Mito Ca++ accumulation could be a late event resulting from cell death. The present aim was, therefore, to determine the sequence of changes in Mito function in ischemic acute renal failure (ARF) induced by 45 min of bilateral renal pedicle clamping in the rat. Animals were studied at the end of clamping, 1, 4, and 24 hr after reflow. By 24 hr, the serum creatinine level had risen progressively to almost ten times control values and fractional excretion of sodium and water were increased. Mito respiration (state 3, adenosine diphosphate-stimulated; acceptor control ratio, state 3/state 4; and uncoupled, FCCP) was severely depressed immediately after 45 min of clamping but improved significantly at 1 and 4 hr after reflow although remaining below sham-operated controls. At 24 hr, when ischemic ARF was established, Mito respiration was again severely depressed. Mito Ca++ was increased slightly but significantly at the end of clamping and increased progressively at 1, 4, and 24 hr after reflow. The Mito Ca++ accumulation was not only demonstrated to occur very early after the ischemic insult, but was relatively selective since it was not associated with Mito Mg++ accumulation. Moreover, the increased Mito Ca++ during reperfusion (1, 4, and 24 hr) demonstrated a significant correlation with the decreased state 3 respiration and the rising serum creatinine level (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1973

The occurrence of a stepwise-decreasing respiration rate during oxidative assimilation of different substrates by resting Klebsiella aerogenes in a system open to oxygen.

The addition of an oxidizable substrate to a continuous culture of Klebsiella aerogenes is known to cause an increased respiration rate that decreases in discrete steps as the added substrate is being exhausted. We have used a simple new technique to show that this phenomenon is also produced by washed, resting cells harvested from batch or continuous growth culture. The stepwise-decreasing respiration rate is caused by the exhaustion of different pools of intermediates. Each plateau of respiration rate is a measure of the activity of one or more enzymes that are rate limiting in the exhaustion of pools of intermediates. If the identities of the enzymes that are rate limiting at the different plateaux are known, the method may allow the determination, in one experiment, of the activities of up to six different enzymes in the intact bacteria. Integration of the respiration-rate measurements yields the total amount of O(2) taken up. After the addition of glucose to the washed resting bacteria 37% of the amount of O(2) required for the complete oxidation of the glucose was taken up. Acetate, pyruvate and succinate were all oxidized to the extent of 51%.

Acetates↗
PubMed1980

The H+/e- stoicheiometry of respiration-linked proton translocation in the cytochrome system of mitochondria.

1. The -->H(+)/e(-) quotients for proton release from mitochondria associated with electron flow from succinate and duroquinol to O(2), ferricyanide or ferricytochrome c, and from NNN'N'-tetramethyl-p-phenylenediamine+ascorbate to O(2), were determined from rate measurements of electron flow and proton translocation. 2. Care was taken to avoid, or to take into account, unrelated electron flow and proton translocation, which might take place in addition to the oxido-reductions that were the subject of our analysis. Spectrophotometric techniques were chosen to provide accurate measurement of the rate of consumption of oxidants and reductants. The rate of proton translocation was measured with fast pH meters with a precision of 10(-3) pH unit. 3. The -->H(+)/O quotient for succinate or duroquinol oxidation was, at neutral pH, 4, when computed on the basis of spectrophotometric determinations of the rate of O(2) consumption or duroquinol oxidation. Higher -->H(+)/O quotients for succinate oxidation, obtained from polarographic measurements of O(2) consumption, resulted from underestimation of the respiratory rate. 4. The -->H(+)/2e(-) quotient for electron flow from succinate and duroquinol to ferricyanide or ferricytochrome c ranged from 3.9 to 3.6. 5. Respiration elicited by NNN'N'-tetramethyl-p-phenylenediamine+ascorbate by antimycin-inhibited mitochondria resulted in extra proton release in addition to that produced for oxidation of ascorbate to dehydroascorbate. Accurate spectrophotometric measurement of respiration showed that the -->H(+)/e(-) ratio was only 0.25 and not 0.7-1.0 as obtained with the inadequate polarographic assay of respiration. Proton release was practically suppressed when mitochondria were preincubated aerobically in the absence of antimycin. Furthermore, the rate of scalar proton consumption for water production was lower than that expected from the stoicheiometry. Thus the extra proton release observed during respiration elicited by NNN'N'-tetramethyl-p-phenylenediamine+ascorbate is caused by oxidation of endogenous hydrogenated reductants. 6. It is concluded that (i) the -->H(+)/O quotient for the cytochrome system is, at neutral pH, 4 and not 6 or 8 as reported by others; (ii) all the four protons are released during electron flow from quinol to cytochrome c; (iii) the oxidase transfers electrons from cytochrome c to protons from the matrix aqueous phase and does not pump protons from the matrix to the outer aqueous phase.

Animals↗
PubMed1983

alpha-adrenergic stimulation of respiration in isolated rat hepatocytes.

1. The alpha-adrenergic agonists noradrenaline (in the presence of beta-blocker) and phenylephrine cause a transient stimulation of the respiration in isolated rat hepatocytes. After a lag period of 12s, this activation first attains its maximal value (+24%) for about 1 min and then falls to a sustained value (+15%). The effect is blocked by the alpha-antagonists phenoxybenzamine and phentolamine. It is dose-dependent, with an half-maximal stimulation by 16 nM-noradrenaline, which is similar to that found for other cell responses to the hormone. 2. Vasopressin and ATP, which in common with alpha-agonists are believed to increase intracellular [Ca2+], induce similar activation in the respiration rate. 3. The alpha-adrenergic-mediated respiration depends on extracellular Ca2+. The activation is decreased or abolished when extracellular [Ca2+] is decreased by adding EGTA, or when the Ca2+ antagonists Mn2+ and La3+ are present in the incubation medium. 4. It is suggested that the activation of the mitochondrial respiration rate results from the increase in cytosolic Ca2+ concentration, presumably via Ca2+ influx or Ca2+ release from the plasma membrane or endoplasmic reticulum.

Adenosine Triphosphate↗
PubMed1984

The relationship between the rate of respiration and the protonmotive force. The role of proton conductivity.

It is shown by titrating a suspension of rat liver mitochondria with either ADP or an uncoupler that a specific rate of respiration may not have a unique associated value of the protonmotive force. Alternatively, a specific protonmotive force may not be associated with a unique rate of respiration. It seems that the rate of respiration and the protonmotive force are more sensitive to the agents used for the titrations than to each other. Such observations are not easily explained by the chemiosmotic hypothesis. It is, however, possible provided that the proton conductivities, i.e. the rates of dissipation of the protonmotive force, are considered to be different for each of the agents used to titrate the rate of respiration at the same protonmotive force, or vice versa.

Adenosine Diphosphate↗
PubMed1984

Hepatic antioxidant-sensitive respiration. Effect of ethanol, iron and mitochondrial uncoupling.

The addition of the antioxidants (+)-cyanidanol-3, butylated hydroxyanisole and ascorbate to the perfused rat liver resulted in a decrease in the rate of oxygen consumption. This basal antioxidant-sensitive respiration of 110-130nmol X min-1 X (g of liver)-1 represents 5-7% of total respiration. Increased antioxidant-sensitive respiratory rates are found after the infusion of increasing concentrations of ethanol (1.8-72.2mM) or iron (35.5-248.5 microM). This respiratory component exhibits a dependence on ethanol or iron concentration, with maximal rates of 200-255 and 330nmol X min-1 X (g of liver)-1 respectively. After the addition of 100 microM-2,4-dinitriphenol, an antioxidant-sensitive respiratory component of 230nmol X min-1 X (g of liver)-1 is found, which is not observed at lower concentrations of the uncoupler (5-50 microM). The lack of effect of the antioxidants used on mitochondrial respiration [the preceding paper, Videla, Villena, Donoso, Giulivi & Boveris (1984) Biochem. J. 223, 879-883] and on the glycolytic rate of the perfused liver suggests that the basal and chemically induced antioxidant-sensitive respiration observed are related to oxygen required for one-electron transfer reactions associated with the generation of active species of oxygen and lipid peroxidation in the liver cell.

2,4-Dinitrophenol↗
PubMed1985

Respiration-dependent uptake of dihydrostreptomycin by Escherichia coli. Its irreversible nature and lack of evidence for a uniport process.

The transport of [3H]dihydrostreptomycin into the cytoplasm of Escherichia coli was distinguished, by its respiration-dependent nature, from binding within the cell envelope. 1. Of the radiolabel in the cytoplasm, 70-90% was dissolved in, or quickly equilibrated with, the cytoplasmic aqueous phase because this proportion rapidly left cells treated with toluene or with butan-1-ol. 2. After a period of respiration-dependent uptake of [3H]dihydrostreptomycin, cells were washed repeatedly by centrifugation and resuspension. Radiolabel did not leave the cells at any appreciable rate. 3. Uptake of dihydrostreptomycin (at an exogenous concentration of 1 mg of base/ml) was monitored for 2h to an apparent equilibrium. Then the specific radioactivity of exogenous dihydrostreptomycin was raised without significantly altering its chemical concentration. There was no exchange of radiolabel between the exogenous pool and the cytoplasmic pool. 4. Dihydrostreptomycin was not taken up by respiring, cytoplasm-free membrane vesicles which accumulated L-proline in control experiments. These data support the view that respiration-dependent uptake of dihydrostreptomycin by E. coli is not simply a secondary translocation process such as uniport.

1-Butanol↗
PubMed1991

Noradrenaline stimulates glucose transport in rat brown adipocytes by activating thermogenesis. Evidence that fatty acid activation of mitochondrial respiration enhances glucose transport.

The mechanisms by which noradrenaline, lipolytic agents and long-chain fatty acids stimulate glucose transport were investigated in rat brown adipocytes. Glucose transport was evaluated with tracer D-[U-14C]glucose and cell respiration was measured polarographically. Noradrenaline increased basal oxygen consumption (8-10-fold) and glucose transport (4-5-fold) in a dose-dependent manner, with a maximal stimulation at 100 nM. The stimulatory effects of noradrenaline on respiration and glucose transport were selectively mimicked by dibutyryl cyclic AMP (DBcAMP), 3-isobutyl-1-methylxanthine, cholera toxin and physiological concentrations of palmitic acid. Cytochalasin B completely blocked the effects of these agents on glucose transport. The beta-adrenergic antagonist propranolol inhibited noradrenaline-induced glucose transport, but did not affect the action of DBcAMP, palmitic acid or cholera toxin on this process. The specific inhibitor of mitochondrial carnitine palmitoyltransferase, 2-tetradecylglycidic acid (McN 3802) (50 microM), inhibited the stimulatory effects of noradrenaline (100 nM) and palmitic acid (0.5 mM) on both glucose transport and mitochondrial respiration. Significantly, McN 3802 failed to affect insulin (1 nM) action under identical experimental conditions. These results demonstrate that (a) the stimulatory effects of noradrenaline on brown-adipocyte respiration and glucose transport can be dissociated from those induced by insulin, and (b) noradrenaline increases glucose transport indirectly, by activating adenylate cyclase via beta-adrenergic pathways and by stimulating mitochondrial oxidation of fatty acids.

1-Methyl-3-isobutylxanthine↗
PubMed1996

Nitric oxide and peroxynitrite exert distinct effects on mitochondrial respiration which are differentially blocked by glutathione or glucose.

Nitric oxide (NO) and peroxynitrite both inhibit respiration by brain submitochondrial particles, the former reversibly at cytochrome c oxidase, the latter irreversibly at complexes I-III. Both GSH (IC50 =10 microM) and glucose (IC50 = 8 mM) prevented inhibition of respiration by peroxynitrite (ONOO-), but neither glucose (100 mM) nor GSH (100 microM) affected that by NO. Thus, unless ONOO- is formed within mitochondria it is unlikely to inhibit respiration in cells directly, because of reactions with cellular thiols and carbohydrates. However, the reversible inhibition of respiration cytochrome c oxidase by NO is likely to occur (e.g. in the brain during ischaemia) and could be responsible for cytotoxicity.

Animals↗