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At least 793 records · Page 44Linked to original sources
PubMed2001

Effect of (+)-pulegone and other oil components of Mentha x Piperita on cucumber respiration.

Peppermint (Mentha x piperita L.) essential oil and main components were assessed for their ability to interfere with plant respiratory functions. Tests were conducted on both root segments and mitochondria isolated by etiolated seedlings of cucumber (Cucumis sativus L.). Total essential oil inhibited 50% of root and mitochondrial respiration (IC50) when used at 324 and 593 ppm, respectively. (+)-Pulegone was the most toxic compound, with a 0.08 and 0.12 mM IC50 for root and mitochondrial respiration, respectively. (-)-Menthone. followed (+)-pulegone in its inhibitory action (IC50 values of 1.11 and 2.30 mM for root and mitochondrial respiration respectively), whereas (-)-menthol was the less inhibitory compound (IC50 values of 1.85 and 3.80 mM respectively). A positive correlation was found for (+)-pulegone, (-)-menthone and (-)-menthol between water solubility and respiratory inhibition. The uncoupling agent. carbonyl-cyanide-m-chlorophenyl-hydrazone (CCCP), lowered (-)-menthol and (-)menthone inhibition and annulled (+)-pulegone inhibition of mitochondrial respiration, whereas salicyl-hydroxamic acid (SHAM) 2-hydroxybenzohydroxamic acid, the alternative oxidase (AO) inhibitor, increased (-)-menthone inhibition and annulled both (+)-pulegone and (-)-menthol inhibitory activity. The possible interaction of (-)-pulegone and (-)-menthol with AO and the mechanism of action of(+)-pulegone, (-)-menthone and (-)-menthol on mitochondrial respiration are discussed.

Cucumis sativus↗
PubMed2002

Nitric oxide inhibition of mitochondrial respiration and its role in cell death.

Nitric oxide (NO) or its derivatives (reactive nitrogen species, RNS) inhibit mitochondrial respiration in two different ways: (i) an acute, potent, and reversible inhibition of cytochrome oxidase by NO in competition with oxygen; and, (ii) irreversible inhibition of multiple sites by RNS. NO inhibition of respiration may impinge on cell death in several ways. Inhibition of respiration can cause necrosis and inhibit apoptosis due to ATP depletion, if glycolysis is also inhibited or is insufficient to compensate. Inhibition of neuronal respiration can result in excitotoxic death of neurons due to induced release of glutamate and activation of NMDA-type glutamate receptors. Inhibition of respiration may cause apoptosis in some cells, while inhibiting apoptosis in other cells, by mechanisms that are not clear. However, NO can induce (and inhibit) cell death by a variety of mechanisms unrelated to respiratory inhibition.

Adenosine Triphosphate↗
PubMed2002

Ultraviolet radiation has no effect on respiratory oxygen consumption or enhanced post-illumination respiration in three species of microalgae.

A 30-min exposure to UV-B radiation (1.1 Wm(-2), unweighted) from a xenon arc lamp caused pronounced inhibition (33-78%) of net photosynthetic oxygen production in three species of microalgae, Phaeodactylum tricornutum Bohlin, Dunaliella tertiolecta Butcher and Wolozynskia sp., however, no statistical differences (t-test, alpha=0.05) in dark-respiration rates were found between the control group and the UV-treated group, for any of the species tested. These results indicate: (i) that the respiratory processes responsible for oxygen consumption do not sustain any appreciable impairment registered in the first half-hour after ultraviolet radiation (UVR) exposure; and (ii) any change in respiration that may occur in response to increased repair demands is not detected in this period. Dark-respiration rates were observed to be significantly higher in all species tested (17-29%; t-test, alpha=0.05) following illumination with photosynthetically active radiation, compared to dark-respiration before illumination. This increase, interpreted as enhanced post-illumination respiration (EPIR), was observed in all three species. The magnitude of this increase was not affected by prior exposure to UVR.

Chlorophyta↗
PubMed2000

Respiration studies of penicillin solid-state fermentation.

An earlier work showed that when the bagasse content (BC) of the solid medium was decreased within a wide range of values, penicillin production by solid-state fermentation was always increased. Respiration studies were performed to understand how BC controls the secondary metabolism in this culture system. CO2 production of solid cultures with different compositions was monitored. In cultures of series A, the initial moisture content was increased and this variation was compensated by decreasing the nutrient and BC of the medium. In series B the initial moisture content was increased while BC was decreased and the nutrient content increased. In addition, penicillin production and respiration was also studied in extreme media (dry and concentrated and humid and diluted), with high and low BC. Criteria for the interpretation of respiration kinetics of the idiophase were established for the first time in this work. For the cumulative form (total CO2/g dry matter vs t) as well as for derivative (CO2/g dm/h vs t) respiration kinetics, the CO2 production rate (Q(CO2)) was determined by calculating the slope of the cumulative curve. Results indicate that Q(CO2) of the tropho- and idiophases was directly related to the BC of the solid medium (and inversely related to penicillin yields). These conclusions were confirmed by analysis of the derivative form, the results of which indicate that a lower but stable metabolic activity is essential for obtaining high penicillin yields in solid-state fermentation (SSF). The results indicate that the derivative CO2 production kinetics proved to be a more precise and sensitive indicator of the culture metabolic activity during idiophase than the cumulative respiration kinetics.

Journal Article↗
PubMed2006

Maturational changes in the rhythms, patterning, and coordination of respiration and swallow during feeding in preterm and term infants.

To study the coordination of respiration and swallow rhythms we assessed feeding episodes in 20 preterm infants (gestational age range at birth 26-33wks; postmenstrual age [PMA] range when studied 32-40wks) and 16 term infants studied on days 1 to 4 (PMA range 37-41wks) and at 1 month (PMA range 41-45wks). A pharyngeal pressure transducer documented swallows and a thoracoabdominal strain gauge recorded respiratory efforts. Coefficients of variation (COVs) of breath-breath (BR-BR) and swallow-breath (SW-BR) intervals during swallow runs, percentage of apneic swallows (at least three swallows without interposed breaths), and phase of respiration relative to swallowing efforts were analyzed. Percentage of apneic swallows decreased with increasing PMA (16.6% [SE 4.7] in preterm infants 35wks; 1.5% [SE 0.4] in term infants; p<0.001). Term infants had significantly lower BR-BR COV (0.405 [SE 0.016]) than preterm infants (0.641 [SE 0.052] at >35wks' PMA; 0.693 [SE 0.059] at <or=35wks' PMA). Phase relation between swallowing and respiration stabilized with increasing PMA, with decreased apnea, and a significant increase in percentage of swallows occurring at end-inspiration. These data indicate that unlike the stabilization of suck and suck-swallow rhythms, which occur before about 36 weeks' PMA, improvement in coordination of respiration and swallow begins later. Coordination of swallow-respiration and suck-swallow rhythms may be predictive of feeding, respiratory, and neurodevelopmental abnormalities.

Analysis of Variance↗
PubMed1986

Differential effects of resact analogues on sperm respiration rates and cyclic nucleotide concentrations.

Analogues of resact (Cys-Val-Thr-Gly-Ala-Pro-Gly-Cys-Val-Gly-Gly-Gly-Arg-LeuNH2) were synthesized to determine whether or not a stimulation of sperm respiration could be obtained independent of elevations of cyclic nucleotide concentrations. Modification of the CO2-terminal leucine NH2 did not alter biological activity; however, substitution of the two cysteinyl residues by Ser or Tyr or methylation of the cysteinyl residues resulted in divergent relative potencies dependent on whether respiration rates or cyclic nucleotide concentrations were measured. [Ser1,Tyr8]resact, as an example, was approximately 40% as potent as resact at stimulating respiration rates but was 1% as effective as resact at causing cyclic GMP elevations. An NH2-terminal fragment (Cys-Val-Thr-Gly-Ala-Pro-Gly) neither stimulated respiration nor elevated cyclic nucleotide levels at concentrations up to 10 microM whereas a CO2-terminal fragment (Cys-Val-Gly-Gly-Gly-Arg-LeuNH2) had approximately 20% of the respiration activity and 0.1% of the cyclic GMP elevating activity of resact. When the CO2- and NH2-terminal fragments were added simultaneously, however, cyclic nucleotide concentrations were elevated at the same relative concentrations as observed with resact. An analogue (125I-[Tyr1,Ser8]resact) was subsequently synthesized and used for receptor binding studies. Both the NH2-terminal and CO2-terminal fragments competed for binding, although they were 0.0004 and 0.025 times as effective as resact, respectively. However, in the presence of 1 microM resact-(1-7), resact-(8-14) was almost as potent as resact in the competitive binding assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Inhibition by light of CO(2) evolution from dark respiration: Comparison of two gas exchange methods.

Two approaches to determine the fraction (mu) of mitochondrial respiration sustained during illumination by measuring CO(2) gas exchange are compared. In single leaves, the respiration rate in the light ('day respiration' rate R(d)) is determined as the ordinate of the intersection point of A-c(i) curves at various photon flux densities and compared with the CO(2) evolution rate in darkness ('night respiration' rate R(n)). Alternatively, using leaves with varying values of CO(2) compensation concentration (Gamma), intracellular resistance (r(i)) and R(n), an average number for mu can be derived from the linear regression between Gamma and the product r(i)cR(n). Both methods also result in a number c* for that intercellular CO(2) concentration at which net CO(2) uptake rate is equal to -R(d). c* is an approximate value of the photocompensation point Gamma* (Gamma in the absence of mitochondrial respiration), which is related to the CO(2)/O(2) specificity factor of Rubisco S(c/o). The presuppositions and limitations for application of both approaches are discussed. In leaves of Nicotiana tabacum, at 22 degrees C, single leaf measurements resulted in mean values of mu = 0.71 and c(*) = 34 mumol mol(-1). At the photosynthetically active photon flux density of 960 mumol quanta m(-2) s(-1), nearly the same numbers were derived from the linear relationship between Gamma and r(i)cR(n). c* and R(d) determined by single leaf measurements varied between 31 and 41 mumol mol(-1) and between 0.37 and 1.22 mumol m(-2) s(-1), respectively. A highly significant negative correlation between c* and R(d) was found. From the regression equation we obtained estimates for Gamma* (39 mumol mol(-1)), S(c/o) (96.5 mol mol(-1)) and the mesophyll CO(2) transfer resistance (7.0 mol(-1) m(2) s).

Journal Article↗
PubMed2001

Acclimatization of soil respiration to warming in a tall grass prairie.

The latest report by the Intergovernmental Panel on Climate Change (IPCC) predicts a 1.4-5.8 degrees C average increase in the global surface temperature over the period 1990 to 2100 (ref. 1). These estimates of future warming are greater than earlier projections, which is partly due to incorporation of a positive feedback. This feedback results from further release of greenhouse gases from terrestrial ecosystems in response to climatic warming. The feedback mechanism is usually based on the assumption that observed sensitivity of soil respiration to temperature under current climate conditions would hold in a warmer climate. However, this assumption has not been carefully examined. We have therefore conducted an experiment in a tall grass prairie ecosystem in the US Great Plains to study the response of soil respiration (the sum of root and heterotrophic respiration) to artificial warming of about 2 degrees C. Our observations indicate that the temperature sensitivity of soil respiration decreases--or acclimatizes--under warming and that the acclimatization is greater at high temperatures. This acclimatization of soil respiration to warming may therefore weaken the positive feedback between the terrestrial carbon cycle and climate.

Acclimatization↗
PubMed1975

Betaine-induced stimulation of respiration at high osmolarities in a halotolerant bacterium.

It was shown that non-penetrating solutes at high concentrations inhibit the respiration of the halotolerant bacterium Ba1. Betaine relieved the inhibition caused by osmotic stress and exhibited in this respect a considerable structural specificity. The rate of oxidation of various substrates was stimulated to different extents. It stimulated the rates of both respiration and growth to a similar extent, leaving the energy yield essentially unchanged. In cells pre-loaded with labelled glutamate, betaine also stimulated the rate of oxidation of this intracellular substrate. Betaine was accumulated by respiring cells, and the maximum amount taken up was correlated with the osmolarity of the medium. As judged by chromatography, accumulated intracellular betaine underwent no chemical modification, and this accumulated betaine could not be exchanged with the betaine in the medium or released by passive efflux when respiration was inhibited. Intracellular betaine caused no stimulation of respiration, whereas betaine added to the medium increased the respiratory rate to the same extent in cells pre-loaded with betaine as that in the nonloaded cells. The above observations suggest that iso-economic adjustment is not involved in the anti-osmotic effect of betaine, and that betaine exerts its action on the cellular membrane from the outside.

Bacteria↗
PubMed1980

Energy transduction in intact synaptosomes. Influence of plasma-membrane depolarization on the respiration and membrane potential of internal mitochondria determined in situ.

A method is described, based on the differential accumulation of Rb+ and methyltriphenylphosphonium, for the simultaneous estimation of the membrane potentials across the plasma membrane of isolated nerve endings (synaptosomes), and across the inner membrane of mitochondria within the synaptosomal cytoplasm. These determinations, together with measurements of respiratory rates, and ATP and phosphocreatine concentrations, are used to define the bioenergetic behaviour of isolated synaptosomes under a variety of conditions. Under control conditions, in the presence of glucose, the plasma and mitochondrial membrane potentials are respectively 45 and 148mV. Addition of a proton translocator induces a 5-fold increase in respiration, and abolishes the mitochondrial membrane potential. The addition of rotenone to inhibit respiration does not affect the plasma membrane potential, and only lowers the mitochondrial membrane potential to 128mV. Evidence is presented that ATP synthesis by anaerobic glycolysis is sufficient under these conditions to maintain ATP-dependent processes, including the reversal of the mitochondrial ATP synthetase. Addition of oligomycin under non-respiring conditions leads to a complete collapse of the mitochondrial potential. Even under control conditions the plasma membrane (Na+ + K+)-dependent ATPase is responsible for a significant proportion of the synaptosomal ATP turnover. Veratridine greatly increases respiration, and depolarizes the plasma membrane, but only slightly lowers the mitochondrial membrane potential. High K+ and ouabain also lower the plasma membrane potential without decreasing the mitochondrial membrane potential. In non-respiring synaptosomes, anaerobic glycolysis is incapable of maintaining cytosolic ATP during the increased turnover induced by veratridine, and the mitochondrial membrane potential collapses. It is concluded that the internal mitochondria must be considered in any study of synaptosomal transport.

Adenosine Triphosphate↗
PubMed1981

Estimation with an ion-selective electrode of the membrane potential in cells of Paracoccus denitrificans from the uptake of the butyltriphenylphosphonium cation during aerobic and anaerobic respiration.

1. Aerobic respiration by cells of Paracoccus dentrificans drives the uptake of the lipophilic cation butyltriphenylphosphonium. Anaerobiosis or addition of an uncoupler of oxidative phosphorylation (carbonyl cyanide p-trifluoromethoxyphenylhydrazone) results in efflux of the cation. Changes in the concentration of butyltriphenylphosphonium in the suspension medium were measured by using an ion-selective electrode, the construction of which is described. 2. If the uptake of butyltriphenylphosphonium is used as an indicator of membrane potential, then at pH 7.3 an estimate of about 160 mV is obtained for cells of P. dentrificans respiring aerobically in 100 mM-Hepes [4-(2-hydroxyethyl)-1-piperazine-ethanesulphonic acid/NaOH or 100mM-NaH2PO4/NaOH. This potential, however, is decreased by more than 20 mV in reaction media containing a high concentration of phosphate (100 mM) together with at least 1 mM-K+. 3. Anaerobic electron transport with NO3-, NO2- or N2O as terminal electron acceptor generates a membrane potential of about 150mV in described suspension media. The presence of these species under aerobic conditions, moreover, has negligible effect upon the extent of uptake of butyltriphenylphosphonium normally driven by aerobic respiration. These data indicate that none of these molecules exert a significant uncoupling effect on the protonmotive force. 4. No 204Tl+ uptake into respiring cells was detected. This adds to the evidence that 204Tl+ is not a freely permeable cation in bacterial cells and therefore not an indicator of membrane potential as has been proposed. The absence of respiration-driven 204Tl+ uptake indicates that P. denitrificans cells grown under the conditions specified in the present work do not possess K+-transport systems of either the Kdp or TrkA types that have been described in Escherichia coli.

Aerobiosis↗
PubMed1993

Is complex II involved in the inhibition of mitochondrial respiration by N-methyl-4-phenylpyridinium cation (MMP+) and N-methyl-beta-carbolines?

It has been reported that N-methyl-beta-carbolinium analogues of the neurotoxic N-methyl-4-phenylpyridinium cation (MPP+) inhibit NADH-linked mitochondrial oxidations, as well as mitochondrial respiration on succinate nearly to the same extent [Fields, Albores, Neafsey and Collins (1992) Arch. Biochem. Biophys. 294, 539-544]. Those authors further claimed that MPP+ itself also blocks respiration through succinate dehydrogenase, in addition to its well-known effect on NADH dehydrogenase (Complex I), and concluded that both effects may contribute to the development of Parkinsonian symptoms. Since N-methyl-beta-carboliniums are thought to be endogenous metabolites, these findings, if verified, would have important implications on the etiology of idiopathic Parkinsonism. We have re-examined these observations, using mitochondria after full activation of succinate dehydrogenase, as well as submitochondrial particles, in which complexities due to membrane transport are not present. We report the following observations. (1) N-Methyl-beta-carboliniums inhibit mitochondrial respiration on NAD(+)-linked substrates in a time-dependent manner, and the inhibition is potentiated by the presence of tetraphenylboron anion (TPB-), as expected for positively charged compounds. (2) Unlike MPP+ itself, however, these compounds are uncouplers at higher concentrations, so that the effects seen in State 3 cannot be assigned exclusively to inhibition of NADH oxidation. (3) The effects on succinate oxidation in mitochondria, in which the full activity of the enzyme is expressed, are 1-1.5 orders of magnitude lower than on respiration via Complex I and are thus unlikely to contribute significantly to the neurotoxicity. (4) The effect of MPP+ on mitochondrial respiration via succinate dehydrogenase is trivial, in accord with previous reports from several laboratories, but contradicting the findings of Fields et al. (cited above). (5) In submitochondrial particles the inhibition of NADH oxidation (via the complete respiratory chain) has been confirmed, but it differs markedly from the action of MPP+ in two respects. First, the enhancement by TPB- is very small; secondly, the inhibition of NADH oxidation measured using ubiquinone (Q) analogues is far lower, suggesting that Complex I is not the only target. (6) In submitochondrial particles the inhibition of succinate oxidation by either O2 or Q analogues is incomplete, trivial or absent. (7) We thus conclude that we find no basis for assigning any potential biological effect of N-methyl-beta-carboliniums to the blockade of succinate oxidation.

1-Methyl-4-phenylpyridinium↗
PubMed1995

The nature of mitochondrial respiration and discrimination between membrane and pump properties.

A new criterion is utilized for the interpretation of flow-force relationships in rat liver mitochondria. The criterion is based on the view that the nature of the relationship between the H+/O ratio and the membrane potential can be inferred from the relationship between ohmic-uncoupler-induced extra respiration and the membrane potential. Thus a linear relationship between extra respiration and membrane potential indicates unequivocally the independence of the H+/O ratio from the membrane potential and the leak nature of the resting respiration [Brand, Chien, and Diolez (1994) Biochem. J. 297, 27-29]. On the other hand, a non-linear relationship indicates that the H+/O ratio is dependent on the membrane potential. The experimental assessment of this relationship in the presence of an additional ohmic leak, however, is rendered difficult by both the uncoupler-induced depression of membrane potential and the limited range of dependence of the H+/O ratio on the membrane potential. We have selected conditions, i.e. incubation of mitochondria at low temperatures, where the extent of non-linearity is markedly increased. It appears that the nature of the resting respiration of mitochondria in vitro is markedly dependent on the temperature: at low temperatures the percentage of resting respiration due to membrane leak decreases and that due to intrinsic uncoupling of the proton pumps increases.

Animals↗
PubMed2000

Health effects of respirator use at low airborne concentrations.

Respirators are considered a personal protective mechanism for preventing occupational disease because of inhaling toxic and hazardous substances. Engineering and work practice controls, in today's industrial environment, often maintain airborne contaminants below occupational hazardous levels. However, even at low concentrations, workers are often required to use respirators. Inappropriate use of respirators, during low exposure concentrations, may result in increased incidence and prevalence of disease from respirator use caused by physiological and psychological stress. This paper examines the hypothetical aspect of increased disease from using respirators at low exposure concentrations, with specific reference to the asbestos abatement industry.

Air Pollutants, Occupational↗
PubMed1980

Cytokinin inhibition of respiration in mitochondria from six plant species.

The influence of 6-benzylaminopurine (BAP) on the respiration by mitochondria from bush bean (Phaseolus vulgaris L.), mung bean (P. aureus Roxburgh), soybean [Glycine max (L.) Merrill], maize (Zea mays L.), pea (Pisum sativum L.), and wheat (Triticum aestivum L.) was examined. BAP, a synthetic cytokinin, consistently inhibited oxygen uptake by mitochondria from all species when malate was used as the substrate. The decrease in respiration was especially evident in the presence of ADP or an uncoupler of oxidative phosphorylation. 6-Isopentenylaminopurine and 6-furfurylaminopurine also inhibited malate oxidation, but zeatin and adenine did not. In certain instances, BAP reduced succinate and NADH oxidation. With succinate as the substrate and with antimycin A present, inhibition by BAP paralleled that caused by salicylhydroxamic acid, an inhibitor of alternative respiration. A suggested scheme features a cytokinin-inhibited point located between NADH dehydrogenase and cytochrome b of the electron transport system. Electrons from the NADH generated by malate oxidation are assumed to flow through this point, with electrons from externally supplied or cytosolic NADH and succinate doing so only under certain conditions such as when alternative respiration is occurring. Cytokinin effects on respiration and perhaps on other phenomena may be mediated by this mechanism.

Journal Article↗
PubMed1998

Nuclear-recessive mutations of factors involved in mitochondrial translation are responsible for age-related respiration deficiency of human skin fibroblasts.

We addressed the question of whether both mitochondrial and cytoplasmic translation activities decreased simultaneously in human skin fibroblasts with the age of the donors and found that the age-related reduction was limited to mitochondrial translation. Then, to determine which genome, mitochondrial or nuclear, was responsible for this age-related, mitochondria-specific reduction, pure nuclear transfer was carried out from mitochondrial DNA (mtDNA)-less HeLa cells to four fibroblast lines, two from aged subjects, one from a fetus, and one from a patient with cardiomyopathy, and their nuclear hybrid clones were isolated. A normal fibroblast line from the fetus and a respiration-deficient fibroblast line from the patient were used as a positive and a negative control, respectively. Subsequently, the mitochondrial translation and respiration properties of the nuclear hybrid clones were compared. A negative control experiment showed that this procedure could be used to isolate even nuclear hybrids expressing overall mitochondrial respiration deficiency, whereas no respiration deficiencies were observed in any nuclear hybrids irrespective of whether their mtDNAs were exclusively derived from aged or fetal donors. These observations suggest that nuclear-recessive mutations of factors involved in mitochondrial translation but not mtDNA mutations are responsible for age-related respiration deficiency of human fibroblasts.

Aging↗
PubMed2000

Direct evidence for the control of mitochondrial respiration by mitochondrial creatine kinase in oxidative muscle cells in situ.

The efficiency of stimulation of mitochondrial respiration in permeabilized muscle cells by ADP produced at different intracellular sites, e.g. cytosolic or mitochondrial intermembrane space, was evaluated in wild-type and creatine kinase (CK)-deficient mice. To activate respiration by endogenous production of ADP in permeabilized cells, ATP was added either alone or together with creatine. In cardiac fibers, while ATP alone activated respiration to half of the maximal rate, creatine plus ATP increased the respiratory rate up to its maximum. To find out whether the stimulation by creatine is a consequence of extramitochondrial [ADP] increase, or whether it directly correlates with ADP generation by mitochondrial CK in the mitochondrial intermembrane space, an exogenous ADP-trap system was added to rephosphorylate all cytosolic ADP. Under these conditions, creatine plus ATP still increased the respiration rate by 2.5 times, compared with ATP alone, for the same extramitochondrial [ADP] of 14 microM. Moreover, this stimulatory effect of creatine, observed in wild-type cardiac fibers disappeared in mitochondrial CK deficient, but not in cytosolic CK-deficient muscle. It is concluded that respiration rates can be dissociated from cytosolic [ADP], and ADP generated by mitochondrial CK is an important regulator of oxidative phosphorylation.

Adenosine Diphosphate↗
PubMed1985

Magnitude of ouabain-sensitive respiration in the liver of growing, lactating and starved sheep.

Oxygen consumption and ouabain-sensitive respiration was measured for liver biopsies from lactating and non-lactating ewes and for hepatocytes isolated from mature, dry ewes. O2 consumption, ouabain-sensitive respiration and 86Rb+ uptake were also measured for hepatocytes isolated from lambs, fed adult sheep and adult sheep starved for 5 d. Ouabain-sensitive respiration in the liver of ewes at peak lactation accounted for 45% of the total liver O2 consumption. This percentage was 24-37% higher (P less than 0.05) than measurements made during late lactation and during the non-lactating period. Total O2 consumption and ouabain-sensitive respiration rates of lamb hepatocytes were greater (P less than 0.05) than similar measurements for hepatocytes isolated from adult sheep. Ouabain-sensitive 86Rb+ uptake by hepatocytes from fed sheep was up to six times greater (P less than 0.05) than that by cells from starved sheep. The magnitude of ouabain-sensitive respiration of hepatocytes from starved sheep was 62% lower (P less than 0.05) than that for hepatocytes from fed sheep.

Animals↗