A few species with the most powerfully thermogenic flowers also exhibit temperature regulation, which is the maintenance of a relatively constant temperature in the flower, regardless of external air temperature. Rather precise thermoregulation has been discovered in P. Knutson ; Ito et al. At low ambient temperatures during the night, heat production by the flower rises to about 1 Watt. Respiration clearly responds to ambient temperature, not time of day Seymour and Schultze-Motel However, it is apparent that the flowers do not detect ambient temperature directly, but instead respond to changes in the temperature of their own cells.
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Close examination of the data reveals that there is a small decrease in flower temperature that occurs with falling ambient temperature see Figure 3. Therefore is it clear that respiration in these species is negatively related to tissue temperature, opposite to the usual positive relationship between temperature and rates of biochemical reactions.
Recent results from three thermoregulatory species show steeply decreasing respiration as tissue temperature increases Figure 4. What causes this inhibition is still unknown, but it is entirely reversible, and temperature regulation occurs within a relatively narrow range of tissue temperature. As environmental temperature decreases, the rate of heat loss increases, causing a decrease in tissue temperature.
But this in turn causes heat production to rise to a level that matches the rate of heat loss, and tissue temperature stabilizes. Further decreases in environmental temperature cause further decreases in tissue temperature and rises in respiration rate. Thus below the switching temperature, thermoregulation is impossible. The dashed line is isothermal, showing that evaporative heat loss predominates at high ambient temperatures, but metabolic heat production prevails at low ambient temperature.
The means were derived from intact flowers in the field, during the thermoregulatory period associated with female receptivity. The inset shows a flower cut in half, revealing the yellow receptacle that is obviously warm in the thermal image. From Seymour and Schultze-Motel The curves fitted to the data indicate the precision of temperature regulation, with Nelumbo being the most precise, followed by Symplocarpus and Dracunculus. From Seymour et al.
Heat production in thermogenic plants has been generally considered to be associated with an increase in activity of the cyanide-resistant electron transport pathway in mitochondria Vanlerberghe and McIntosh The free energy created by the flow of electrons from ubiquinol to AOX does not generate ATP; instead, it is lost as heat. The AOX pathway seems to be present in all plants in varying capacities, although it is particularly active in thermogenic species see Web Topic Plant AOX activity is generally regulated not only through transcriptional control but also by two interrelated posttranslational mechanisms.
To date, AOX activities have been analyzed at the molecular level in four thermogenic species: Sauromatum guttatum , Symplocarpus renifolius , Nelumbo nucifera , and Arum maculatum. Among these plants, only N. In contrast, A. Recent bioinformatic and functional analyses have suggested that an element consisting of three adjacent residues, termed ENV Glu-Asn-Val , is critical for the regulation Albury et al.
Filled red circles show the di-iron center. The black star marks the position of the ENV motif.
Pyruvate-sensitive, succinate-sensitive, and pyruvate-insensitive and constitutively active AOXs are boxed in red, blue, and green, respectively. Ubiquinone UQ is a redox intermediate of the mitochondrial respiratory chain that translocates electrons from dehydrogenases to the cytochrome pathway and AOX. In contrast, the UQ pool in the thermogenic appendices of A. As mentioned before, plant AOXs are more active in their reduced forms, so a highly reduced UQ pool facilitates maximal AOX activity for thermogenesis. However, analysis of the redox state of the UQ pool in vivo has shown that the reduction level in the thermogenic and post-thermogenic spadices of S.
Data from Wagner et al. UQ reduction levels in thermogenic Hot and post-thermogenic Post tissues are represented by white circles and black triangles, respectively. The reduction state of UQ is a reflection of the metabolic balance between the rate at which the upstream dehydrogenases reduce oxidized UQ and the rate at which reduced UQ is oxidized by the AOX and cytochrome c oxidase pathways. The regulatory mechanisms that control the redox status of the UQ pool in thermoregulating S.
A recent comparative study of respiratory component expression in mitochondria showed abundant expression of a type II NAD P H dehydrogenase NDB found on the external face of the mitochondrial inner membrane in A. Therefore, it is possible that such factors, which control electron flow in the mitochondrial respiratory chain, are involved in the molecular mechanisms of thermoregulation in plants. Points were experimentally determined rates as follows: a , nonmitochondrial Fig. Mitochondrial membrane potential with oligomycin was assumed to be similar to that determined for mitochondria within synaptosomes A mV potential drop was assumed sufficient for maximal respiration Because substrate oxidation rate is a linear function of membrane potential 22 , 44 , potentials associated with points d-f were set according to this slope i.
The nonlinear control proton leak curve ii was drawn based on points a-c , whereas the curve after glutamate treatment iii was drawn based on points a and d , assuming that respiration driving the leak is similar to the control curve at potentials giving maximal respiration. Pyruvate supplementation did not significantly affect basal respiration, indicating that in this state glycolysis provides adequate substrate to the mitochondrion. However, during uncontrolled respiration glycolytic substrate supply to the mitochondria limits respiratory chain activity because pyruvate significantly enhanced the FCCP effect.
Moreover, under the present incubation conditions, which prevent induction of apoptosis, these CGN preparations had insufficient glycolytic activity to maintain prolonged basal function in the presence of oligomycin Fig. Most important, pyruvate decreases cell death Fig. Acute Effects of Glutamate —A key finding from this study is that under the present conditions glutamate exposure acutely stimulates CGN respiration submaximally.
Pyruvate supplementation did not further increase the response to glutamate Fig. Thus, glycolysis was capable of supplying necessary substrate to sustain the higher respiratory chain activity, and oxidative phosphorylation was capable of supplying sufficient ATP to meet the energy demand imposed by glutamate.
Atlante et al. Surprisingly, they observed a total inhibition of respiration by ouabain both in control and glutamate-exposed neurons, suggesting that their assay was insufficiently sensitive to detect the respiration under conditions of low ATP demand.
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The decreased state 3 rate could reflect either an inhibited respiratory chain or a decreased yield of mitochondria because of cell death. In a related study, Almeida et al. They reported a modest decrease in respiration, but the ability of the preparation to respond to succinate indicated extensive damage resulting from the manipulations. Clearly ion influx through this receptor stimulates ATP turnover but not to such a degree that demand exceeds supply.
The analysis to distinguish ATP turnover from uncoupled respiration was performed. The second analysis was performed by acute addition of oligomycin to inhibit ATP synthase Fig. The CGN preparations used in Fig. Oligomycin blocked oxidative phosphorylation after a short delay Figs.gatsbybuild.co.uk/chin-chin-el-teporocho-novela.php
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Chronic Glutamate Exposure —An important finding of this study is that mitochondria in surviving CGNs do not show diminished respiratory capacity after 3 h of continuous glutamate exposure. Previous attempts to monitor the effects of glutamate exposure on neuronal respiration e. These cells retain protonophore-releasable respiratory control.
From this perspective, the assumption that glutamate-treated cells that undergo these changes do not respire seems valid. Although this uncertainty does not affect our conclusions that cells exposed to glutamate retain normal mitochondrial function until cell death, it is clear that more experiments are required to determine the variable s that more accurately differentiate an oxygen-consuming cell from one that is truly dead. Glycolytic failure did occur with oligomycin because uncontrolled respiration with pyruvate supplementation was much greater than with glucose alone Fig.
In Fig. The plateau was not sustained in the cell depicted in Fig. Careful inspection of the respiration traces in Fig. In both cases the increase amounted to 0. Taken together, the data indicate that glutamate-induced DCD is associated with a loss of respiration rather than pronounced uncoupling. Chronic Glutamate Exposure with Pyruvate —Pyruvate supplementation significantly attenuates glutamate excitotoxicity Table I.
This protection cannot be attributed to enhanced mitochondrial substrate supply because glutamate did not maximally stimulate respiration and pyruvate did not further enhance glutamate-stimulated rate, in contrast to its effects on uncontrolled respiration. Surprisingly, cells that remained viable after 3 h of continuous glutamate exposure exhibited a pronounced reduction in maximal respiratory capacity Fig. Clearly, pyruvate protection from glutamate excitotoxicity cannot be ascribed to improved mitochondrial function, as indicated by respiratory capacity.
This is not surprising given that chronic glutamate exposure imposed very little energy demand above the basal state Fig. Previous studies 18 , 38 - 42 have shown that pyruvate-supplemented media protect neurons from glutamate- or NMDA-mediated excitotoxicity. Conclusions —The oxygen electrode has proven over the years to be the most versatile apparatus for investigating the function of isolated mitochondria and cells that exist in suspension.
The lack of a similar device for cultured neurons and other cells attached to a substrate has restricted investigations of in situ mitochondrial function in such preparations. The hypotheses that glutamate stimulates CGN respiration maximally, that the increase is entirely the result of increased ATP demand, and that excitotoxicity is associated with a loss of reserve ATP-generating capacity are not valid for the present experimental conditions, although the data support the hypothesis that the NMDA receptor is a significant contributor to the overall energy demand imposed by glutamate.
It has not escaped our attention that studies to investigate neuronal bioenergetic changes associated with apoptosis and other stresses are equally feasible with this technique. The costs of publication of this article were defrayed in part by the payment of page charges. Section solely to indicate this fact.
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