Respiration parallels, inhibition

The mitochondrial Mg2+ ATPase activity from liver and brain was inhibited by about 50-60% after an administration of 100 mg Al kg 1 body weight in the diet for a period of 90-120 days. By contrast, in the heart mitochondria, the ATPase activity increased from 73 to 212% after this treatment [38]. In this work, it was also found that ADP phosphorylation rates were decreased by 46% and that the changes in the ATPase activity, in general, were paralleled to those of the respiratory rates. The author suggested that these results imply that the effects of Al3+ treatment on respiratory activity and the ATPase activity go hand in hand. Curiously, liver and brain mitochondria presented doubled aluminum concentration and impaired respiration rate, whereas the heart mitochondria, that accumulated 11 times higher amount of aluminum, presented stimulation of respiration. Thus, an indirect action of aluminum in this tissue could be suggested. 

The mitochondrial respiratory chain consists of three proton pumps which act in series with respect to the electron flow and in parallel with respect to the proton circuit (Fig. 2.2a). Two limiting states are frequently referred to for isolated mitochondria - State 4 in which the proton current is limited by the inhibition of proton re-entry through the ATP synthase (due to either actual inhibition of the synthase or to the attainment of equilibrium), and State 3 in which there is ready proton re-entry into the matrix and hence brisk respiration. The State 3 condition can be due to an induced proton leak in the membrane or to the maintenance of AG tp below that required to equilibrate with AfiH+ (by either removing ATP, or following the addition of ADP. 

Whatever the operating mode, each respiration test requires several individual measurement units working in parallel. Each unit always includes a bioreactor and a measurement or trapping system for the criterion of interest, either C02 or 02. Several parallel units are required to test not only the material sample,but also to control the viability of the microorganisms, inherent carbon dioxide production, inhibition, etc. 

Contrary to what had earlier been supposed, there is no parallel between the anaesthetic doses of a series of depressants and their inhibition of the various enzymes isolated from the respiratory chain (see review by Butler, 1950). The concentrations of depressants required to inhibit respiration in tissues, in vitro, has always proved to be much higher than those used to produce surgical anaesthesia in humans. Thus the observed drop in cellular respiration caused by depressants is more likely to be a result of reduced nervous activity rather than a cause of it (Mcllwain, 1962). 

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