Processes contributing to metabolic depression in hepatopancreas cells from the snail Helix aspersa.

Cells isolated from the hepatopancreas of the land snail Helix aspersa strongly depress respiration both immediately in response to lowered P(O2) (oxygen conformation) and, in the longer term, during aestivation. These phenomena were analysed by dividing cellular respiration into non-mitochondrial and mitochondrial respiration using the mitochondrial poisons myxothiazol, antimycin and azide. Non-mitochondrial respiration accounted for a surprisingly large proportion, 65+/-5 %, of cellular respiration in control cells at 70 % air saturation. Non-mitochondrial respiration decreased substantially as oxygen tension was lowered, but mitochondrial respiration did not, and the oxygen-conforming behaviour of the cells was due entirely to the oxygen-dependence of non-mitochondrial oxygen consumption. Non-mitochondrial respiration was still responsible for 45+/-2 % of cellular respiration at physiological oxygen tension. Mitochondrial respiration was further subdivided into respiration used to drive ATP turnover and respiration used to drive futile proton cycling across the mitochondrial inner membrane using the ATP synthase inhibitor oligomycin. At physiological oxygen tensions, 34+/-5 % of cellular respiration was used to drive ATP turnover and 22+/-4 % was used to drive proton cycling, echoing the metabolic inefficiency previously observed in liver cells from mammals, reptiles and amphibians. The respiration rate of hepatopancreas cells from aestivating snails was only 37 % of the control value. This was caused by proportional decreases in non-mitochondrial and mitochondrial respiration and in respiration to drive ATP turnover and to drive proton cycling. Thus, the fraction of cellular respiration devoted to different processes remained constant and the cellular energy balance was preserved in the hypometabolic state.