Cellular oxygen exposure

The effects of berbamine on energy metabolism in isolated rat alveolar type II cells (cells which play a critical role in the maintenance of normal lung function) were studied. Incubation of type II cells with berbamine produced a reduction in cellular ATP content, but there was no effect of the alkaloid on cellular oxygen consumption. Berbamine produced an increase in internal calcium levels of type II cells, and incubation of the cells with calcium ionophore, 4-bromo A-23187, led to increased amounts of cellular calcium and reductions in ATP levels, with no effect on oxygen consumption. Exposure of isolated lung mitochondria to calcium produced a concentration-dependent reduction in ATP synthesis with no effect on mitochondrial oxygen... 

The reduction of the energy metabolism of normal lung tissue as indicated by decreasing oxygen-values, reflects reduced energy requirement due to reduced cellular synthesis during Rn/Rn-d exposure. 

The precise technical name of HCN is Hydrocyanic Acid. The cyanides are true protoplasmic poisons, combining in the tissues with the enzymes associated with cellular oxidation. They thereby render the oxygen unavailable to the tissues, and cause death through asphyxia. Inhaling concentrations of more than 180 ppm of HCN will lead to unconsciousness in a matter of minutes, but the fatal effects would normally be caused by carbon monoxide poisoning after HCN has made the victim unconscious. Exposure to HCN concentrations of 100 to 200 ppm for periods of 30 to 60 minutes can also cause death. 

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