Abstract
The diamine putrescine inhibits accumulation of the herbicide paraquat into slices of rat lung. Putrescine was also shown to be accumulated into rat lung slices by an uptake process which obeyed saturation kinetics. The apparent K m for the process was 7 μM with a V max of 330 nmoles/g wet wt of lung/hr. The uptake of putrescine was enhanced when the slices were incubated in sodium deficient medium and was inhibited by iodoacetate (1 mM) together with KCN (1 mM), rotenone (100 μM), and by paraquat. Putrescine was not accumulated by slices of liver, kidney, heart or spleen to concentrations much above that in the medium. It was accumulated however by a KCN sensitive process into brain slices although the accumulation was less than that which occurred in lung slices. Lung slices taken from rats given an amount of paraquat known to damage both type I and type II lung alveolar epithelial cells were less able to accumulate putrescine or paraquat than lung slices taken from control rats. This reduction in uptake was similar for both compounds. These data have led us to conclude that (1) the process in the lung and brain which accumulates paraquat is that which is normally responsible for the uptake of putrescine in particular and diamines in general, and (2) it is the alveolar type I and type II cells of the lung which possess a receptor for the active uptake of the diamine putrescine.
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