Fig. 6. Working model of Cu²⁺ uptake by lobster hepatopancreatic epithelial cells and sequestration within hepatopancreatic mitochondria by transport mechanisms described in the present investigation and reported previously (Klein and Ahearn, 1999; Chavez-Crooker et al., 2001). Cu²⁺ has previously been shown to be transported across epithelial brush-border membranes (BBMs) by an antiport process that exchanges external Cu²⁺ with intracellular cations such as Na⁺ on an electroneutral, amiloride-insensitive 1Cu²⁺/2Na⁺ antiporter. Ca²⁺ derived from the luminal medium may enter the cells through a verapamil-sensitive channel and either allosterically activate the exchanger or serve as a transport substrate. Intracellular Ca²⁺ and Cu²⁺ may enter hepatopancreatic mitochondria via three possible pathways: (i) an electrogenic, Ruthenium-Red-sensitive uniporter, (ii) a diltiazem-sensitive, electroneutral 1Ca²⁺(1Cu²⁺)/2Na⁺ exchanger and a diltiazem-insensitive, electroneutral 1Ca²⁺(1Cu²⁺)/2H⁺ exchanger. Ruthenium Red (RR) appears to interact with all three transport processes. Dilt, diltiazem.

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