Relationship of thermal and chemical tolerance to transepithelial transport by cultured flounder renal epithelium.

We tested the effects of mild heat shock (MHS) on tolerance of epithelial transport processes to a chemical inhibitor and, reciprocally, chemical stress effects on tolerance to severe thermal stress. Flounder renal tubules were cultured as monolayers on native collagen for 12 to 14 days at 22 degrees C and mounted in Ussing chambers in which transepithelial electrical characteristics and unidirectional [35S]sulfate fluxes were measured. 2,4-dichlorophenoxyacetic acid (0.5 mM) lowered net active sulfate secretion 25% (93.6 +/- 7.64-69.0 +/- 9.08 nmol/cm2/hr); MHS (27 degrees C for 6 hr followed by 1.5 hr at 22 degrees C) prevented this inhibition (92.4 +/- 5.72 nmol/cm2/hr) and stimulated transport 30% (125.7 +/- 11.06 nmol/cm2/hr). Cycloheximide or actinomycin D prevented the enhancing and protective effects of MHS. Preincubation in 100 microM ZnCl2 for 6 hr at 22 degrees C followed by 1.5 hr in zinc-free medium (mild zinc stress) enhanced net sulfate flux, protected transport from severe heat stress (32 degrees C for 1.5 hr followed by 1.5 hr at 22 degrees C) and prevented 2,4-dichlorophenoxyacetic acid inhibition in a manner similar to MHS. Mild zinc shock induced heat shock protein synthesis the same as MHS. Cycloheximide prevented the mild zinc shock effect on transport. The data show that thermal or chemical stressors can independently induce tolerance of transepithelial transport to both thermal and chemical insults and that stress-induced "protection" is due to enhancement of normal function rather than prevention of damage.