RELATIONSHIP OF THERMAL AND CHEMICAL TOLERANCE TO TRANSEPITHELIAL TRANSPORT BY CULTURED FLOUNDER RENAL EPITHELIUM

Citation
Jl. Renfro et al., RELATIONSHIP OF THERMAL AND CHEMICAL TOLERANCE TO TRANSEPITHELIAL TRANSPORT BY CULTURED FLOUNDER RENAL EPITHELIUM, The Journal of pharmacology and experimental therapeutics, 265(2), 1993, pp. 992-1000
Citations number
39
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00223565
Volume
265
Issue
2
Year of publication
1993
Pages
992 - 1000
Database
ISI
SICI code
0022-3565(1993)265:2<992:ROTACT>2.0.ZU;2-Q
Abstract
We tested the effects of mild heat shock (MHS) on tolerance of epithel ial transport processes to a chemical inhibitor and, reciprocally, che mical stress effects on tolerance to severe thermal stress. Flounder r enal tubules were cultured as monolayers on native collagen for 12 to 14 days at 22-degrees-C and mounted in Ussing chambers in which transe pithelial electrical characteristics and unidirectional [S-35]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) p revented this inhibition (92.4 +/- 5.72 nmol/cm2/hr) and stimulated tr ansport 30% (125.7 +/- 11.06 nmol/cm2/hr). Cycloheximide or actinomyci n D prevented the enhancing and protective effects of MHS. Preincubati on in 100 muM ZnCl2 for 6 hr at 22-degrees-C followed by 1.5 hr in zin c-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 sh ock protein synthesis the same as MHS. Cycloheximide prevented the mil d zinc shock effect on transport. The data show that thermal or chemic al stressors can independently induce tolerance of transepithelial tra nsport to both thermal and chemical insults and that stress-induced '' protection'' is due to enhancement of normal function rather than prev ention of damage.