Km. Gaudio et al., ROLE OF HEAT-STRESS RESPONSE IN THE TOLERANCE OF IMMATURE RENAL TUBULES TO ANOXIA, American journal of physiology. Renal, fluid and electrolyte physiology, 43(6), 1998, pp. 1029-1036
The stress response was studied in suspensions of tubules from immatur
e (IT) and mature (MT) rats after noninjury, heat, oxygen, and anoxia.
Under all conditions, IT exhibited more exuberant activation of heat
shock transcription factor (HSF) than MT. Characterization of activate
d HSF in immature cortex revealed HSF1. Also, 2 h after each condition
, heat shock protein-72 (HSP-72) mRNA was twofold in IT. As the metabo
lic response to 45 min of anoxia, 20-min reoxygenation was assessed by
measuring O-2 consumption (O2C). Basal O2C was manipulated with ouaba
in, nystatin, and carbonylcyanide p-chloromethyoxyphenylhydrazone (CCC
P). Basal O2C in IT were one-half the value of MT. After anoxia, basal
O2C was reduced by a greater degree in MT. Ouabain reduced O2C to hal
f the basal value in both noninjured and anoxic groups. Basal O2C was
significantly stimulated by nystatin but not to the same level followi
ng anoxia in MT and IT. Basal O2C was also stimulated by CCCP, but aft
er anoxia, CCCP O2C was significantly less in MT with no decrease in I
T, suggesting mitochondria are better preserved in IT. Also, O2C devot
ed to nontransport activity was better maintained in IT.