Ehrlich carcinoma and EL-4 thymoma ascites cells were subjected in vit
ro to heat shock, ATP depletion, oxidative stress, Ca2+ overloading an
d iodoacetamide treatment. After the transient stresses, Triton (X-100
)-insoluble (TIS) fractions were isolated from the cells and analysed
by electrophoresis and immunoblotting. All stresses used caused rapid
aggregation of cell proteins. This was manifested in a signficant rise
in protein content in the TIS fractions. The protein increase was mos
tly due to an increase in the insolubility of actin, 57 kDa protein of
intermediate filaments, 70 kDa heat shock protein (HSP 70), and some
specific proteins whose insolubilization was a characteristic sign for
each type of cell injury. Different survival rates in the cell lines
after either stress correlated well with differences in their TIS prot
ein accretion. Possible mechanisms for stress-induced protein aggregat
ion and its relationship with cell viability are suggested.