{'fraction_non_alphanumeric': 0.03064066852367688, 'fraction_numerical': 0.0350974930362117, 'mean_word_length': 5.507246376811594, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Constitutive and inducible hsp70s are involved in oxidative resistance evoked by heat shock or ethanol.

Improved cardiac post-ischemic recovery after whole-body hyperthermia is correlated with an increased expression of the heat shock proteins (hsps). The inducible hsp70 (hsp70i) has a known cardioprotective effect against ischemia/reperfusion injury. Here, we studied whether other hsps are also involved in cardioprotection. Using rat heart-derived H9c2 myocytes, we observed that preheating at 43 degreesC for 20 min conferred resistance to hydrogen peroxide (H2O2). The resistance to mild H2O2 toxicity (3-5 micro mol/10(7) cells) appeared early and persisted, whereas the resistance to moderate H2O2 toxicity (6-9 micro mol/10(7) cells) was detectable only at 20-44 h post heat shock. No resistance was observed at higher doses of hydrogen peroxide (10-12 micro mol/10(7) cells), indicating that severe toxicity exceeds the capacity of the induced protective mechanism. Coincidentally, this thermal regimen elicited a rapid and prolonged increase in the cellular level of hsp70i, and a delayed and transient induction of the constitutive hsp70 (hsp70c). Nuclear translocations of hsp70i and hsp70c also occurred upon heat stimulation. A homogeneous distribution of the accumulated hsp70i and hsp70c throughout the nuclei and cytoplasm paralleled the development of heat-induced resistance to moderate H2O2 challenge. Application of another hsp inducer, ethyl alcohol, evoked a similar pattern of H2O2 resistance, and hsp induction and distribution. Our results suggest that induction and subcellular distribution of hsp70s contribute importantly to cellular antioxidant defenses, and that a co-operation between hsp70i and hsp70c may improve cardiac preservation during oxidative insult.