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At least 19 recordsLinked to original sources
PubMed1993

Effect of amino acid analogs on the development of thermotolerance and on thermotolerant cells.

Exposure of HA-1 Chinese hamster fibroblasts to amino acid analogs has been shown to have a heat-sensitizing effect as well as inducing the heat shock response (Li and Laszlo, 1985a). In this study, we have examined the effect of amino acid analogs on the development of thermotolerance after a brief heat shock or exposure to sodium arsenite and the effect of amino acid analogs on cells that are already thermotolerant. Exposure of HA-1 cells to amino acid analogs inhibited the development of thermotolerance following a mild heat shock or treatment with sodium arsenite. However, cells that were already thermotolerant were resistant to the sensitizing action of amino acid analogs. The refractoriness of thermotolerant cells to amino acid analog treatment developed in parallel with thermotolerance. The uptake of the arginine analog, canavanine, and its incorporation into proteins was not altered in the thermotolerant cells. Furthermore, another biological consequence of exposure to amino acid analogs, sensitization to ionizing radiation, also was not altered in the thermotolerant cells. The inhibition of the development of thermotolerance by amino acid analogs and the refractoriness of thermotolerant cells to the heat-sensitizing action of amino acid analogs lend further support the role of heat-shock proteins in the phenomenon of thermotolerance.

Amino Acids↗
PubMed2004

Salicylic acid dependent signaling promotes basal thermotolerance but is not essential for acquired thermotolerance in Arabidopsis thaliana.

Salicylic acid (SA) is reported to protect plants from heat shock (HS), but insufficient is known about its role in thermotolerance or how this relates to SA signaling in pathogen resistance. We tested thermotolerance and expression of pathogenesis-related (PR) and HS proteins (HSPs) in Arabidopsis thaliana genotypes with modified SA signaling: plants with the SA hydroxylase NahG transgene, the nonexpresser of PR proteins (npr1) mutant, and the constitutive expressers of PR proteins (cpr1 and cpr5) mutants. At all growth stages from seeds to 3-week-old plants, we found evidence for SA-dependent signaling in basal thermotolerance (i.e. tolerance of HS without prior heat acclimation). Endogenous SA correlated with basal thermotolerance, with the SA-deficient NahG and SA-accumulating cpr5 genotypes having lowest and highest thermotolerance, respectively. SA promoted thermotolerance during the HS itself and subsequent recovery. Recovery from HS apparently involved an NPR1-dependent pathway but thermotolerance during HS did not. SA reduced electrolyte leakage, indicating that it induced membrane thermoprotection. PR-1 and Hsp17.6 were induced by SA or HS, indicating common factors in pathogen and HS responses. SA-induced Hsp17.6 expression had a different dose-response to PR-1 expression. HS-induced Hsp17.6 protein appeared more slowly in NahG. However, SA only partially induced HSPs. Hsp17.6 induction by HS was more substantial than by SA, and we found no SA effect on Hsp101 expression. All genotypes, including NahG and npr1, were capable of expression of HSPs and acquisition of HS tolerance by prior heat acclimation. Although SA promotes basal thermotolerance, it is not essential for acquired thermotolerance.

Acclimatization↗
PubMedDate not supplied

Protocol for freezing thermotolerant cells and maintaining thermotolerance following thawing.

Two independent laboratories have demonstrated that suspension-grown, Chinese hamster ovary (CHO) cells can be made thermotolerant, frozen and subsequently thawed such that they still express thermotolerance. Thermotolerance was determined as the ability to protect cells against hyperthermic cell killing (colony formation assay) and the ability to reduce protein aggregation within the nuclei of heated cells. Cells were frozen either following development of full or partial thermotolerance. In the former case frozen cells maintained thermotolerance upon thawing and in the latter case cells subsequently developed full thermotolerance following thawing and incubation at 37.0 degrees C. After thawing, frozen cells displayed a temporal course of thermotolerance development and decay that was similar to that for never-frozen cells. Success was obtained using either asynchronous or synchronous cell populations, and the heat sensitivity of the cells was not altered by the freezing procedure. The experimental results demonstrate the plausibility of utilizing a frozen stock of thermotolerant cells to make thermotolerance experiments more convenient.

Animals↗
PubMed1991

Differences in thermotolerance induced by heat or sodium arsenite: correlation between redistribution of a 26-kDa protein and development of protein synthesis-independent thermotolerance in CHO cells.

In previous studies, we have demonstrated the differences in thermotolerance induced by heat and sodium arsenite (Lee et al., Radiat. Res. 121, 295-303, 1990). In this study, we investigated whether a 26-kDa protein might play an important role in evincing these differences. Chinese hamster ovary (CHO) cells treated for either 1 h with 100 microM sodium arsenite (ARS) or 10 min at 45.5 degrees C became thermotolerant to a test heat treatment at 43 degrees C administered 6 or 12 h later, respectively. After the test heating at 43 degrees C for 1.5 h, the level of 26-kDa protein in the nucleus was decreased by 92% in nonthermotolerant cells, 78% in ARS-induced thermotolerant cells, and 3% in heat-induced thermotolerant cells. Inhibiting protein synthesis with cycloheximide (CHM, 10 micrograms/ml) after ARS treatment eliminated thermotolerance to 43 degrees C and delayed restoration of the 26-kDa protein in the nucleus. In contrast, CHM neither prevented the development of thermotolerance nor inhibited the restoration of the 26-kDa protein in heat-induced thermotolerant cells. However, when cells were exposed to cold (4 degrees C), immediately after initial heating, restoration of the 26-kDa protein and development of thermotolerance did not occur. These results demonstrate a good correlation between the restoration and/or the presence of this 26-kDa protein and the development of protein synthesis-independent thermotolerance.

Acclimatization↗
PubMed1994

Chemical induction of stress proteins does not induce splicing thermotolerance under conditions producing survival thermotolerance.

Cell survival during a severe heat stress can be enhanced when heat shock proteins are induced prior to the severe heat treatment. Induction can be accomplished either by heat or chemical treatments. The increase in survival at these severe elevated temperatures after pretreatment has been referred to as thermotolerance, which we now refer to as survival thermotolerance. It has also been shown previously that mild heat treatment allows splicing in cells subjected to a severe heat treatment, now referred to as splicing thermotolerance. The experiments shown here demonstrate that even though chemical induction of the heat shock proteins leads to survival thermotolerance, this same treatment does not induce splicing thermotolerance. These are the first results that demonstrate at least two distinct aspects of thermotolerance.

Animals↗
PubMedDate not supplied

Expression of thermotolerance following microinjection of poly(A)RNA isolated from thermotolerant CHO cells.

Poly(A)RNA was isolated from thermotolerant cells and microinjected into recipient non-tolerant Chinese hamster ovary (CHO) cells. The injected cells expressed thermotolerance to a subsequent test heat treatment both in terms of the end-points of colony formation (cell survival) and resumption of protein synthesis after test heating (translational labelling). The magnitude of thermotolerance expression was dependent on the experimental end-point (increase up to 3.8-fold for translational labelling and approximately 2-fold for survival) and on the time between microinjection and the test heat treatment. Control experiments showed that poly(A)RNA from non-tolerant cells did not alter the heat response of microinjected cells. Proteins corresponding to the poly(A)RNA from thermotolerant cells were analysed by in vitro translation and by labelling of microinjected cells, followed by SDS-PAGE. In vitro translations showed high levels of transcripts for classical heat-shock proteins (HSP 70/72, 89, 110) in poly(A)RNA from thermotolerant versus control cells. However, proteins synthesized in intact cells showed no detectable differences when cells were microinjected with poly(A)RNA from thermotolerant versus control cells, or not injected at all. In principle the data show that microinjection of specific poly(A)RNA fractions can be used for defining the contribution of individual gene products to the cellular heat response.

Animals↗
PubMed1989

[Thermotolerant kinetics of HEp-2 cells and effect of thermotolerance on cytotoxicity of nitrocaphane].

The thermotolerant kinetics of HEp-2 cells and its effect on cytotoxicity of Nitrocaphane (NC) were studied by colony formation assay. HEp-2 cells were exposed to two equal thermal doses (44 degrees C, 30 min) spaced at 0-24 hr intervals during which the cells were incubated at 37 degrees C. The maximum thermotolerance developed at the 8th hr and then gradually declined. Thermal dose survival curve even up to 2.5 hr of continuous exposure to 44 degrees C, no development of thermotolerance was demonstrated. If the cells were preheated at 44 degrees C for 30 min, and returned to 37 degrees C for 10 hr and then received the second heating at 44 degrees C for 3 hr, the slope of survival curve decreased (D0 = 2.26 hr). Thermotolerant ratio was 5.9. Thermosensitive HEp-2 cells were turned into thermotolerant cells by preheating at 44 degrees C, 30 min and returning to 37 degrees C for 10 hr. The thermotolerant cells showed resistance to drug or heat when they were exposed to NC or NC combined with heat.

Antineoplastic Agents↗
PubMedDate not supplied

Effects of cis-diamminedichloroplatinum (CDDP) and cis-diammine (1,1-cyclobutanedicarboxylate) platinum (CBDCA) on thermotolerance development and thermosensitivity of the thermotolerant cells.

The interactive effects of combined treatment with heat and CDDP (0.5 micrograms/ml) or CBDCA (10 micrograms/ml) were examined on the surviving fractions of V-79 cells. Both CDDP and CBDCA treatment induced a slight enhancement in thermosensitivity of thermotolerant cells. The development of thermotolerance during step-up heating was partially inhibited by simultaneous treatment with CDDP or CBDCA throughout the heating process. Simultaneous heat treatment at 42 degrees C with either drug showed marked interactive effect and inhibited the thermotolerance developed during 42 degrees C heating.

Animals↗
PubMed1997

Physiological and biochemical characterization of intergeneric hybrids of thermotolerant and non-thermotolerant yeasts.

Kluyveromyces-like intergeneric hybrids of thermotolerant Kluyveromyces marxianus and non-thermotolerant Saccharomyces cerevisiae, produced in a previous study by protoplasmic fusion, have been characterized. On molasses, these strains produced ethanol in excess of 6% (v/v) both at 30 and 45 degrees C as against 3% and 4.2% (v/v) by the former parent at 30 and 45 degrees C, respectively. In hybrids, the increase in ethanol production appeared to be a sequel to increased activities of alcohol dehydrogenase and pyruvate kinase, derived probably from S. cerevisiae parent. Hybrid ADH-isozyme pattern on polyacrylamide gel corroborated the presence of S. cerevisiae ADH in the tested hybrids. Regression analyses indicated a positive correlation between ethanol production and ADH or PK or both (r approximately 0.76-0.84).

Hybridization, Genetic↗
PubMedDate not supplied

Time-temperature relationships for step-down heating in normal and thermotolerant cells.

Normal and thermotolerant H35 cells were submitted to step-down heating (SDH). SDH can significantly reduce the induction and expression of thermotolerance. For SDH a sensitizing treatment (ST) at 44.6 degrees C was followed by a test treatment (TT) at a lower hyperthermic temperature. The comparison between the thermotolerant and non-thermotolerant condition was based on isosurvival ST doses. For both conditions dose-effect relationships were obtained by plotting the ST-surviving fraction against the D0 of a TT. The TT was at either 41 or 42.5 degrees C, representing respectively, a permissive or a non-permissive condition for chronic induction of thermotolerance (CIT). The complex dose-effect relationships are partly exponential. In non-thermotolerant cells tested at 42.5 degrees C the dose-effect relationship between ST and TT is relatively weak. At 41 degrees C, however, the expression of CIT is strongly inhibited after a ST that kills < 20% of the cells. At higher ST doses the response is comparable with that at 42.5 degrees C. In thermotolerant cells a high degree of thermosensitization is also observed for relatively low ST doses, but in contrast with non-thermotolerant cells a stronger dose-effect relationship remains at the higher ST doses. Ultimately this results in a comparatively higher degree of thermosensitization that can be achieved in non-thermotolerant cells. For example, at an isosurviving fraction of 0.15 the reduction of D0 is non-thermotolerant cells at 42.5 degrees C is less than five times, whereas in thermotolerant cells, the D0 reduction is between 40 and 50 times. A similar reduction is found in non-thermotolerant cells tested at 41 degrees C. Subsequently, an isosurvival ST dose of about 40% was used in combination with a TT that was varied between 39 and 44 degrees C. D0's were plotted in an Arrhenius diagram to obtain a time-temperature relationship for the effect of SDH on thermotolerant and non-thermotolerant cells. The four plots are all biphasic with a downward inflection. Thermotolerance causes an upward shift of the inflection point of 2 degrees C relative to single-heated cells, whereas SDH causes a downward shift of 1 degree C in single-heated cells and of 2 degrees C in thermotolerant cells. For most of the temperature range, i.e. 39-43.5 degrees C, SDH decreases the activation energies.

Animals↗
PubMed1990

Differences in thermotolerance induced by heat or sodium arsenite: cell killing and inhibition of protein synthesis.

Chinese hamster ovary (CHO) cells became thermotolerant after treatment with either heat for 10 min at 45.5 degrees C or incubation in 100 microM sodium arsenite for 1 h at 37 degrees C. Thermotolerance was tested using heat treatment at 45 degrees C or 43 degrees C administered 6-12 h after the inducing agent. At 45 degrees C thermotolerance ratios at 10(-2) isosurvival levels were 4.2 and 3.8 for heat and sodium arsenite, respectively. Recovery from heat damage as measured by resumption of protein synthesis was more rapid in heat-induced thermotolerant cells than in either sodium arsenite-induced thermotolerant cells or nonthermotolerant cells. Differences in inhibition of protein synthesis between heat-induced thermotolerant cells and sodium arsenite-induced thermotolerant cells were also evident after test heating at 43 degrees C for 5 h. At this temperature heat-induced thermotolerant cells were protected immediately from inhibition of protein synthesis, whereas sodium arsenite-induced thermotolerant cells, while initially suppressed, gradually recovered within 24 h. Furthermore, adding cycloheximide during the thermotolerance development period greatly inhibited sodium arsenite-induced thermotolerance (SF less than 10(-6] but not heat-induced thermotolerance (SF = 1.7 X 10(-1] when tested with 43 degrees C for 5 h. Our results suggest that both the development of thermotolerance and the thermotolerant state for the two agents, while similar in terms of survival, differed significantly for several parameters associated with protein synthesis.

Animals↗
PubMed1989

Influence of cellular, microenvironmental, and growth parameters on thermotolerance kinetics in vivo in human melanoma xenografts.

The kinetics of thermotolerance in five human melanoma xenograft lines grown in BALB/c-nu/nu/BOM mice was studied in vivo. Local hyperthermia was given by immersing the tumor-bearing leg of the mice into a thermostatically regulated water bath. Specific growth delay was used as the end point for tumor response. Thermotolerance ratio (TTR), i.e., the ratio of the slopes of dose-response curves (specific growth delay versus heating time) for single-heated and preheated tumors, was used as a quantitative measure of thermotolerance. All melanoma lines developed thermotolerance; TTR reached a maximum (TTRmax) 16 to 24 h after the conditioning heat treatment and then decayed slowly. TTRmax and the time necessary to reach TTRmax tended to increase with increasing conditioning heat dose, whereas the half-time of thermotolerance decay did not change with the conditioning heat dose. The kinetics of thermotolerance differed considerably among the melanoma lines. After a conditioning heat treatment of 43.5 degrees C for 30 min, TTRmax ranged from 2.3 +/- 0.5 to 7.0 +/- 1.2, the half-time of thermotolerance decay from 53 +/- 13 h to 142 +/- 30 h and the time necessary to reach complete decay of the thermotolerance from 5 days to more than 14 days. TTRmax showed no correlation to heat sensitivity or any known growth and microenvironmental parameter of the melanoma lines. On the other hand, TTRmax was positively correlated to TTRmax measured in vitro when cells from the melanomas were studied in soft agar. However, TTRmax in vivo was always somewhat lower than TTRmax in vitro. Consequently, the development of thermotolerance in the melanomas in vivo was governed mainly by the intrinsic ability of the tumor cells to develop thermotolerance and was just slightly modified by the tumor microenvironment. The rate of thermotolerance decay was independent of TTRmax. The half-times of thermotolerance decay in vivo were longer than, and not correlated to, those measured in vitro. However, the decay half-time in vivo tended to increase with increasing tumor volume-doubling time, and to decrease with increasing growth fraction and vascular density. There was no relationship between decay half-time and fraction of radiobiologically hypoxic cells. Consequently, the rate of thermotolerance decay in the melanomas in vivo was governed mainly by tumor growth parameters and not by intrinsic characteristics of the tumor cells. The considerable difference in the kinetics of thermotolerance observed among the melanoma lines suggests that fractionated hyperthermia cannot be expected to give optimum clinical results until individualized treatment regimens are being used.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Kinetics of thermotolerance in normal and tumor tissues: a review.

Thermotolerance is a phenomenon in which cells become resistant to elevated temperatures as a result of prior or continuous exposure to hyperthermia. Thermotolerant cells exhibit a decreased slope of the cell survival curve. Recent studies disclosed that thermotolerance developed in rodent tumors and normal tissues as well. Thermotolerance develops during the treatment at a temperature below approximately equal to 43.0 degrees C, or it develops rapidly after the first heat treatment. The decay of thermotolerance is slow and is incomplete over 7 days in many normal tissues, while it appears to be completed in murine tumors. The kinetics of thermotolerance is modified by various factors. In general, the greater the initial heat damage (independently of temperature), the greater is the magnitude of thermotolerance and the longer is the time to reach maximum and the time to decay. Although thermotolerance develops less extensively in cultured cells in low pH medium and the average tumor tissue pH is lower than the normal tissue pH, the magnitude of thermotolerance in tumors thus far examined is at least equal to that in the normal tissues. Data on the interaction between thermotolerance and radiosensitivity are contradictory, although thermotolerance appears to reduce thermal radiosensitization. The kinetics of reduced sensitization is similar to that of thermotolerance. The interaction between chemotherapeutic agents and thermotolerance appears to depend on the drug and the temperature. Experimental data on this topic are still sparse and extensive studies are required.

Animals↗
PubMed1995

Thermotolerance and nuclear protein aggregation: protection against initial damage or better recovery?

Heat-induced nuclear protein aggregation and subsequent disaggregation were measured in nonpreheated and preheated (thermotolerant) HeLa S3 cells. The effect of thermotolerance on the formation of and recovery from heat-induced nuclear protein aggregates was related to the cellular levels of hsp27, hsp60, hsp70, hsc70, and hsp90. Cells heated at different time points after the thermotolerance trigger showed various levels of protection against heat-induced nuclear protein aggregation. This protection, however, did not parallel the development and decay of thermotolerance on cell survival. The protection was maximal when the thermotolerance level already had started to decay. The level of protection against nuclear protein aggregation did however parallel the cellular level of hsp70 indicating that hsp70 may be involved in this process. At all stages during the development and decay, thermotolerant cells showed a more rapid recovery (disaggregation) from the heat-induced nuclear protein aggregates than non-thermotolerant cells. The rates of disaggregation during development and decay of thermotolerance paralleled the cellular levels of hsp27 suggesting that hsp27 is somehow involved in this recovery process from heat-induced nuclear protein aggregates. The total cellular levels of none of the individual hsp's completely correlate with development and decay of thermotolerance, indicating that overexpression of any of these hsp's alone does not determine the level of thermotolerance. Clonogenic cell survival paralleled the rates of disaggregation, leading to the notion that recovery processes are the most important determinant for the thermotolerant state of HeLa S3 cells. The best correlation with clonogenic survival was found when both initial aggregation and subsequent disaggregation were taken into account, suggesting that the combined action of various hsp's in these two processes have to be included in thermotolerance development and decay.

HeLa Cells↗
PubMed1992

Splicing thermotolerance maintains Pre-mRNA transcripts in the splicing pathway during severe heat shock.

Thermotolerance, the ability of cells and organisms to withstand severe elevated temperatures after brief exposure to mild elevated temperatures, has been studied in numerous laboratories. Survival thermotolerance is defined as the increase in cell or organism survival at severe elevated temperatures after a pretreatment at mild elevated temperatures. This study examines splicing thermotolerance in Drosophila melanogaster, the ability to splice pre-mRNAs made at the severe temperature (38 degrees C) after a brief pretreatment at a milder temperature (35 degrees C). It is probably one of a number of mechanisms by which cells adapt to heat shock. These experiments demonstrate that pre-mRNAs synthesized at the severe temperatures in splicing thermotolerant cells, although protected in splicing-competent complexes, are not actually processed to mature mRNAs until the cells are returned to their normal temperature. We have also studied the kinetics of acquisition and loss of splicing thermotolerance. As little as 10 min of pretreatment at 35 degrees C was sufficient to provide full splicing thermotolerance to a 30-min severe heat shock of 38 degrees C. Pretreatments of less than 10 min provide partial splicing thermotolerance for a 30-min severe heat shock. Full splicing thermotolerance activity begins to decay about 4 h after the cessation of the 35 degrees C incubation and is completely lost by 8 h after the pretreatment. The kinetics experiments of pre-mRNAs synthesized during the 38 degrees C treatment in splicing thermotolerant cells indicate that one or more splicing thermotolerance factors are synthesized during the 35 degrees C pretreatment which interact with pre-mRNA-containing complexes to keep them in a splicing-competent state. These kinetic experiments also indicate that in cells which are partially splicing thermotolerant, the pre-mRNAs synthesized early during the 38 degrees C incubation are protected, whereas those synthesized late are not. In the absence of splicing thermotolerant factors, the pre-mRNA-containing complexes leave the normal splicing pathway and are allowed to exit to the cytoplasm.

Animals↗
PubMedDate not supplied

Characteristic synthesis and redistribution of 70 kd heat shock protein in thermotolerant Chinese hamster V79 cells.

Upon exposure to heat shock the increased rate of hsp70 synthesis decreased more rapidly in thermotolerant V79 cells than in the non-thermotolerant cells. However, the levels of hsp70 in the thermotolerant cells at 12 h after a heat shock were almost the same as those in the non-thermotolerant cells. On the other hand, the migration of hsp70 from cytoplasm to nucleoli after a heat shock was very rapid in both thermotolerant and non-thermotolerant cells, but hsp70 in the nucleoli disappeared faster in the thermotolerant cells than in the non-thermotolerant cells, and this coincided with the faster decline of hsp70 synthesis in the thermotolerant cells. For the characteristic distribution of hsp70, protein synthesis was not required. Furthermore, the induction and expression of thermotolerance by the cells were little affected by the inhibition of protein synthesis. Thus, the synthesis of hsp70 itself seemed not to be essential for the induction and expression of thermotolerance of the cells, although hsp70 may be essential for thermoresistance of cells. The rapid decrease of hsp70 synthesis and the rapid disappearance of hsp70 from the nucleoli after a heat shock may be essential for the expression of thermotolerance of the cells.

Animals↗
PubMedDate not supplied

Effects of step-down and step-up heating on the development of thermotolerance in a C3H mammary carcinoma in vivo.

The effects of step-down (SDH) and step-up heating (SUH) on the development of thermotolerance were investigated in a C3H mammary carcinoma in vivo. The endpoint was tumour growth time, i.e. the time for a tumour to reach a volume five times that of the first treatment day. SDH consisted of 44.5 degrees C/5 min followed immediately by 41.0 degrees C/120 min. SUH consisted of the same heat treatments but in reverse sequence. Thermotolerance was detected by subsequent heating at 43.5 degrees C at variable intervals following the primary SDH or SUH. The degree of thermotolerance was quantified by the thermotolerance ratio (TTR) calculated as a ratio between the slope of the dose-response curve for tumours heated at 43.5 degrees C and tumours preheated with either SDH or SUH followed by 43.5 degrees C. Both SDH and SUH induced thermotolerance. However, the maximal degree of thermotolerance and the time interval to reach maximum thermotolerance were different. For SUH maximal thermotolerance was observed at 8 h with a TTR of 3.6. For SUH, thermotolerance peaked at 24-28 h with a TTR of 7.3. In both cases thermotolerance had decayed with a 120 h interval. The SDH priming induced about 2.5 times more heat damage than SUH. The results are therefore in agreement with previous data obtained in the same tumour model by single heating showing that both the degree and the time to reach maximal thermotolerance increases with pretreatment heat damage. In addition, the results indicate that thermotolerance and thermosensitization are independent phenomena.

Animals↗