Cardiac stress in glass bangle workers

The cardiac cost of work and recovery pulse rates were evaluated in 38 glass bangle workers (mean age 27.8 years, SD 3.4) exposed to radiant heat (46.2 degrees C, SD 5.1) and high ambient temperature (38.2 degrees C, SD 3.4) for a mean period of 11.0 years, SD 3.5 in the glass bangle industry. A reference group of 15 controls (mean age 27.0 years, SD 3.5 unexposed to occupational heat stress served as a comparison. The results showed that the pulse rate increased from a mean basal value of 80.0 beats.min-1, SD 2.7 to 113.2 beats.min-1, SD 11.4 in the exposed workers while in the controls the increase was negligible. Thus the cardiac cost of work was found to be 33.2 beats.min-1, SD 11.1 in the exposed group which was significantly higher (P less than 0.001) than 7.8 beats.min-1, SD 4.2 observed in the control group. Among the exposed workers, 'belanias', who were engaged in the strenuous job of manually rotating the iron roller in the Belan furnace so that the molten glass could be wound in a spiral form, showed the maximum increase in the pulse rate (42.0 beats.min-1, SD 7.5) over the work-shift followed by 'muthias' (31.1 beats.min-1, SD 4.0) who were engaged in removing the glass spirals from the Belan furnace. However, wireman ('tarkashs'), who were engaged in the highly skilled job of making very fine threads of molten glass with the help of an iron roller, showed the smallest increase (19.5 beats.min-1, SD 3.4) in pulse rate over the work-shift.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermal stress and physiological strain of children exposed to hot environments in a glass bangle factory

A group of 19 male children (mean age 12.1 years SEM 1.6 years) occupationally exposed to an excessively hot environment for an average duration of 2.5 years SEM 1.7 years in the glass bangle factory in Firozabad, India, were studied to evaluate the physiological strain induced by the thermal radiation (mean radiant temperature 46.2 degrees SEM 5.1 degrees C) and high ambient temperature (38.2 degrees SEM 3.4 degrees C) prevailing in the factory. Over a work-shift the mean increase in oral temperature was 0.90 degrees C in the exposed children, in comparison with the 0.40 degrees C increase recorded in the control children (p less than 0.05). The maximum increase in oral temperature was recorded in 'gulliwalas' (0.90 degrees C) and the minimum in 'battiwalas' (0.80 degrees C). The mean peak value of oral temperature (37.5 degrees C) was observed at 1600 hours. A significant increase in the pulse rate (25.9 beats.min-1) during the work-shift was observed in the exposed children in comparison with a mean increase of 9.4 beats.min-1 in the control group. Ventilatory studies showed pulmonary hyperventilation in the exposed workers. The increase in pulmonary ventilation was in the form of an increase in tidal volume and respiratory frequency induced by high environmental temperatures and thermal radiation. The cardio-respiratory responses showed physiological strain induced by the high ambient temperature and radiant heat prevailing in the glass bangle factory.     

Photosynthetic acclimation to high temperatures associated with heat tolerance in creeping bentgrass

Photosynthetic responses to increasing temperatures play important roles in regulating heat tolerance. The objectives of this study were to determine photosynthetic acclimation to increasing temperatures for creeping bentgrass (Agrostis stolonifera L.) and to examine changes in major photosynthetic components (photosynthetic pigments, photochemical efficiency, ribulose-1,5-bisphosphate carboxylase/oxygenase (rubisco) activity, and activation state of rubisco) involved in heat responses of photosynthesis. 'Penncross' was exposed to 20, 25, 30, and 35 degrees C for 7d at each temperature (acclimated) before being exposed to 40 degrees C for 28d or directly exposed to 40 degrees C for 28d from 20 degrees C (non-acclimated) in growth chambers. Leaf net photosynthetic rate (Pn), photochemical efficiency, rubisco activity, rubisco activation state, chlorophyll content, and carotenoid content decreased when grasses were subjected to severe heat stress at 40 degrees C for 28d. The declines in rubisco activity and activation state were most dramatic among different photosynthetic components examined in this study. Heat-acclimated plants were able to maintain significantly higher Pn, the content of chlorophyll and carotenoid, and the level of rubisco activity and activation state during subsequent exposure to severe heat stress, compared to non-acclimated plants. These results suggested that photosynthetic acclimation to increasing temperatures contributed to creeping bentgrass tolerance to severe heat stress, which was associated with the maintenance of both higher light-harvesting capacity and carbon fixation activity during heat stress.     

Characterization of high temperature induced stress impairments in thylakoids of rice seedlings.

Exposure of isolated thylakoids or intact plants to elevated temperature is known to inhibit photosynthesis at multiple sites. We have investigated the effect of elevated temperature (40 degrees C) for 24 hr in dark on rice seedlings to characterize the extent of damage by in vivo heat stress on photofunctions of photosystem II (PSII). Chl a fluorescence transient analysis in the intact rice leaves indicated a loss in PSII photochemistry (Fv) and an associated loss in the number of functional PSII units. Thylakoids isolated from rice seedlings exposed to mild heat stress exhibited >50% reduction in PSII catalyzed oxygen evolution activity compared to the corresponding control thylakoids. The ability of thylakoid membranes from heat exposed seedlings to photooxidize artificial PSII electron donor, DPC, subsequent to washing the thylakoids with alkaline Tris or NH2OH was also reduced by approximately 40% compared to control Tris or NH2OH washed thylakoids. This clearly indicated that besides the disruption of oxygen evolving complex (OEC) by 40 degrees C heat exposure for 24 hr, the PSII reaction centers were impaired by in vivo heat stress. The analysis of Mn and manganese stabilizing protein (MSP) contents showed no breakdown of 33 kDa extrinsic MSP and only a marginal loss in Mn. Thus, we suggest that the extent of heat induced loss of OEC must be due to disorganization of the OEC complex by in vivo heat stress. Studies with inhibitors like DCMU and atrazine clearly indicated that in vivo heat stress altered the acceptor side significantly. [14C] Atrazine binding studies clearly demonstrated that there is a significant alteration in the QB binding site on D1 as well as altered QA to QB equilibrium. Thus, our results show that the loss in PSII photochemistry by in vivo heat exposure not only alters the donor side but significantly alters the acceptor side of PSII.     

Higher induction of heat shock protein 72 by heat stress in cisplatin-resistant than in cisplatin-sensitive cancer cells

Induction of the heat shock proteins (HSPs) is involved in the increased resistance to cancer therapies such as chemotherapy and hyperthermia. We used two human ovarian cancer cell lines; a cisplatin (CDDP)-sensitive line A2780 and its CDDP-resistant derivative, A2780CP. The concentration of intracellular glutathione (GSH) is higher (2.7-fold increase) in A2780CP cells than in A2780 cells. A mild treatment with a heat stress (42 degrees C for 30 min) induced synthesis of both the heat shock protein 72 (Hsp72) mRNA and the HSP72 protein in A2780CP cells, but not in A2780 cells. In contrast, a severe heat stress (45 degrees C for 30 min) increased synthesis of the HSP72 protein in the two cell lines. The induced level of the HSP72 protein by the severe treatment was higher in A2780CP than in A2780 cells. The gel mobility shift assay showed that DNA binding activities of the heat shock factor (HSF) in the two cell lines were induced similarly and significantly by the mild heat stress. Immunocytochemistry using an anti HSF1 antibody also indicated that mild heat stress activated the HSF1 translocation from the cytosol to the nucleus similarly in the both cell lines. Pretreatment of CDDP-sensitive A2780 cells with N-acetyl-L-cysteine, a precursor of GSH, effectively enhanced induction of the Hsp72 mRNA by the mild heat stress. The present findings demonstrate that induction of the Hsp72 mRNA by the mild heat stress was more extensive in CDDP-resistant A2780CP cells. It is likely that the higher GSH concentration in A2780CP cells plays an important role in promoting Hsp72 gene expression induced by the mild heat stress probably through processes downstream of activation of HSF-DNA binding.     

Identification and characterization of an expansin gene AsEXP1 associated with heat tolerance in C3 Agrostis grass species

Plant tolerance of heat stress involves various changes at physiological and molecular levels. The objective of this study was to examine the expression of a gene encoding expansin protein in relation to heat tolerance in two C(3) grass species and genotypes differing in heat tolerance. Heat-tolerant, thermal Agrostis scabra, adapted to high temperatures in geothermal areas in Yellowstone National Park, was subjected to 20 degrees C (control) or 40 degrees C (heat stress) for 7 d in a growth chamber. Differential display analysis identified that a gene, AsEXP1, encoding an expansin protein, was strongly up-regulated in leaves exposed to heat stress in thermal A. scabra. Virtual northern hybridization and RT-PCR confirmed that AsEXP1 was a heat-inducible gene in leaves. The expression of AsEXP1 was induced at 1 h of plant exposure to heat stress and reached the highest level of expression at 4 h of treatment. A 1.3 kb full-length cDNA of AsEXP1 was isolated, which encodes a 251 amino acid protein. Two ecotypes of thermal A. scabra and 10 genotypes of Agrostis stolonifera (creeping bentgrass), a widely used turfgrass species in cool climatic regions, varying in the level of heat tolerance, were exposed to 40 degrees C for 7 d to examine the level of AsEXP1 expression in relation to heat tolerance. Genetic variation in heat tolerance was evaluated by measuring cell membrane stability, photochemical efficiency, and leaf growth. RT-PCR analysis revealed that the level of AsEXP1 in different genotypes was positively correlated with the level of heat tolerance in both grass species. The results first identified a heat-related expansin gene in grass species and suggest that AsEXP1 may be useful as a molecular marker to select for heat-tolerant grass germplasm.     

Heat stress preconditioning does not protect renal epithelial Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters from their modulation by severe heat stress

This study compares the effects of heat and osmotic stress on heat stress protein (HSP) production while examining the putative protective action of HSPs on modulation of Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters in Madin-Darby canine kidney (MDCK) epithelial cells by severe heat stress (46 degrees C, 15 min). Preconditioning heat stress (43 degrees C, 20 min) followed by 4 h recovery at 37 degrees C led to a 35-fold increase of HSP70 mRNA expression measured by Northern blot analysis. The protein content of HSP70 and HSP27, assessed by Western blots, was augmented by 5- and 2-fold, respectively, after 6 h of recovery. In contrast to preconditioning heat stress, hyperosmotic stress (520 vs. 320 mosm) elevated HSP70 mRNA content only by 7-fold and did not significantly affect the protein content of HSP70 or HSP27. Neither cell survival, assessed as lactate dehydrogenase (LDH) release, nor the basal activities of the ion transporters and their modulation by protein kinase C, P(2)-purinoceptor and cell volume were altered by preconditioning heat stress. Severe heat stress increased extracellular LDH content from 3+/-2 to 23+/-5% and enhanced Na(+),K(+),Cl(-) and Na(+),P(i) cotransport activity by 2-3-fold. The volume- and protein kinase C-dependent regulation of these carriers was abolished by severe heat stress while regulation by P(2)-purinoceptors was preserved. Preconditioning heat stress diminished severe heat stress-induced LDH release to 11+/-4% but did not protect Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters from activation by severe heat stress and did not prevent severe heat stress-induced inactivation of protein kinase C- and volume-dependent signaling pathways. These results show that in MDCK cells, preconditioning heat stress-induced HSPs are not involved in the regulation of Na(+),K(+),Cl(-) and Na(+),P(i) cotransporters and do not protect them from modulation by severe heat stress.     

Ascorbic acid decreases heat shock protein 70 and plasma corticosterone response in broilers (Gallus gallus domesticus) subjected to cyclic heat stress

It is known that ascorbic acid (AA) supplementation can ameliorate the chicken's responses to heat stress. The influence of AA on heart heat shock protein 70 (hsp70) and plasma corticosterone (CS) was evaluated in young male broiler chickens fed either no AA (N-AA) or 500 mg AA /kg (AA) and exposed to cyclic high temperatures (21 to 30 to 21 degrees C) over a 3.5 h period on three consecutive days. Dietary AA supplementation elevated plasma AA and maintained it at high levels after heating, but in N-AA birds, only heat elevated plasma AA. In N-AA fed chickens, plasma CS was elevated and was further increased by heat stress as compared with AA-fed birds. Heart hsp70 expression was greater in N-AA-fed chickens compared to AA-fed chickens, and heat stress further elevated hsp70 in both N-AA- and AA-fed birds. The hsp70 increase after heat was two-fold greater in N-AA- vs. AA-fed birds. Plasma CS and heart hsp70 were positively correlated, plasma AA and heart hsp70 were negatively correlated, and plasma CS and AA were negatively correlated. It was concluded that chickens experience a less severe stress response after exposure to high temperatures when they are provided dietary AA.     

Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress

The aim of this study was to elucidate the interactive effect of central hypovolemia and plasma hyperosmolality on regulation of peripheral vascular response and AVP secretion during heat stress. Seven male subjects were infused with either isotonic (0.9%; NOSM) or hypertonic (3.0%; HOSM) NaCl solution and then heated by perfusing 42 degrees C (heat stress; HT) or 34.5 degrees C water (normothermia; NT) through water perfusion suits. Sixty minutes later, subjects were exposed to progressive lower body negative pressure (LBNP) to -40 mmHg. Plasma osmolality (P(osmol)) increased by approximately 11 mosmol/kgH(2)O in HOSM conditions. The increase in esophageal temperature before LBNP was much larger in HT-HOSM (0.90 +/- 0.09 degrees C) than in HT-NOSM (0.30 +/- 0.07 degrees C) (P < 0.01) because of osmotic inhibition of thermoregulation. During LBNP, mean arterial pressure was well maintained, and changes in thoracic impedance and stroke volume were similar in all conditions. Forearm vascular conductance (FVC) before application of LBNP was higher in HT than in NT conditions (P < 0.001) and was not influenced by P(osmol) within the thermal conditions. The reduction in FVC at -40 mmHg in HT-HOSM (-9.99 +/- 0.96 units; 58.8 +/- 4.1%) was significantly larger than in HT-NOSM (-6.02 +/- 1.23 units; 44.7 +/- 8.1%) (P < 0.05), whereas the FVC response was not different between NT-NOSM and NT-HOSM. Plasma AVP response to LBNP did not interact with P(osmol) in either NT or HT conditions. These data indicate that there apparently exists an interactive effect of P(osmol) and central hypovolemia on the peripheral vascular response during heat stress, or peripheral vasodilated conditions, but not in normothermia.     

Thermotolerance of pulp cells and phagocytosis of apoptotic pulp cells by surviving pulp cells following heat stress

Apoptosis is known to be associated with wound healing and regeneration of dental pulp. We examined the effects of heat stress on clonal dental pulp cell line (RPC-C2A cells) to clarify the pulp wound healing process. RPC-C2A cells were exposed to heat stress at 43 degrees C for 45 min. After several time intervals, the inhibition of cell proliferation and apoptosis induction were analyzed by cell viability assay, DNA gel electrophoresis, nuclear staining, and terminal deoxynucleotidyl transferase mediated labeling assay. RPC-C2A cells showed the thermotolerance following heat stress. We found that apoptosis was induced in some RPC-C2A cells, whereas others remained alive, and observed the engulfment of apoptotic cells by scavenger-like RPC-C2A cells following heat stress. We also analyzed the phagocytotic activity of RPC-C2A cells and found that they had an ability to engulf apoptotic RPC-C2A cells, which was stimulated by heat stress. These results suggest that heat stress induces apoptosis of RPC-C2A cells, which are phagocytosed by the surviving RPC-C2A cells.     

Association of plasma antibodies against the inducible Hsp70 with hypertension and harsh working conditions

Autoantibodies against certain stress or heat shock proteins (Hsps) may play a role in the pathogenesis and/ or prognosis of some diseases. Using immunoblotting with human recombinant Hsps and univariate and multivariate logistic regression models, we have investigated the presence of antibodies against Hsp70, the inducible member of the 70-kDa family of heat shock proteins, and analyzed its possible association with hypertension and working conditions. Plasma and serum were collected from 764 steel mill workers from 6 work sites exposed to (1) severe noise; (2) severe noise and dust; (3) noise, dust, and heat; (4) noise and heat; (5) severe noise and heat; and (6) office conditions (control). Workers with prolonged exposure to stresses such as noise, dust, and high temperature and a combination of these in the workplace had a high incidence (26.6% to 40.2%) of antibodies to Hsp70 compared to the lowest incidence (18.6%) of antibodies to Hsp70 in the control group of office workers. Moreover, there was a statistical association of antibodies against Hsp70 with hypertension. The statistical correlation between the presence of antibodies to Hsp70 and hypertension is higher in the group of workers with blood pressure of 160/95 mmHg than in the 140/90-mmHg group after excluding possible effects of the workplace stresses. These results suggest that harsh workplace conditions can increase the production of antibodies against Hsp70 and that the presence of antibodies to this stress protein may be associated with hypertension. The precise mechanism for the elevation of antibodies against Hsps by environmental and workplace stresses and their relation to hypertension remains to be established.     

Induced thermotolerance in bovine two-cell embryos and the role of heat shock protein 70 in embryonic development

Induced thermotolerance is a phenomenon whereby exposure to a mild heat shock can induce heat shock proteins (HSP) and other cellular changes to make cells more resistant to a subsequent, more severe heat shock. Given that the 2-cell bovine embryo is very sensitive to heat shock, but can also produce HSP70 in response to elevated temperature, experiments were conducted to test whether 2-cell embryos could be made to undergo induced thermotolerance. Another objective was to test the role of the heat-inducible form of heat shock protein 70 (HSP70i) in development and sensitivity of bovine embryos to heat shock. To test for induced thermotolerance, 2-cell bovine embryos were first exposed to a mild heat shock (40 degrees C for 1 hr, or 41 degrees C or 42 degrees C for 80 min), allowed to recover at 38.5 degrees C and 5% (v/v) CO2 for 2 hr, and then exposed to a severe heat shock (41 degrees C for 4.5, 6, or 12 hr). Regardless of the conditions, previous exposure to mild heat shock did not reduce the deleterious effect of heat shock on development of embryos to the blastocyst stage. The role of HSP70i in embryonic development was tested in two experiments by culturing embryos with a monoclonal antibody to the inducible form of HSP70. At both 38.5 degrees C and 41 degrees C, the proportion of 2-cell embryos that developed to blastocyst was reduced (P < 0.05) by addition of anti-HSP70i to the culture medium. In contrast, sensitivity to heat shock was not generally increased by addition of antibody. In conclusion, bovine 2-cell embryos appear incapable of induced thermotolerance. Lack of capacity for induced thermotolerance could explain in part the increased sensitivity of 2-cell embryos to heat shock as compared to embryos at later stages of development. Results also implicate a role for HSP70i in normal development of bovine embryos.     

Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS.

The physiological mechanisms that might be involved in an association between heat stress and sudden infant death syndrome (SIDS) are obscure. We tested the hypothesis that a combination of acute hypoxia and elevated body temperature (T(B)) might prevent autoresuscitation from hypoxic apnea (AR). We exposed 21-day-old mice (total = 216) to hyperthermia (40.5-43.5 degrees C), hypoxia, or a combination of the two. Neither hyperthermia alone (40.5-42.5 degrees C) nor hypoxia alone was found to be lethal, but the combination produced failure to AR during the first hypoxic exposure with increasing frequency as T(B) increased. The ability to withstand multiple hypoxic exposures was also reduced as T(B) increased. In contrast, heat stress causing moderate T(B) increase (40.5 degrees C) had no effect on survival. Increased T(B) (43.5 degrees C) reduced gasping duration and number of gasps. It increased heart rate during anoxia but did not alter gasping rate. Furthermore, the oxygen-independent increase in heart rate observed before gasping failure was usually delayed until after the last gasp in hyperthermic animals. Mild dehydration occurred during T(B) elevation, but this did not appear to be a primary factor in AR failure. We conclude that a thermal stress, which by itself is nonlethal, frequently prevents AR from hypoxic apnea. This may be due, at least in part, to decreased gasp number and duration as well as to hyperthermia-related asynchrony of reflexes regulating heart and gasping frequencies during attempted AR.     

Genetic variation in fertility of heat-stressed male mice

The damaging effects of heat stress on male fertility are evident in developing spermatozoa expressed in ejaculates 18-28 days post-stress in mice. Our objectives were to: (1) assess genetic variation in fertility of heat-stressed male mice and (2) determine response to selection for fertility after heat stress in male mice. Mature male mice were exposed to heat stress (35+/-1 degrees C; n=50) or control (21+/-1 degrees C; n=10) conditions for 24h (day 0) and then hemicastrated for tissue collection. Two periods of mating tests followed, period 1 (from days 3 to 11) when no reductions in fertility were anticipated, and period 2 (days 18-26) when variation in fertility was expected. Period 2 pregnant females were sacrificed in late gestation. Males were indexed by multiplying overall mean ovulation rate by pre-implantation survival and number of pregnant period 2 mates. The five highest and five lowest ranking males were identified as heat stress resistant and susceptible, respectively. Resistant males were 61.2units superior in the index, 57.5% greater in pregnancy rate, and 57.6 total fetuses greater than susceptible males. Progeny of resistant sires were superior to progeny of susceptible sires in estimated breeding value by 4.5units for the index, 4.1% for pregnancy rate, and 5.2 fetuses (P<0.0001). Heritability estimates for the index, pregnancy rate, and number of fetuses ranged from 0.09 to 0.13, suggesting male fertility following heat stress is heritable and responds to selection.     

Temperature Dependent Alterations in the Pattern of Photochemical and Non-Photochemical Quenching and Associated Changes in the Photosystem II Conditions of the Leaves

The alterations in the PSII activity of leaves, subsequent toa mild or severe heat stress were characterized by monitoringthe Chl a fluorescence and thermoluminescence emission fromintact leaves. The Chl a fluorescence measurements were carriedout in leaves adapted to either ‘state I’ or ‘stateII’ since under these two conditions the photosyntheticapparatus is known to have distinctly different structure-functionrelationships. The pattern of Chl a fluorescence induction instate II-adapted leaves was different from that of state I-adaptedleaves due to the alterations in the extent of photochemical(q_Q) and non-photochemical (q_E) quenching during the time courseof induction. The pattern of changes in q_Q and q_E values wasalso altered by heat treatment depending on the severity ofheat stress; severe heat stress (47°C) suppressing theseparameters drastically. Mild heat treatment (42°C) did notaffect the ability of leaves to undergo state I to state IItransition whereas the severe heat stress totally abolishedsuch transition. The fluorescence and thermoluminescence characteristicsof the leaves that have been exposed to the severe heat stresssuggest that a large number of affected PSII units retain afunctional water-oxidizing complex at the donor side. (Received June 14, 1994; Accepted July 19, 1995)     

Characterization of goldfish heat shock protein-30 induced upon severe heat shock in cultured cells

Temperature-dependent changes of growth rate and protein components were investigated for primary cultured cells derived from goldfish caudal fin. When the culture temperature was shifted from 20 degrees C to 35 degrees C and 40 degrees C, the growth rate was increased at 35 degrees C as compared with that at 20 degrees C, but no cell growth was observed at 40 degrees C. The differential scanning calorimetry demonstrated the onset of the endothermic reaction for goldfish cellular components at 40 degrees C. Therefore, the temperature shift to 40 degrees C was found to be of severe heat shock for goldfish cultured cells. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis revealed that, although expression of 70-kDa components was slightly induced at 35 degrees C, the temperature shift to 40 degrees C markedly induced the expression of the 30-kDa component in addition to that of 70-kDa component. The N-terminal amino acid sequencing identified the 30- and 70-kDa components to be heat shock protein (Hsp)-30 and Hsp70, respectively. Northern blot analysis revealed that the enhanced Hsp30 messenger ribonucleic acid (mRNA) levels were only observed at 40 degrees C, whereas Hsp70 mRNA was slightly accumulated at 35 degrees C. These results indicated that Hsp30 might have important functions under severe heat stress condition.     

Cellular localization of HSP23 during Drosophila development and following subsequent heat shock

The low-molecular-weight heat-shock protein HSP23 is synthesized in the absence of heat shock during Drosophila development. Here, I present a quantitative analysis of this phenomenon and describe the cellular localization of this protein during normal development and after a subsequent heat shock. HSP23 is first detected in the late third instar larvae and continues to accumulate reaching a maximum level in late pupae. In a 1-week-old adult, HSP23 can no longer be detected. Following lysis of whole pupae, HSP23 is found in the soluble lysate fraction in a form which sediments between 10 and 20 S. Exposure of larvae, pupae, and the adult fly to heat stress (37 degrees C) results in an increased amount of HSP23 which, however, is recovered in an insoluble particulate form following insect lysis. During recovery from heat shock, HSP23 is again found in the soluble 10- to 20-S lysate fraction. In pupae which are exposed to a severe heat stress (41 degrees C) HSP23 remains in the pellet fraction after the heat stress and no pupae are able to emerge as adult flies. However, when pupae are first exposed to a mild heat-shock treatment prior to the 41 degrees C stress, the thermotolerance process is induced and HSP23 is again rapidly found in the soluble lysate fraction during the recovery from heat shock. These observations suggest a possible correlation between the survival of pupae after heat shock and the recovery of HSP23 in the soluble lysate fraction as 10- to 20-S structures after the heat shock.