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PubMed1987

The influence of pH on heat denaturation of anti-haemophilic cryoprecipitate.

The influence of pH on heat denaturation of anti-haemophilic cryoprecipitate (CP) was studied by using phosphate and citrate buffers at three different pH levels for processing lyophilized, heat treated CP. The solubility and the content of FVIII:C and fibrinogen were determined following heating at 68 degrees C for 24 hours and compared to "ordinary", non-heated CP. Both the solubility and the biological activity were best preserved in the most acidic samples (pH 5.7-6.7), these batches equalled non-heated CP. At higher pH, heat treatment resulted in reduced solubility and a more pronounced loss of FVIII:C and fibrinogen. Amino acids (Syntamin 17) have previously been shown to stabilize CP during heat treatment. Some of the stabilizing effect seems to be due to a large buffering capacity, maintaining a low pH during lyophilization and heating. Raising the pH level in Syntamin-CP from 6.6 to 7.8 resulted in decreased solubility and FVIII:C content. The quality of heat treated, acidic Syntamin-CP was comparable to that of heated, acidic phosphate- and citrate-CP. We conclude that buffers used for processing heat treated CP should be of low pH, and that acidic buffers may replace Syntamin without lowering the quality of the heated product.

Amino Acids↗
PubMed1980

Translational control of protein synthesis in response to heat shock in D. melanogaster cells.

In response to elevated temperature, Drosophila cells synthesize a small set of proteins known as the heat-shock proteins, while synthesis of most other proteins ceases. In vitro translation has been used to demonstrate that the messenger RNAs encoding the normal (25 degrees) spectrum of proteins are not broken down or irreversibly inactivated in response to the temperature change. During the heat shock only the heat-shock mRNAs plus a small number of preexisting mRNAs are translated, while most other messages are stored and can be reactivated upon return of the cells to their normal temperature. After recovery from heat shock, cells translate both the normal mRNA and the remaining heat-shock mRNA. The translational control operating in intact cells has been reproduced in cell-free translation systems directed by purified mRNA from normal and heat-shocked cells. Lysates prepared from heat-shocked Drosophila cells preferentially translated the heat-shock messages, while the lysate made from normally growing Drosophila cells indiscriminately translated both normal and heat-shock messages. Therefore there must be stable alterations in the translational components of heat-shocked cells which are capable of causing selective translation of the heat-shock messages. In addition there must be information encoded in the heat-shock messages that allows their selection.

Animals↗
PubMed2001

Changes in cytosolic calcium in response to noxious heat and their relationship to vanilloid receptors in rat dorsal root ganglion neurons.

Heat transduction mechanisms in primary nociceptive afferents have been suggested to involve a vanilloid receptor channel with high calcium permeability. To characterize the changes in free cytosolic calcium evoked by noxious heat stimuli (< or =51 degrees C, 10s), we performed microfluorometric measurements in acutely dissociated small dorsal root ganglion neurons (< or =32.5 microm) of adult rats using the dye FURA-2. Only neurons that responded with a reversible increase in intracellular calcium to high potassium were evaluated. Heat-induced calcium transients (exceeding mean + 3S.D. of the temperature dependence of the dye) were found in 66 of 105 neurons. These transients increased non-linearly with temperature. In contrast, heat-insensitive neurons showed a small linear increase of intracellular calcium throughout the range of 12-49 degrees C, similar to cardiac muscle cells. The vanilloid receptor agonist capsaicin induced calcium transients in 72 of 99 neurons. Capsaicin sensitivity and heat sensitivity were significantly associated (P<0.001, chi(2)-test), but 16 of 34 heat-insensitive cells responded to capsaicin and four of 49 heat-sensitive cells were capsaicin insensitive. The competitive vanilloid receptor antagonist capsazepine (10 microM) reversibly reduced the heat-induced calcium transients by 47+/-13%. In contrast, high potassium-induced calcium transients were not affected by pre-incubation with capsazepine. In calcium-free extracellular solution, the heat-induced rise in intracellular calcium was reduced by 76+/-5%. Heat-induced calcium transients were also reversibly reduced by 75+/-6% in sodium-free solution and by 62+/-7% with the L-type calcium channel blocker nifedipine (5 microM). These results indicate that noxious heat rapidly increases intracellular calcium in nociceptive primary sensory neurons. Heat-sensitive vanilloid receptors are involved in the induction of calcium transients, and calcium is also released from intracellular stores, but the main fraction of calcium passes through voltage-operated calcium channels.

Animals↗
PubMed1990

Heat sensitivity and thermotolerance in vitro of human breast carcinoma, malignant melanoma and squamous cell carcinoma of the head and neck.

Heat sensitivity and the development of thermotolerance of cells isolated directly from surgical specimens of human breast carcinoma, malignant melanoma and squamous cell carcinoma of the head and neck were studied in vitro using the Courtenay soft agar colony assay. The plating efficiency of some of the tumours was sufficiently high (0.3-20.4%) for survival curves covering up to two to three decades to be established. Experiments repeated with cells stored in liquid nitrogen showed that the survival assay gave highly reproducible results. Heat sensitivity of thermotolerant cells was studied by giving cells a conditioning heat treatment of 43.5 degrees C for 60 min and, after incubation at 37 degrees C for 24 h, second graded heat treatments at 43.5 degrees C. Significant differences in heat sensitivity and development of thermotolerance between the three tumour types were not found. However, the heat sensitivity, whether the cells were thermotolerant or not, differed considerably among individual tumours of each histological category. Do at 43.5 degrees C was found to be in the ranges of 23-59 min (breast carcinoma), 20-63 min (malignant melanoma) and 20-57 min (squamous cell carcinoma) for single-heated cells and 105-476 min (breast carcinoma). 102-455 min (malignant melanoma) and 87-400 min (squamous cell carcinoma) for thermotolerant cells. The heat sensitivity of cells made thermotolerant showed no significant correlation to the surviving fraction after the conditioning heat treatment. The study indicated that histological category is a poor parameter for assessment of clinical heat responsiveness of tumours. Breast carcinoma, malignant melanoma and squamous cell carcinoma are probably, from a thermobiological point of view, equally good candidates for clinical trial aimed at studying the potential usefulness of hyperthermia as an adjunct to radiation therapy and/or chemotherapy. The large differences in heat sensitivity and development of thermotolerance observed among individual tumours, irrespective of histological origin, suggested that an in vitro predictive assay for heat responsiveness would be very useful for stratification purposes in such clinical trials.

Breast Neoplasms↗
PubMed2006

Body temperature responses in spinal cord injured individuals during exercise in the cold and heat.

The aim of this study was to assess the effect of arm exercise on the heat balance in spinal cord-injured (SCI) individuals with complete lesions at ambient temperatures of 10 and 35 degrees C. Four SCI with a high lesion (> or = T6) (SCI-H), seven with a low lesion (< T6) (SCI-L), and ten able-bodied controls (AB) performed arm-cranking exercises at 40 % of the maximal power output for 45 min, once in 10 degrees C and once in 35 degrees C. Oxygen uptake, rectal temperature, and skin temperature (chest, upper arm, thigh, calf) were measured at rest and 15, 30, and 45 min after the onset of exercise. Metabolism, heat production, skin temperature, mean body temperature (a combination of rectal and skin temperature), and body heat content were calculated. Heart rate at 10 degrees C was 103 b/min in SCI-H, 120 in SCI-L and 112 in AB, while in 35 degrees C, heart rate was 112 b/min in SCI-H, 144 in SCI-L and 134 in AB. The increase in rectal temperature in 35 degrees C was larger in SCI-L (+ 0.07 degrees C) and SCI-H (+ 0.08 degrees C) than in AB (+ 0.06 degrees C). The decrease in mean body temperature at 10 degrees C was larger in SCI-H (33.0 +/- 0.68 degrees C) than in SCI-L (33.6 +/- 0.29 degrees C) and AB (34.5 +/- 0.31 degrees C). During exercise in 35 degrees C, mean body temperature increased in all three groups. The increase in body temperature in SCI-L was larger than in AB. During exercise in 10 degrees C, body heat content decreased in SCI-H (80.0 +/- 15.1 kJ) and SCI-L (89.2 +/- 9.1 kJ) but remained constant in AB (97.0 +/- 16.1 kJ). During exercise in 35 degrees C, body heat content increased in all three groups. The increase in body heat content after exercising in 35 degrees C was not significantly different between the three groups. In summary, mean body temperature and body heat content in the cold decreased in SCI, despite exercising. In the heat, mean body temperature and body heat content seems to increase more in SCI than in AB. We can conclude that SCI are at a greater risk for a disturbed heat balance during exercise in the cold and in the heat than AB. Both in the cold and in the heat, precautions should be taken even earlier and be more intensive for SCI than for AB.

Adult↗
PubMed2001

Release of heat, moisture and carbon dioxide in an aviary system for laying hens.

1. Production of total heat, divided into sensible and latent heat, together with carbon dioxide and animal activity were determined at different ambient temperatures under full-scale conditions in an aviary system with loose-housed laying hens. 2. Sensible heat production decreased approximately linearly with increasing ambient temperature and was lower during the day than at night. One explanation may be that some sensible heat produced by the hens was converted to latent heat by evaporation of moisture due to increased activity of the hens during the day (scratching in the bedding and drinking/waste water). 3. Latent heat production increased with increasing ambient temperature and was higher during the day than at night. This confirms that the hens, by agitating the bedding during the day and by spilling drinking water, transferred some sensible heat to latent heat by evaporation. 4. Total heat production decreased with increasing temperature because the hens by thermoregulation decreased their metabolism in order to maintain a constant body temperature. The difference between day and night values of total heat production was less pronounced than in the case of sensible and latent heat. In comparison with current guidelines the measurements showed a higher total heat production (22% higher at 20 degrees C). 5. There was a large diurnal variation in carbon dioxide production, closely correlated to measured animal activity; on average carbon dioxide production during the 12-h dark period was only 66% of the production during the day.

Animals↗
PubMed1999

Benefit of heat acclimation is limited by the evaporative potential when wearing chemical protective clothing.

Heat acclimation-induced sweating responses have the potential of reducing heat strain for chemical protective garment wearers. However, this potential benefit is strongly affected by the properties of the garment. If the clothing ensemble permits sufficient evaporative heat dissipation, then heat acclimation becomes helpful in reducing heat strain. On the other hand, if the garment creates an impenetrable barrier to moisture, no benefit can be gained from heat acclimation as the additional sweating cannot be evaporated. Ten subjects were studied exercising on a treadmill while wearing two different chemical protective ensembles. Skin heat flux, skin temperature, core temperature, metabolic heat production and heart rate were measured. It was found that the benefit of heat acclimation is strongly dependent on the ability of the body to dissipate an adequate amount of heat evaporatively. The evaporative potential (EP), a measure of thermal insulation modified by moisture permeability, of the clothing ensemble offers a quantitative index useful to determine, a priori, whether heat acclimation would be helpful when wearing protective clothing system. The data show that when EP is < 15%, heat acclimation affords no benefit. An evaporative potential graph is created to aid in this determination.

Acclimatization↗
PubMed1992

Effect of heat on induction and repair of DNA strand breaks in X-irradiated CHO cells.

Chinese hamster ovary cells were exposed to various heat treatments followed by X-irradiation, and the induction and repair of DNA strand breaks was studied using the alkaline unwinding technique. Heat treatments alone were found to cause DNA strand breakage only for temperatures greater than or equal to 43 degrees C, whereas the number of radiation-induced strand breaks was unaffected by additional heating. Strand break repair was studied for irradiated cells preheated at temperatures ranging from 42 degrees C to 45 degrees C. The total repair curve could be separated into three phases, a fast (t = 0-15 min), an intermediate (t = 15-120 min) and a slow (t greater than or equal to 120 min) phase. All phases were altered when cells were heated either prior to or after irradiation. The fast and the intermediate phase could be well interpreted by the assumption that irradiation leads to both primary and secondary single-strand breaks, the latter being generated by enzymatic incision at sites of damaged bases. For irradiation alone, the ratio of all secondary strand breaks to all primary breaks was fsec = 1.5 +/- 0.5. This ratio was not altered by preceding heat treatments (mean fsec = 1.7 +/- 0.2). The main effect of heating on the repair kinetics of single-strand breaks was an increase in the repair half-time of primary and secondary breaks (maximum increase by a factor of 3.4), whereas the generation of secondary breaks was only slightly retarded (factor 1.3). The slow repair phase, which is assumed to represent the repair of DNA double-strand breaks, was best described by a single exponential component. The half-time of this component was found to increase from tau slow = 170 +/- 70 min for non-heated cells to tau slow = 345 +/- 80 min for cells heated at 45 degrees C for 20 min, indicating that heat inhibited the repair of double-strand breaks. For irradiation alone, the initial fraction of the slow component was fslow = 0.065 +/- 0.004. This fraction was enhanced by additional heating, with a maximum increase by a factor of 2.7 for cells heated at 45 degrees C for 20 min. This elevation cannot be the result of an enhanced induction of double-strand breaks, but must be associated with an additional formation of slowly repaired strand breaks during repair incubation. These additional strand breaks must arise from strand breaks which in non-heated cells are repaired during the fast or intermediate phase.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

A mathematical model for cell killing by heat applied to a C3H mammary carcinoma in vivo.

Jung (1986) has proposed a mathematical model for cell killing by hyperthermia which assumes that heat killing involves two steps: the production (p) of non-lethal lesions at random and a subsequent conversion (c) into lethal lesions. The p & c model has been shown to predict the survival of CHO cells heated in vitro even when complicated biological phenomena such as thermotolerance and step-down heating (SDH) are involved (Jung 1986, 1991). In the present study the objective was to test the p & c model's ability to describe the effect of single heating and SDH in an experimental tumour in vivo. The endpoint was tumour growth delay (GD). The doubling times (DT) for untreated and heated tumours were similar, and the surviving fraction (SF) could therefore be estimated using: SF = -in(2).GD/DT. SF was fitted to the model by non-linear regression. The p & c model adequately described the GD obtained by SDH (39-44.5 degrees C) and single heating above 42.5 degrees C. Multiple linear regression showed that the residuals for single heating and SDH were independent of both heating time and temperature. However, the residuals for single heating (41-44.5 degrees C) were significantly correlated to heating time when analysed separately. The GD obtained by the use of extended single heating times at or below 42.5 degrees C was therefore overestimated by the model. Development of chronic thermotolerance during heating may account for the observed divergence. The Arrhenius plots for both p and c were log-linear with activation energies of 678 and 311 kJ/mol, respectively. Jung (1986) has previously reported similar p and c activation energies above 42.5 degrees C for CHO cells in vitro.

Animals↗
PubMed1995

Large blood vessel cooling in heated tissues: a numerical study.

Large blood vessels can produce steep temperature gradients in heated tissues leading to inadequate tissue temperatures during hyperthermia. This paper utilizes a finite difference scheme to solve the basic equations of heat transfer and fluid flow to model blood vessel cooling. Unlike previous formulations, heat transfer coefficients were not used to calculate heat transfer to large blood vessels. Instead, the conservation form of the finite difference equations implicitly modelled this process. Temperature profiles of heated tissues near thermally significant vessels were calculated. Microvascular heat transfer was modelled either as an effective conductivity or a heat sink. An increase in perfusion in both microvascular models results in a reduction of the cooling effects of large vessels. For equivalent perfusion values, the effective conductivity model predicted more effective heating of the blood and adjacent tissue. Furthermore, it was found that optimal vessel heating strategies depend on the microvascular heat transfer model adopted; localized deposition of heat near vessels could produce higher temperature profiles when microvascular heat transfer was modelled according to the bioheat transfer equation (BHTE) but not the effective thermal conductivity equation (ETCE). Reduction of the blood flow through thermally significant vessels was found to be the most effective way of reducing localized cooling.

Animals↗
PubMed1999

An investigation of the flow dependence of temperature gradients near large vessels during steady state and transient tissue heating.

Temperature distributions measured during thermal therapy are a major prognostic factor of the efficacy and success of the procedure. Thermal models are used to predict the temperature elevation of tissues during heating. Theoretical work has shown that blood flow through large blood vessels plays an important role in determining temperature profiles of heated tissues. In this paper, an experimental investigation of the effects of large vessels on the temperature distribution of heated tissue is performed. The blood flow dependence of steady state and transient temperature profiles created by a cylindrical conductive heat source and an ultrasound transducer were examined using a fixed porcine kidney as a flow model. In the transient experiments, a 20 s pulse of hot water, 30 degrees C above ambient, heated the tissues. Temperatures were measured at selected locations in steps of 0.1 mm. It was observed that vessels could either heat or cool tissues depending on the orientation of the vascular geometry with respect to the heat source and that these effects are a function of flow rate through the vessels. Temperature gradients of 6 degrees C mm(-1) close to large vessels were routinely measured. Furthermore, it was observed that the temperature gradients caused by large vessels depended on whether the heating source was highly localized (i.e. a hot needle) or more distributed (i.e. external ultrasound). The gradients measured near large vessels during localized heating were between two and three times greater than the gradients measured during ultrasound heating at the same location, for comparable flows. Moreover, these gradients were more sensitive to flow variations for the localized needle heating. X-ray computed tomography data of the kidney vasculature were in good spatial agreement with the locations of all of the temperature variations measured. The three dimensional vessel path observed could account for the complex features of the temperature profiles. The flow dependences of the transient temperature profiles near large vessels during the pulsed experiments were consistent with the temperature distributions measured in the steady state experiments and provided unique insights into the process of convective heat transfer in tissues. Finally, it was shown that even for very short treatment times (3-20 s), large vessels had significant effects on the tissue temperature distributions.

Angiography↗
PubMed1980

Earliest event in the heat denaturation of myosin.

In a previous paper (Kimura, I., Arai, K., & Watanabe, S. (1979) J. Biochem. 86, 1629-1638), we reported that when myosin was subjected to heat treatment, inactivation of actomyosin ATPase occurred in two steps; an early fast inactivation, followed by a slow inactivation. A further study was conducted on the fast inactivation in the early stage of heat treatment of myosin, and the following results were obtained: 1. As the weight ratio of actin to heat-treated myosin increased, the rate of early inactivation of actomyosin ATPase increased. 2. The superprecipitation activity of actomyosin was also decreased in two steps by heat treatment of myosin: an early fast inactivation and a subsequent slow inactivation were distinguishable. 3. The turbidity of myosin suspensions in 0.05 M KCl increased during heat treatment of myosin. The increase also proceeded in two distinct steps, and the rate constants for the two steps of increase were comparable to those for inactivation of actomyosin ATPase. 4. In an electron microscopic study, a new change in the morphology of "thick filaments" of myosin was detectable in the early period of heat treatment, when the fast inactivation of actomyosin ATPase was found to occur; myosin filaments were shorter and thinner than the "regular thick filaments" of untreated myosin, and their size was much more heterogeneous. Heterogeneity of myosin aggregates was also detectable in the sedimentation patterns. 5. The actin-binding ability of myosin or HMM remained unaffected during heat treatment of myosin. The binding ability was estimated in three different ways; by measuring the ATP-induced changed in the turbidity of actomyosin solution, the actin-inhibition of EDTA-ATPase of myosin, and the actin-activation of Mg-ATPase of HMM. 6. In a sedimentation study, formation of myosin dimers was not detectable in the early period of heat treatment of myosin, and was detectable only in the later period. Likewise, increase in the light scattering intensity of myosin solutions occurred only in the later period of heat treatment of myosin. 7. Heat treatment caused a decrease in the ATP-induced enhancement of the HMM fluorescence. The decrease was fitted by a single exponential (first-order reaction), and not by two exponentials. 8. Heat-induced change was not detectable either in the light scattering intensity of LMM solutions in 0.5 M KCl or in the turbidity of LMM suspensions in 0.05 M KCl. Based on these results, it is strongly suggested that the earliest event in heat denaturation of myosin is loss of the ability of myosin to form "regular thick filaments."

Actins↗
PubMed1994

Effect of heating rate on the thermal inactivation of Listeria monocytogenes.

In order to quantify the effect of heating rate on the thermal inactivation of Listeria monocytogenes an accurate means of describing the inactivation kinetics at near instantaneous heating was used. Survivor curves for L. monocytogenes, at near instantaneous heating, were obtained over the temperature range 50-64 degrees C. The use of a linear function to describe the data would have given only a poor approximation of the true inactivation kinetics. With a model based on a logistic algorithm extremely accurate descriptions were made. In processes which had rates of heating < or = 5.0 degrees C min-1, significant deviations of real kill from predicted kill were observed. Predicted kill assumed that heating rate did not affect the inactivation kinetics of a thermal process. At rates of heating between 5.0 and 0.7 degrees C min-1 the deviation greatly increased as the rate of heating decreased; approximately a 1.7 x 10(5)-fold difference at 0.7 degrees C min-1. Maximum thermotolerance was induced at rates of heating < or = 0.7 degrees C min-1. The increased thermotolerance during slow rates of heating was analogous to the induction of the heat-shock response. The models described in this work allow for confident assessments of safety to be made not only at near instantaneous heating but also when the heating rate varies.

Colony Count, Microbial↗
PubMed1995

Estimation of metabolic energy cost and heat production during a 3-day-event.

The metabolic power required for sustained exercise in the horse is proportional to running speed. Moderately fast speeds require substantial energy expenditure and result in the generation of a massive metabolic heat load. Quantitative estimates of energy expenditure and heat production of horses at various running speeds were developed using empirically derived data from treadmill studies. Total metabolic power represents the sum of aerobic power indicated by the rate of oxygen consumption and net anaerobic power indicated by the rate of plasma lactate accumulation. These data were applied to typical running speeds and distances for each of the 4 phases of the endurance day of an Olympic level (CCI) 3-day-event to provide an estimate of the energy expenditure and heat production during each phase. In a given horse, the rates of energy expenditure and heat production are determined by running speed, while total energy expenditure and heat production are determined by a combination of running speed and duration of exercise at that intensity. The highest calculated rate of energy expenditure and heat production occurred during Phase B, the steeplechase, followed closely by Phase D, the cross-country course. Interestingly, the highest total energy expenditure and heat production occurred on Phase C, Roads and Tracks, which is usually considered a period for cool down and recovery between the relatively high speed steeplechase and the demanding cross-country course. Nevertheless, because the rate of energy expenditure is low during this phase, the horses would be expected to lose heat and lower body temperature during this interval. In hot and humid climates, dissipation of the exercise-induced heat load may be compromised, leading to a narrower range of safety between the rate of heat production and the ability of the horse to dissipate this heat to the environment. The results of this study could be used, should environmental conditions dictate, to provide quantitative guidelines as to how specific alterations of speed or distance of the various phases of the event would affect heat production.

Animals↗
PubMed1996

Force-dependent and force-independent heat production in single slow- and fast-twitch muscle fibres from Xenopus laevis.

1. The origin of labile heat production, i.e. a heat component which rapidly decays after the onset of stimulation, and of stable (maintenance) heat production was investigated in intact single fast-twitch (type 1) and slow-twitch (type 3) iliofibularis muscle fibres from Xenopus laevis, at 20 degrees C, by varying stimulation frequency and by varying sarcomere length and the concentration of 2,3-butanedione 2-monoxime (BDM) added. 2. The labile heat produced consisted of a force-independent and a force-dependent part. The average parvalbumin (PA) content found in type 1 fibre bundles (0.84 +/- 0.08 mM; mean +/- S.E.M.; n = 5) and in type 3 fibre bundles (0.12 +/- 0.02 mM; n = 5) indicates that the force-independent labile heat is explained by Ca(2+)-Mg2+ exchange on PA, and amounts to a molar enthalpy change of -78 kJ (molPA)-1. 3. Force-dependent labile heat during fused contractions was similar to the calculated heat production resulting from the formation of force-generating cross-bridges, assuming an enthalpy change associated with cross-bridge formation of -30 kJ mol-1. 4. Activation heat, i.e. the part of the total stable heat that is not related to the contractile apparatus, and of which the calcium sequestration by the sarcoplasmic reticulum is the most important contributor, determined by varying sarcomere length or BDM concentration, was identical. For fused contractions the fraction activation heat of the stable maintenance rate of heat production was 34 +/- 4% (mean +/- S.E.M.; n = 13) in type 1 fibres, and 52 +/- 4% (n = 15) in type 3 fibres. In unfused contractions this was 48 +/- 5% (n = 13) in type 1 fibres, and 35 +/- 2% (n = 11) in type 3 fibres. 5. From the force-dependent stable rate of heat production the economy of cross-bridge cycling, expressed as the force-time integral for a single myosin head per ATP molecule hydrolysed, was calculated. It followed that cross-bridge interaction in type 3 fibres is more economical than in type 1 fibres, and that fused contractions are more economical than unfused contractions.

Animals↗
PubMed1996

Mechanism by which gamma irradiation increases the sensitivity of Salmonella typhimurium ATCC 14028 to heat.

Effects of irradiation and heating on survival of Salmonella typhimurium ATCC 14028 were examined by measuring DNA damage and the integrity of the cytoplasmic membrane. S. typhimurium cells fell into two distinct groups following heating: (i) heat-sensitive cells, which were rapidly inactivated at 65 degrees C and (ii) heat-resistant cells, which were only slowly inactivated at 65 degrees C. Radiation sensitivity of S. typhimurium was greater in the presence of air than in the presence of N2 gas (radiation doses required to inactivate 90% of the cells, 0.394 +/- 0.029 in air and 0.561 +/- 0.035 in N2). Recovery of the covalently closed circular form of plasmid pBR322 from S. typhimurium transformants (Ampr Tetr) was decreased by irradiation but not by heating. Heating prior to irradiation significantly decreased the recovery of plasmid DNA without affecting survival of S. typhimurium. Transformability of the recovered plasmid pBR322 was affected by neither irradiation nor heating, and mutation of antibiotic resistance genes was not detected in S. typhimurium. Heating, but not irradiation, caused destabilization of the cytoplasmic membrane, allowing penetration of hydrophobic dye. These results suggest that lethality of heating followed by irradiation for S. typhimurium was additive, reflecting irradiation-induced DNA damage and heat-induced membrane destabilization. When irradiation preceded heating in the absence of air, more cells were inactivated than was expected, because of heat-inactivating radiation-damaged DNA.

DNA Damage↗
PubMed1972

Specific effects of heating of transformable streptococci on their ability to discriminate between homospecific, heterospecific, and hybrid deoxyribonucleic acid.

Heating competent bacteria of the Challis strain of Streptococcus at a temperature of 48 C causes them to lose their transformability and mainfest a slight retardation of growth rate without loss of viability. The heat-induced loss of transformability is due to diminution in the ability of the bacteria to bind deoxyribonucleic acid (DNA) irreversibly. Another effect of heat is upon a step in the transformation process subsequent to binding, a step in which DNA molecules will compete if they multiply infect an unheated cell. Despite the reduction in irreversible binding exhibited by heated cells, competition between DNA molecules to transform these cells is decreased. Neither of these sites affected by heat exhibits any specificity with regard to origin of DNA. Since heat treatment causes a relative stimulation of transformation by heterospecific DNA, a third effect of heat must be envisaged. The amount of heat-induced stimulation is dependent upon the amount of heterospecific material in the transforming DNA. Linkage of heterospecific markers is increased as a consequence of heating the recipients. Transformation by markers of different transforming efficiency in homospecific DNA is also affected by heat treatment in a differential manner. Taken together, these results point to a heat-sensitive intracellular mechanism that recognizes DNA base sequences during transformation. The effect of heat upon discrimination against heterospecific DNA has been found to occur also in the pneumococcus and in Bacillus subtilis.

Bacillus subtilis↗
PubMed1966

Heat stability and species range of purified staphylococcal alpha-toxin.

Cooper, Louis Z. (New England Medical Center Hospital, Boston, Mass.), Morton A. Madoff, and Louis Weinstein. Heat stability and species range of purified staphylococcal alpha-toxin. J. Bacteriol. 91:1686-1692. 1966.-Heating of high-titer purified staphylococcal alpha-toxin at 60 and 80 C resulted in a double-sloped curve of inactivation of the hemolytic effect on rabbit erythrocytes. Early inactivation was less at the lower temperature, but activity persisted for a longer time at 80 C. Toxin inactivated at 60 C showed renewed activity when heated briefly at 80 C. A precipitate which formed during heating of alpha-toxin at 60 or 80 C yielded hemolytic activity when resuspended and heated at 80 but not at 60 C. Supernatant fluid of heat-precipitated toxin was heat-labile and did not regain activity when heated at 80 C. The results indicate that the "paradoxical effect" of heating of staphylococcal alpha-toxin is not due to a thermolabile inhibitor, but results from alteration of the toxin molecule to a heat-stable active form. Demonstration of renewed activity by 80 C heating of purified toxin requires potent toxin preparations and brief heating periods. Hemolysis of erythrocytes of several animal species by purified alpha-toxin was generally similar to that produced by impure toxin. Rabbit cells were most susceptible. Human and horse erythrocytes hemolyzed to less than 0.1% of the extent of rabbit cells. Blood cells of other species were intermediate in their response to the lytic effect of alpha-toxin.

Animals↗