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In response to a variety of hyperthermic treatments, rat embryonic fibroblasts synthesize heat shock proteins (hsps), including those with molecular weights of 68,000 (hsp 68), 70,000 (hsp 70) and 89,000 (hsp 89). Hyperthermic stresses, which produce the hsps, also cause expression of thermotolerance. The dependence of thermotolerance expression on hsp synthesis was investigated in this mammalian cell line under different heating conditions. Temperature shift experiments showed that hsp synthesis and thermotolerance expression were dependent not only on the absolute hyperthermic temperature, but also on the difference between the initial incubation temperature and the hyperthermic temperature. Small temperature differences which produced no cell killing did not cause detectable synthesis of hsp 68. Increasing the difference of the initial and hyperthermic temperatures reduced cell survival and increased the synthesis of hsp 68. Thermotolerance could be expressed by surviving cells following an initial heat stress even when both heat shock and general protein synthesis were inhibited. Cells exposed to cycloheximide were heated, incubated at their initial temperature for six hours and reheated in the presence of the drug. The inhibitor was then removed and the cells plated for colony formation. The hsps were expressed during this latter incubation period. The regulation of hsp 70 in rat fibroblasts was investigated next. Hsp 70 synthesis rates correlated with the amount of hsp 70 encoding mRNA. The time course of heat shock synthesis and general protein synthesis recovery were each dependent on the duration of the heat stress. Inhibiting protein synthesis with cycloheximide resulted initially in the accumulation of the RNA encoding hsp 70 but did not effect the normal turnover of this RNA species. The conclusions based on these findings are that thermal survival adaptation can be expressed in the absence of hsp 68 synthesis. Hsp 68 is expressed by cells that will ultimately die (see Chapter 2). The hsps do not appear to protect cells against subsequent heat stress. They may function in a repair capacity (see Chapter 3). Hsp 70 expression is primarily regulated by transcription in Rat-1 cells. Hsp 70 does not act to regulate its own turnover (see Chapter 4).

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Capture of wildlife often leads to high animal mortality. In many species, capture is associated with development of a high body temperature. This stress-induced hyperthermia appears to form an integral part of capture-related mortalities, since it occurs before, during and after exposure to capture. I used two wildlife species, impala and blesbok, and exposed them to darting and net capture so as to investigate thermal and haematological changes that occur during capture. We implanted the animals with temperature-sensitive data loggers within the abdominal cavity (for core body temperature) and caudal aspect of the thigh (for muscle temperature). Activity loggers were tethered to the abdominal wall to measure locomotor activity. Blood samples were taken after capture when the animal became recumbent and another sample 10 minutes after the first sample in order to determine haematological changes. Impala had higher abdominal body temperatures during net capture in comparison to darting, whereas blesbok abdominal body temperatures did not differ between capture methods. Different species and individuals of the same species respond differently to various capture procedures. However, I found that irrespective of the capture event or whether impala or blesbok were captured, human presence before capture caused abdominal body temperatures to rise. Similar to thermal responses, there also was high variability between individuals in terms of blood variable concentrations used to quantify physiological responses to capture. Overall, blood variable changes (total protein, sodium, lactate, haematocrit, noradrenaline, adrenaline, potassium, creatine phosphokinase, pH) were similar for impala and blesbok in response to the two capture procedures. Cortisol values in blesbok however showed a greater response during darting whereas impala showed a greater response during net capture. Similarly, osmolality values showed a greater response during net capture whereas impala showed a greater response during darting. Both the species showed that sodium and lactate correlated positively as well as noradrenaline and adrenaline correlated positively. The correlation between two variables allows us to measure only one of the variables, predicting the change of another. Unpredictable differences in thermal and blood variable measurements of impala and blesbok between different capture procedures did not allow me to correlate the thermal responses after a capture event to stress-related blood variables. The issue of obtaining a practical and accurate measurement of the hyperthermic response during capture also often arises. Rectal temperature is currently the method of choice to determine body temperature in the field. I aimed to investigate whether muscle temperature measurement can be used as an alternative body temperature measurement in the field. When abdominal core body temperatures were high, muscle temperature measurements were close to and even slightly higher than the abdominal body temperature measurements in both the species. However, low abdominal body temperatures, muscle temperature measurements were at lower and much less accurate in predicting abdominal body temperatures. Muscle temperatures can therefore predict abdominal body temperatures with sufficient accuracy during a capture event, since animals respond to capture with elevated body temperatures thus increasing the similarity between the abdominal and muscle temperature measurements measured. One potential problem with muscle temperature, is that it may reflect exercise-induced temperature increases during capture, independently of a rise in abdominal body temperature. I found that the rise in muscle temperature was not only a result of the increase in activity during a capture event but rather as a result of stress-induced hyperthermia. The increase in activity only contributes to the overall hyperthermia of the animal. The degree to which stress-induced hyperthermia contributes to mortality during capture is unclear. During my study, five impala died unexpectedly. Four impala died during the first trial while the fifth impala died before the completion of the last trial. I therefore compared the hyperthermic and haematological changes in surviving and non-surviving individuals. Both non-surviving and surviving impala in my study showed a rise in abdominal body temperature during the capture however the highest abdominal body temperatures occurred in individuals in both the surviving and non-surviving group. Very high abdominal body temperatures greater than 41ºC and 43ºC occurred in individuals of both the non-surviving and surviving animals, respectively. Some animals with an abdominal body temperature of 43ºC, therefore survived whereas other individuals died when experiencing abdominal body temperature of less than 41ºC. Blood variable responses (Creatine phosphokinase, glucose, potassium, calcium, sodium, lactate, osmolality, noradrenaline, adrenaline, pH) of the non-surviving individuals showed high values in comparison to the blood variable measurements of the surviving group. The blood variable measurements were however sampled late which will affect the measurements but can still be used to predicted mortality in the non-surviving impala. The blood variable measurements therefore were associated with mortality in the non-surviving impala. In conclusion, whether stress-induced hyperthermia can be used as a sole measure to identify a compromised individual during a capture event and concomitantly enable us to give appropriate treatment is unclear. It is evident from my study that capture induced a hyperthermic response in excitable impala as well as in the much less excitable blesbok. My study is one of few systematic studies on capture stress and shows that body temperature used in conjunction with other parameters may be useful in estimating the degree of stress in captured animals, and thus predicting likelihood of mortality or morbidity. My study also revealed that muscle temperature, possibly measured in the field by a needle-stab method, may provide an index of core body temperature.

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An attempt has been made to alter the degree of unsaturation of the body fats of goldfish (Carassius auratus) and correlate these changes with any modifications of heat tolerance subsequently exhibited by the fish. The goldfish were fed three different diets each containing a fat of different degree of unsaturation. The fats used were pilchard oil (iodine value of 181.7), herring oil (iodine value of 128.4.) and lard (iodine value of 66.2). Heat resistance was tested by holding the fish at a constant high temperature and observing the time to death. Variations in the ability of the groups to withstand high temperature were then compared to differences in the degree of unsaturation of their extracted fats. It was found that while diet could effect changes in the degree of unsaturation of the goldfish fats to approximately 54% of the theoretical level, and that these changes in turn modified the heat resistance of the goldfish, no quantitative relationship was established. / Science, Faculty of / Zoology, Department of / Graduate

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LD2668 .T4 1966 B64 / Master of Science

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