Thermal Tolerance and Repair of Thermal Damage by Cultured Cells

Harisiadis, Leon; Sung, Duk Ii; Hall, Eric J.

doi:10.1148/123.2.505

Cited by 60 publications

(9 citation statements)

References 13 publications

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“…The damage produced by hyperthermia results from the effects of increased temperature on protein unfolding and cell cycle arrest (Westra and Dewey ; Harisiadis et al. ; Landry et al. ).…”

Section: Introductionmentioning

confidence: 99%

“…Hyperthermia contributes to significant cellular damage and death in a manner that is dependent on both the amount and duration of temperature elevation (Palzer and Heidelberger 1973;Sapareto et al 1978). The damage produced by hyperthermia results from the effects of increased temperature on protein unfolding and cell cycle arrest (Westra and Dewey 1971;Harisiadis et al 1977;Landry et al 1982). Accordingly, if METH-induced hyperthermia plays a significant role in the liver damage and increases in ammonia observed during drug exposure, this may represent a mechanism by which hyperthermia contributes significantly to the neurotoxicity of METH.…”

Section: Introductionmentioning

confidence: 99%

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Methamphetamine causes acute hyperthermia‐dependent liver damage

Halpin

Gunning

Yamamoto

2013

Pharmacology Res & Perspec

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Methamphetamine-induced neurotoxicity has been correlated with damage to the liver but this damage has not been extensively characterized. Moreover, the mechanism by which the drug contributes to liver damage is unknown. This study characterizes the hepatocellular toxicity of methamphetamine and examines if hyperthermia contributes to this liver damage. Livers from methamphetamine-treated rats were examined using electron microscopy and hematoxylin and eosin staining. Methamphetamine increased glycogen stores, mitochondrial aggregation, microvesicular lipid, and hydropic change. These changes were diffuse throughout the hepatic lobule, as evidenced by a lack of hematoxylin and eosin staining. To confirm if these changes were indicative of damage, serum aspartate and alanine aminotransferase were measured. The functional significance of methamphetamine-induced liver damage was also examined by measuring plasma ammonia. To examine the contribution of hyperthermia to this damage, methamphetamine-treated rats were cooled during and after drug treatment by cooling their external environment. Serum aspartate and alanine aminotransferase, as well as plasma ammonia were increased concurrently with these morphologic changes and were prevented when methamphetamine-induced hyperthermia was blocked. These findings support that methamphetamine produces changes in hepatocellular morphology and damage persisting for at least 24 h after drug exposure. At this same time point, methamphetamine treatment significantly increases plasma ammonia concentrations, consistent with impaired ammonia metabolism and functional liver damage. Methamphetamine-induced hyperthermia contributes significantly to the persistent liver damage and increases in peripheral ammonia produced by the drug.

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“…The damage produced by hyperthermia results from the effects of increased temperature on protein unfolding and cell cycle arrest (Westra and Dewey ; Harisiadis et al. ; Landry et al. ).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Methamphetamine causes acute hyperthermia‐dependent liver damage

Halpin

Gunning

Yamamoto

2013

Pharmacology Res & Perspec

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“…Two different phenomena have been reported. For prolonged heating at temperatures below 43.5°C there is a decrease in the slope of the cell survival curve after three to four hours (Palzer and Heidelberger, 1973;Gerweck, 1977;Harisiadis et al, 1977). This effect is not observed at higher temperatures.…”

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confidence: 99%

Induced thermal resistance in the mouse ear

Law¹,

Coultas²,

Field³

1979

BJR

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The mouse ear (pinna) was used to investigate the effect of two hyperthermic treatments. Heating was by immersion in hot water at 43.5 degrees C. A single treatment of about 50 minutes was required to cause necrosis in 50% of the ears heated. When heat treatment was given in two equal fractions the total heating time had to be increased if the interval between fractions was greater than four hours. By 24 hours a total treatment of about 100 minutes was required, indicating almost complete recovery from the first heating. Priming treatments at 43.5 degrees C induced thermal resistance to a second heat treatment at 43.5 degrees C. Maximum resistance was observed one day after a 20 minute priming and two days after a 40 minute priming, when the heating time had to be increased to 120 minutes, an increase by a factor of 2.4. Shorter priming treatments induced less resistance, the minimum heating time to produce an effect being two minutes. In all cases the effect decreased during the next four to five days. These results indicate that the reduced response of tissues to fractionated hyperthermia is due both to the repair of sublethal heat damage and induction of thermal resistance.

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“…The extent of CIT was found to increase with increasing temperature and incubation time of the chronic pre-treatment but to decrease with increasing temperature of the second treatment (Harisiadis et al 1977, Joshi and Jung 1979, Li et al 1982, Spiro et al 1982.…”

Section: Thermotolerancementioning

confidence: 96%

Thermotolerance and Thermosensitization in CHO and R1H Cells: A Comparative Study

Dikomey¹,

Eickhoff²,

Jung³

1984

International Journal of Radiation Biology and Related Studies

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In CHO and R1H cells thermotolerance was induced by a pre-incubation at 40 degrees C, by an acute heat shock at 43 degrees C followed by a time interval at 37 degrees C, and during continuous heating at 42 degrees C. Thermotolerance, which was tested at 43 degrees C, primarily causes an increase in D0 of the heat-response curve. The degree of maximum thermotolerance was found to be generally more pronounced in CHO than in R1H cells, but the time interval at 37 degrees C, as well as at 40 degrees C, to reach this maximum level was the same in both cell lines. CHO and R1H cells could be sensitized to 40 degrees C by a pre-treatment at 43 degrees C. When compared for the same survival rate after pre-treatment at 43 degrees C alone the degree of thermosensitization was about the same in both cell lines. In either cell line thermosensitization was found to be suppressed when cells were made thermotolerant by a previous incubation at 40 degrees C for 16 hours.

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Thermal Tolerance and Repair of Thermal Damage by Cultured Cells

Cited by 60 publications

References 13 publications

Methamphetamine causes acute hyperthermia‐dependent liver damage

Methamphetamine causes acute hyperthermia‐dependent liver damage

Induced thermal resistance in the mouse ear

Thermotolerance and Thermosensitization in CHO and R1H Cells: A Comparative Study

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