The response of human and rodent cells to hyperthermia

Roizin-Towle, Laurie; Pirro, John P.

doi:10.1016/0360-3016(91)90018-y

Cited by 87 publications

(58 citation statements)

References 18 publications

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“…It has been used by other authors in this special issue for addressing mechanistic factors related to thermal inactivation (cell killing) as well thermal enhancement of other anti-tumour modalities such as radiation and chemotherapeutic drugs. It is also useful for comparing the differing effects of heat shock amongst different cell types, as is demonstrated by the data of Roizin-Towle and Pirro [11], which is shown in Figure 1 for four rodent cell lines and eight human cell lines. Examination of this data leads to several important conclusions which directly impact clinical application:…”

Section: Heat Cytotoxicity Dose and The Arrhenius Relationshipmentioning

confidence: 94%

The heat shock response: Role in radiation biology and cancer therapy

Corry

Armour

2005

International Journal of Hyperthermia

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Since prehistoric times, elevated temperatures have been used to treat cancer in a variety of forms. In modern times (the last 40 years) efforts have concentrated on combining heat with other anti-tumour modalities, principally ionizing radiation and some chemotherapeutic drugs. Despite the emphasis on combined therapy, rodent data relating to heat sensitivity and thermal tolerance development assumed principal importance. These considerations suggested treating at 43 degrees C as a target temperature and fractionation schemes emphasizing thermal tolerance avoidance. Concomitantly crucial data on heat-induced tumour reoxygenation and its temperature dependence were largely ignored. In reality these were unrealistic and undesirable goals. The preponderance of evidence now suggests that lower temperatures (40-42 degrees C) administered more frequently, optimally immediately before and during each administration of ionizing radiation, are likely to yield optimal results. Factoring in trimodality therapy and other combinations of chemotherapeutic drugs will require some modifications of such fractionation schemes.

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Section: Heat Cytotoxicity Dose and The Arrhenius Relationshipmentioning

confidence: 94%

The heat shock response: Role in radiation biology and cancer therapy

Corry

Armour

2005

International Journal of Hyperthermia

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“…The degree of cell death varied with only a 0.5 • C change in temperature. Moreover, thermotherapy potentiated radiation effects on both normal and cancer cells in vitro (127,371). Efficacy of heat for cancer was related to the cellular oxygen and pH of the microenvironment.…”

Section: Brain Tumors and Heat Stressmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…Recent research studies have indicated that, in comparison with rodent cells, most human cells are more resistant to higher temperature >42"C (Hahn et al 1989, Raaphorst et al 1989, Roizin-Towle and Pirro 1991 but are more sensitive to lower temperature, long duration mild hyperthennia (Mackey et al 1992a, 1992b, Armour et al 1993. Mackey et al (1992aMackey et al ( , 1992b demonstrated that HeLa cells were more sensitive to mild hyperthermia than Chinese hamster ovary cells.…”

Section: Discussionmentioning

confidence: 97%

“…Since most basic research in hyperthermia oncology has been performed on rodent cells (Hahn 1982, Hall 1994, it is important to evaluate the interaction between heat and LDRI in human cell lines because the heat dependent response of human cell lines is substantially different from that of rodent cell lines (Raaphorst and Azzam 1983, Hahn et al 1989, Raaphorst et al 1989, Roizin-Towle and Pirro 1991, Mackey et al 1992a, Armour et al 1993. Recent research studies have indicated that, in comparison with rodent cells, most human cells are more resistant to higher temperature >42"C (Hahn et al 1989, Raaphorst et al 1989, Roizin-Towle and Pirro 1991 but are more sensitive to lower temperature, long duration mild hyperthennia (Mackey et al 1992a, 1992b, Armour et al 1993.…”

Section: Discussionmentioning

confidence: 99%

Enhanced cytotoxicity in combination of low dose-rate irradiation with hyperthermia in vitro

Sakurai

Mitsuhasi

Takahashi

et al. 1996

International Journal of Hyperthermia

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We have pursued an in vitro investigation using a rodent cell line to characterize the interaction of simultaneous low dose-rate irradiation (LDRI) and hyperthermia and to determine the role of LDRI in the development of thermotolerance in a fractionated hyperthermia schedule. Yoshida sarcoma cells growing in vitro were used in this study. Cell survivals were estimated by the Courteney soft agar clonogenic assay. A treatment device for LDRI treatment, which held eight 137Cs sources and agar plus containing the cells, gave an irradiation dose of 51.8 cGy/h to the cells. In the experiment of simultaneous LDRI and hyperthermia, the LDRI cytotoxicities were enhanced by hyperthermia over a non-lethal temperature range. High synergistic effects were observed in a lower temperature range (40, 41 and 41.5 degrees C) in contrast to higher temperature (42, 43 and 44 degrees C). In the experiment of alternate LDRI and hyperthermia, thermotolerance induced by initial heating was well developed during the LDR exposure but less expressed in comparison with the cells which had no LDRI exposure. The treatment of LDRI for 8 h may have affected the thermotolerance development in our experimental condition.

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The response of human and rodent cells to hyperthermia

Cited by 87 publications

References 18 publications

The heat shock response: Role in radiation biology and cancer therapy

The heat shock response: Role in radiation biology and cancer therapy

Cerebral Vascular Control and Metabolism in Heat Stress

Enhanced cytotoxicity in combination of low dose-rate irradiation with hyperthermia in vitro

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