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Biomedical subjects

G C Li

Publications and source records attributed to G C Li.

At least 127 records · Page 7Linked to original sources
PubMed1982

Induced thermal tolerance and heat shock protein synthesis in Chinese hamster ovary cells.

We have performed experiments to determine the kinetics of induction of thermal tolerance in Chinese hamster HA-1 cells, and the effects of heat treatments on the recovery of protein synthesis, with particular attention to whether heat induces specific proteins, perhaps the heat shock proteins (HSP). The kinetics of the development of thermal tolerance were measured by increases in cellular survival. In parallel experiments, the effects of heat treatment on the recovery of protein synthesis in HA-1 cells were examined. After heating (45 degrees, 20 minutes), some of these cells were immediately labeled with 35S-methionine (10 microCi/ml) for 1 hour at 37 degrees, while the others were incubated at 37 degrees for 1-8 hours and then labeled. The cell samples were prepared for electrophoresis on a gradient SDS gel. The incorporation of label into HA-1 cell proteins was drastically inhibited by the 45 degrees heat treatment, but recovered gradually during the 8-hour incubation period at 37 degrees C. A comparison of the proteins synthesized following heat shock with those synthesized by non-heated cells showed that the levels of synthesis of certain proteins were greatly enhanced following the 45 degrees treatment. By 8 hours, it was qualitatively apparent that three proteins, with molecular weights of 59K, 70K and 87K, were synthesized in greater amounts than in untreated cells. The kinetics of HSP synthesis were compared to the kinetics of thermal tolerance; these showed good correlation. Overall protein synthesis also increased during this time, although at a rate slower than the synthesis of the HSP. The question of whether the HSP play a causative role in the development of thermal tolerance and if so, what role might be, has not been answered.

Adaptation, Physiological↗
PubMed1982

Correlation between synthesis of heat shock proteins and development of thermotolerance in Chinese hamster fibroblasts.

Synthesis of a family of proteins called "heat shock" proteins is induced or enhanced in cells in response to various environmental stresses, suggesting that these proteins may perform functions essential to cell survival. Because a brief, nonlethal heat treatment can dramatically induce a transient resistance to a subsequent lethal heat treatment (thermotolerance), we examined the effect of heat treatment (41-46 degrees C) on protein synthesis and cell survival in plateau-phase Chinese hamster fibroblast (HA-1) cells. After heat treatments that either drastically inhibited total protein synthesis (46 degrees C) or did not suppress it (41 degrees C), the synthesis of heat shock proteins was greatly enhanced over that in unheated cells, and cell survival was increased 10(2)- to 10(6)-fold when cells were challenged by a subsequent lethal heat treatment. The synthesis of heat shock proteins correlated well with the development of thermotolerance, and the stability of these proteins correlated well with the persistence of thermotolerance up to 36 hr. Sodium arsenite, hypoxia, and ethanol also induced both the synthesis of heat shock proteins and transient thermotolerance. A qualitative analysis of individual proteins suggests that the synthesis and persistence of polypeptides of Mr 70,000 or 87,000 most closely conformed to the kinetics of thermotolerance.

Animals↗
PubMed1982

Interactions of hyperthermia and drugs: treatments and probes.

At temperatures above 37 degrees C, the abilities of many, but not of all, anticancer drugs to kill cells increases substantially. The increased cytotoxic rate can vary smoothly with temperature (e.g., nitrosoureas or cis-platinum(II) diamminedichloride) or show a marked threshold near 43 degrees C (e.g., adriamycin or bleomycin). Clinically, the increased cell killing rate can be used in the combination of localized hyperthermia and systemic chemotherapy. Drugs can also be useful in the study of cell killing by heat. Aliphatic alcohols which mimic and interact with heat, tend to be localized in lipid-rich regions of the cell, i.e., membranes. Heat modifies the rate at which plant lectins agglutinate cells and also modifies capping rates; most likely, these changes reflected membrane alterations. Because other data strongly imply that proteins are involved in cell death, we think that the first step in hyperthermic killing of cells involves damage to specific membrane-associated proteins.

Alcohols↗
PubMed1981

Temperature-induced homeoviscous adaptation of Chinese hamster ovary cells.

Exponential and plateau phase Chinese hamster ovary cells were maintained for 3 days at 32, 37, 39 or 41 degrees C. The effect of growth temperature on the fluidity and composition of the cellular membranes, and on the ability of the cells to resist a subsequent heat treatment at 43 degrees C, was measured. Cells grown at temperatures above 37 degrees C displayed increased resistance or tolerance to a 43 degree C heat treatment, whereas cells grown at 32 degrees C were sensitized to heat. Extensive cell division was not required for expression of heat tolerance. Membrane fluidity, as determined by the degree of rotational mobility of the fluorescent probe diphenylhexatriene, decreased with increasing growth temperatures, but the relationship did not hold in exponential phase cells grown at 32 degrees C. The cholesterol : phospholipid molar ratio correlated with the fluorescence polarization values, suggesting that the cells are able to adjust membrane fluidity by varying the concentration of cholesterol. The results are compatible with the concept of homeoviscous adaptation: that organisms strive to maintain an optimal level of membrane fluidity and when grown at a different temperature will alter the lipid composition in order to maintain this level. Up until now, cholesterol has not been implicated in this process.

Animals↗
PubMed1980

A proposed operational model of thermotolerance based on effects of nutrients and the initial treatment temperature.

The phenomenon of thermotolerance in mammalian cells has been extensively documented in the literature. Because of its potential clinical importance as well as the fundamental biological interest, we pursued additional studies investigating pH and nutritional effects. Split-dose experiments were performed using plateau phase Chinese hamster HA-1 cells. The effects of the nutritional environment during the initial 43 degrees incubation and the second 43 degree treatment on the induction of thermotolerance were studied by comparing survival in full medium at pH 7.4 or in Hanks' balanced salt solution at pH 6.7. In additional experiments, we examined the effect on thermotolerance of changing the temperature of the initial treatment to 41 degrees. Thermotolerance was induced independently of the nutrient conditions of the first treatment. However, survival at the time of maximum expression of thermotolerance depended primarily on the duration and temperature of the initial treatment. Temperatures of 43 degrees or higher inhibited the development of thermotolerance during the first heat exposure. In contrast, if the initial exposure was at 41 degrees, thermotolerance was almost fully expressed by the end of this initial treatment. Changing pH in Hanks' balanced salt solution from 6.7 to 7.4 did not affect survival. On the basis of these and other data, we suggest that thermotolerance can be divided into three complementary and sometimes competing processes: an initial event ("trigger"); the expression of resistance ("development"); and its disappearance ("decay"). Trigger is induced at all hyperthermic temperatures while development requires a permissive temperature, i.e., less than 43 degrees for HA-1 cells. This model can provide plausible interpretations of several currently puzzling aspects of the survival kinetics of heat-exposed mammalian cells.

Adaptation, Physiological↗