1. Long-term maintenance of rats on a diet containing ethanol did not cause compensatory changes in brain synaptic membrane lipid composition, nor was there any change in membrane lipid order as measured by steady-state fluorescence polarization of DPH. 2. The lipid composition of MC7 tumour plasma membranes was also determined in ethanol-fed and then sucrose pair-fed controls. Dietary ethanol caused no change in the composition of phospholipid classes. There was, however, a tendency for an increase in C18 fatty acids and an increase in monounsaturated at the expense of unsaturated and polyunsaturated fatty acids. There was no significant change in cholesterol content. 3. Tumour membranes from ethanol-fed rats were not different in lipid order from their pair-fed controls. Tumour membranes were, however, significantly less ordered than synaptic membranes. 4. A single heat treatment of 44 degrees C for 1 h increased the survival time of rats bearing both MC7 and D23 foot tumours. No difference in their survival was seen between ethanol-fed and sucrose pair-fed controls.

Alcoholism↗

PubMedDate not supplied

Effect of dietary modulation of membrane lipid composition on the thermostability of HTC cells and of a membrane enzyme.

Growth of hepatoma tissue culture (HTC) cells in the presence of linoleic (18:2) or arachidonic (20:4) acids for 36 h caused an increased cell thermosensitivity. Plasma membrane-rich fractions were purified (15-20-fold) with high yield (30%) from control and fatty acid-supplemented cells. Contamination with membranes from mitochondria, lysosomes and endoplasmic reticulum was low. Supplementation significantly increased the level of the supplemented fatty acid and decreased the level of oleic acid (18:1) in plasma membrane phospholipids (PL), causing a significant decrease in the oleic acid:PUFA (polyunsaturated fatty acid) ratio. No significant changes occurred in other parameters such as cholesterol:PL, cholesterol:protein or PL:protein ratios. Plasma membranes from PUFA-supplemented cells exhibited a lower membrane order, compared with control cell membranes, as determined by DPH fluorescence polarization over the temperature range 4-40 degrees C. Isothermal inactivation of alkaline phosphodiesterase I in plasma membranes from control and supplemented cells showed curvilinear kinetics. The change in membrane composition and order following supplementation with arachidonic acid was associated with increased thermosensitivity of this enzyme. These data are discussed with respect to the suggestion that the plasma membrane may be a target for cellular thermal injury and death.

Animals↗

PubMedDate not supplied

Long-term effects of flavone acetic acid on the growth of a rat tumour.

A rat tumour (MC7 sarcoma), growing subcutaneously, has been shown to be sensitive to a single application of flavone acetic acid. Thirteen rats were still alive after 50 days and 8 of these were tumour free, as compared with control rats which survived for 15.7 +/- 2.53 days. The 8 tumour free animals were rechallenged with MC7 sarcoma 40 weeks later, without further FAA treatment. The tumour grew initially but in all cases the animals became tumour free within 24 days. After a further 30 days they were rechallenged with D23 hepatoma which grew as effectively as in the controls.

Animals↗

PubMedDate not supplied

The effect of local anaesthetics on the thermal sensitivity of HTC cells.

Local anaesthetics caused death of HTC cells, and the order of toxicity (dibucaine > tetracaine > procaine) correlated with their oil:water partition coefficients. Cytotoxic effects of hyperthermia were enhanced by subtoxic levels of anaesthetics and again, their potency was related to the oil:water partition coefficients. DPH fluidity in plasma membranes at 37 degrees C was increased by dibucaine and tetracaine but not by procaine up to 5mM. At 43 degrees C, plasma membrane fluidity was increased by dibucaine but not by tetracaine or procaine. The results suggest that fluidisation of the hydrophobic core of the membrane may contribute to anaesthetic potentiation of heat cell death.

Anesthetics, Local↗