Changes in Glucose and Lactate Content of Ascites Fluid and Blood Plasma During Growth and Decay of the ELD Ascites Tumour

Abstract

WHEN considering the nutritional and transport facilities of tumours one is struck by the diverging conditions developing in ascites and solid tumours with time. Early transplants of both solid and ascites tumours seem close enough to the vascular svstem of the host. In the case of solid tumours, with increasing age and size, vascular occlusion and deranged interstitial transport facilities (Goldacre andSylven, 1959, 1962) lead to starvation and cell death in central tumour regions. In ascites tumours the regressive changes during later stages have for various reasons not been extensively recognized. However, Lucke and Berwick (1954) found a decrease in the number of free ascites cells in the later stages of growth of the Ehrlich-Landschutz (ELD) ascites tumour. Hauschka et al. (1957) reported no such fall in cell number when describing the growth of ELD ascites, but Revesz and Klein (1954) found a decrease in ascites lymphomas.The present communication will draw attention to the spontaneous cellular decay and decrease in tumour cell numbers occurring during later stages of ELD ascites growth some time before the animals succumb. In addition, it became of interest to make serial assays of the content of glucose and lactate (LA) in blood plasma and ascites fluid in order to obtain rough information as to the nutritional supply and magnitude of glycolysis, respectively, along the growth curve. The latter parameters may be compared with previous data on the glucose and LA concentrations in the interstitial fluid from different regions of solid malignant mouse tumours recently assayed (Burgess and Sylven, 1962). MATERIAL AND METHODSMice and tumour strains.-The experiments were performed using only C3H mice or F1 hybrids of C3H x DBA mice. The hyperdiploid Ehrlich-Landschutz (ELD) ascites tumour was employed.Results obtained from 4 experimental series of animals are reported. Each series consisted of 50 animals inoculated with about 25 x 106 cells obtained from mice bearing 10 day ascites. This was an excess of mice, as some died during the course of the experiment. The times when these died were noted.Nutritional conditions. All mice were given food and water ad libitum. It was the aim of this work to study the growth of the ascites tumour under ordinary laboratory conditions. The results will show that the animals were in a state

Moderate endurance training reduced hepatic tumourigenesis associated with lower lactate overload compared to high‐intensity interval training

“…Excess lactate in muscle is excreted, leading to a rapid increase in blood lactate levels and the acidification of the microenvironment. Previous studies have shown that a significant amount of cancer lactate is released into the blood 39,40 . Furthermore, endurance training has also been shown to reduce circulating lactate concentrations, consistent with our findings 19 .…”

Metabolic alterations in a noncachectic animal tumor system

“…In tumorbearing mice, the results are unclear, with some investigators reporting no change in fasting plasma lactic acid levels,*L and others reporting increased levels. 43 In one study with a rat sarcoma model, the authors demonstrated elevated plasma levels, but this was done with very large tumors, and the nutritional status was not ~t a t e d . "~ In this model, tumor-bearing animals demonstrated a significant elevation of blood lactic acid concentration when compared with controls.…”

Oxygen diffusion and the distribution of cellular radiosensitivity in tumours

“…it is much higher than the concentration of 3 mg/100 ml. required to sustain glycolysis of Ehrlich ascites cells (Kemp and Mendel, 1957;Burgess and Sylven, 1962). Thus glucose deficiency and injurious concentrations of carbon dioxide or lactic acid appear not to be primary causes of cell death in tumours.…”