Abstract
(AxT6)F1 hybrid mice received s.c. transplants from (AxT6)F1 mammary carcinomas. At 1, 2 or 4 weeks after tumour transplantation, the mice were bled to obtain plasma and then challenged with 25 micron E. coli lipopolysaccharide (LPS) endotoxin i.v. The mice were killed 24 hr later, further plasma was obtained and their liver ratios and spleen ratios were determined. A similar procedure was carried out on non-tumour-bearing mice. Progressive tumour growth was associated with an increase in the liver ratio. In parallel, mice with 4-week tumour transplant showed increased uptake of colloidal carbon particles and 51Cr-labelled sheep red blood cells in the liver. The plasma amino aspartate transaminase (AST) and the ornithine carbamoyl transferase (OCT) showed a constant rise in all groups of mice after LPS injection. However, at 24 hr after LPS injection, the AST level showed the greatest rise in mice with 4-week tumour transplants. By contrast, OCT, which is liberated only from hepatocytes, showed the greatest rise in non-tumour-bearing mice.
Highlights
Summary.-(AxT6)Fl hybrid mice received s.c. transplants from (AxT6)Fl mammary carcinomas
Hepatocellular damage can occur during local macrophage hyperphagocytosis and it has been proposed that this is due to phagocytosis-induced release of cytotoxic factors from the hepatic macrophages (Bradfield & Wells, 1978)
This paper is concerned with the proposition that the growth of tumours can lead to the activation of hepatic macrophages, making the liver susceptible to damage during clearance of endotoxin from the circulation
Summary
Summary.-(AxT6)Fl hybrid mice received s.c. transplants from (AxT6)Fl mammary carcinomas. Activation of hepatic macrophages during tumour growth in mice, as shown by increased colloidal carbon clearance (Old et al, 1960) suggests that these macrophages participate in the hosts' immune response to the tumour. It was decided to investigate whether (AxT6)Fl mice bearing early transplants of (AxT6)Fl mammary carcinomas showed any evidence of activation of hepatic macrophages, and whether this was associated with increased sensitivity to liver damage by injected lipopolysaccharide (LPS). Such a sequence of events might explain some of the morbidity associated with neoplasia
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