M. Manteuffelcymborowska et al., TUMOR EFFECT ON ARGININE ORNITHINE METABOLIC RELATIONSHIP IN HYPERTROPHIC MOUSE KIDNEY/, Molecular and cellular biochemistry, 168(1-2), 1997, pp. 51-57
Tumor effect on arginine/ornithine metabolic relationship in hypertrop
hic mouse kidney. The presence of a tumour significantly changes nitro
gen metabolism, including that of amino acids and polyamines, in host
animals. In this study, we examine whether developing tumours affect t
he metabolic relationship of arginine and ornithine, precursors of pol
yamines, in the testosterone-induced hypertrophic mouse kidney model.
Androgen-induced changes in the activity of enzymes involved with omit
hine biosynthesis (arginase), its consumption (omithine aminotransfera
se, OAT and omithine decarboxylase, ODC) and the hypertrophy of host m
ouse kidney were not affected by the presence of an ascitic tumour (EA
C) and only slightly by a mammary carcinoma (MaCa). The HPLC determine
d renal level of arginine and ornithine showed a striking homeostasis
and was disturbed neither by testosterone nor EAC. The effect of MaCa
and testosterone on the levels of both amino acids, although significa
nt, was not very pronounced. Developing tumours, especially ascitic, a
ltered the renal activity of OAT and ODC, but not of arginase, in test
osterone-untreated mice. All examined tumours, EAC, L 1210 and MaCa ac
tively metabolized arginine and ornithine. The tumour content of argin
ine which coincided with the activity of arginase, resulted in a marke
d increase of the ornithine/arginine ratio in tumours, when compared w
ith kidneys. These results indicate that the androgen-induced anabolic
response in mouse kidney is preserved, in spite of tumour requirement
s for essential metabolites.