TY - JOUR
T1 - Paradoxical enhancement of S-adenosylmethionine decarboxylase in rat tissues following administration of the specific inhibitor methyl glyoxal bis(guanylhydrazone)
AU - Pegg, A. E.
AU - Corti, A.
AU - Williams-Ashman, H. G.
N1 - Funding Information:
We are very grateful to Dr. manuscript of reference no. 7 prior by the Sir Michael Sobell Fellowship by a research grant (HD-04592) from Mrs. Amelia Schenone for assistance David R. Morris to its publication. of the Cancer the U.S. Public in some of the for allowing us to read a copy of the This research was supported in part Research Campaign (A.E. Pegg) and Health Service. We wish to thank experiments.
PY - 1973/5/15
Y1 - 1973/5/15
N2 - Treatment of rats with large but sublethal doses of methyl glyoxal bis(guanylhydrazone), a potent in vitro inhibitor of animal S-adenosylmethionine decarboxylases, causes marked increases in the enzyme activity of extracts of kidney, ventral prostate, and testis which had been extensively dialyzed to remove any remaining drug. One day after administration of the inhibitor to female rats, the renal S-adenosylmethionine decarboxylase activity was 12 times the normal level and remained greatly enhanced for a further 24 hr. As indicated by decline in decarboxylase activity following depression of protein biosynthesis by injection of cycloheximide, the apparent half-life of the kidney enzyme in normal female rats is roughly 2 hr; in contrast, the apparent half-life of the enzyme is elevated to a value of more than 20 hr in animals that were previously treated with methyl glyoxal bis(guanylhydrazone). The increased renal S-adenosylmethionine decarboxylase activity following administration of the specific enzyme inhibitor in vivo may thus be due, at least in part, to stabilization of the enzyme against intracellular inactivation as a result either of direct combination of the enzyme protein with the inhibitor, or with substance(s) in the tissue whose levels are influenced by treatment with methyl glyoxal bis(guanylhydrazone).
AB - Treatment of rats with large but sublethal doses of methyl glyoxal bis(guanylhydrazone), a potent in vitro inhibitor of animal S-adenosylmethionine decarboxylases, causes marked increases in the enzyme activity of extracts of kidney, ventral prostate, and testis which had been extensively dialyzed to remove any remaining drug. One day after administration of the inhibitor to female rats, the renal S-adenosylmethionine decarboxylase activity was 12 times the normal level and remained greatly enhanced for a further 24 hr. As indicated by decline in decarboxylase activity following depression of protein biosynthesis by injection of cycloheximide, the apparent half-life of the kidney enzyme in normal female rats is roughly 2 hr; in contrast, the apparent half-life of the enzyme is elevated to a value of more than 20 hr in animals that were previously treated with methyl glyoxal bis(guanylhydrazone). The increased renal S-adenosylmethionine decarboxylase activity following administration of the specific enzyme inhibitor in vivo may thus be due, at least in part, to stabilization of the enzyme against intracellular inactivation as a result either of direct combination of the enzyme protein with the inhibitor, or with substance(s) in the tissue whose levels are influenced by treatment with methyl glyoxal bis(guanylhydrazone).
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U2 - 10.1016/0006-291X(73)90768-7
DO - 10.1016/0006-291X(73)90768-7
M3 - Article
C2 - 4711181
AN - SCOPUS:0015925217
SN - 0006-291X
VL - 52
SP - 696
EP - 701
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -