Ornithine decarboxylase activity during kidney growth

Melvin, W.; Thomson, R. Y.

doi:10.1042/bj1290048pa

Cited by 3 publications

(1 citation statement)

References 2 publications

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“…Plasma corticosterone levels also rose rapidly, reaching a peak 2 hr after cycloheximide administration and then falling toward control levels by 8 hr (Fig. 1 (10,17,18) and since there was a substantial early rise in plasma corticosterone after cycloheximide administration, it seemed possible that the subsequent rise in enzyme activity was due, not to cycloheximide itself, but to corticosterone released in response to the stress caused by administration of the drug. To test this hypothesis, we adrenalectomized rats 16 hr before injecting cycloheximide.…”

Section: Resultsmentioning

confidence: 99%

Nature of the increase in renal ornithine decarboxylase activity after cycloheximide administration in the rat.

Levine¹,

Nicholson²,

Orth³

1975

Proc. Natl. Acad. Sci. U.S.A.

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The present study was designed to determine whether the increase in rat renal ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17) activity after cycloheximide administration was a primary effect on the kidney or was a secondary effect of adrenal or pituitary hormones released in response to the drug. Renal ornithine decarboxylase activity was reduced approximately 70% 1 hr after intraperitoneal administration of doses of cycloheximide that also inhibited renal protein synthesis by 68-95% within 1 hr. Protein synthesis began to recover by the second hour, accompanied by a rise in decarboxylase activity that reached a peak about six times greater than pretreatment values at 8 hr, then gradually declined to preinjection levels by 16 hr. Peak ornitlhine decarboxylase activity was directly proportional to cycloheximide doses up to 250 Mg; larger doses, which almost abolished protein synthesis for 8 hr, were inhibitory. Plasma corticosterone rose rapidly after cycloheximide, reached a peak at 2 hr, then fell to baseline by 8 hr. Corticosterone response was also dose-dependent up to 250 Mg, but larger doses were inhibitory. Adrenalectomy did not reduce decarboxylase activity response to cycloheximide, nor did cortisol administration enhance it. Hypophysectomy greatly reduced baseline renal decarboxylase activity within 9 hr and all but abolished the increase in enzyme activity normally seen after cycloheximide administration to the intact rat. The hypophysectomized animal exhibited apparent increased sensitivity to cyclohieximide, since a smaller dose of the drug caused a reduction in renal protein synthesis similar to that seen with a larger dose in the intact rat. As protein synthesis was recovering in the hypophysectomized animals, renal decarboxylase activity responded adequately to the injection of a crude pituitary extract. These data suggest that renal ornithine decarboxylase turnover is rapid, that baseline activity is maintained by new protein synthesis, and that the increase in renal enzyme activity after cyclolieximide is in large part dependent upon pituitary hormone action.

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Section: Resultsmentioning

confidence: 99%

Nature of the increase in renal ornithine decarboxylase activity after cycloheximide administration in the rat.

Levine¹,

Nicholson²,

Orth³

1975

Proc. Natl. Acad. Sci. U.S.A.

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Changes in DNA and RNA synthesis and associated enzyme activities after the stimulation of serum-depleted BHK21/C13 cells by the addition of serum

Howard

Hay

Melvin

et al. 1974

Experimental Cell Research

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Polyamine metabolism in compensatory renal growth

Austin

Goldin

Gaydos

et al. 1983

Kidney International

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The aliphatic polyamines, putrescine, spermidine, and spermine, appear to play an important role in many forms of rapid growth including embryonic, regenerative, hormone-induced, and neoplastic. While the exact biochemical function of polyamines is unclear, current evidence suggests they are probably involved in the biosynthesis and accumulation of nucleic acids and proteins. Increased levels of polyamines and their biosynthetic enzymes are associated with augmented kidney growth stimulated by renal mass extirpation, as well as by various hormones, toxins, and carcinogens. These observations are reviewed and additional data is provided pertaining to alterations in polyamine metabolism during compensatory renal growth following unilateral nephrectomy (uni). To further explore the effect of growth stimuli on renal polyamine synthesis, an in vitro system was employed which previously provided evidence for a circulating renal growth factor after unilateral nephrectomy. These in vitro observations underscore the rapid inducibility of ornithine decarboxylase, the rate limiting enzyme for polyamine biosynthesis; illustrate the association of polyamine and nucleic acid synthesis during enhanced kidney growth; and support the existence of a circulating renal growth regulator which apparently contributes to compensatory responses following loss of functional renal parenchyma.

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Ornithine decarboxylase activity during kidney growth

Cited by 3 publications

References 2 publications

Nature of the increase in renal ornithine decarboxylase activity after cycloheximide administration in the rat.

Nature of the increase in renal ornithine decarboxylase activity after cycloheximide administration in the rat.

Changes in DNA and RNA synthesis and associated enzyme activities after the stimulation of serum-depleted BHK21/C13 cells by the addition of serum

Polyamine metabolism in compensatory renal growth

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