Relationship of Steroid Structure to Induction of Chymotrypsinogen in Embryonic Chick Pancreas in Vitro

Cohen, Amos; Kulka, Richard G.

doi:10.1210/endo-97-2-475

Cited by 15 publications

(10 citation statements)

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“…At present the curative action of trypsin inhibitors-for example, Trasylol, Antilysin-is well established (Beck et al, 1965;Nugent and Atendido, 1965;Baden et al, 1969;Malis et al, 1972). Pancreatic tissue is characterised by a high rate of synthesis of proteins and nucleic acids (Walther et al, 1974;Cohen and Kulka, 1974). It is suggested that drugs interfering with the synthesis of these macromolecules affect the formation of pancreatic enzymes.…”

mentioning

confidence: 99%

Inhibitory effect of various cytostatics and cycloheximide on acute experimental pancreatitis in rats.

Korbová¹,

Kohout²,

Maliś³

et al. 1977

Gut

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SUMMARY Cycloheximide, 5-azacytidine, and 4-methoxybenzoyl-/3-bromoacrylate (Cytembena) block the development of experimental acute pancreatitis in rats when mediated by the administration of 5 % bile solution into the pancreas in vivo. Six hours after drug treatment the pathological changes, evaluated macroscopically or using histological sections of the pancreas, were significantly decreased. The drugs affected the amount of abdominal fluid and lowered its lipase and amylase activity. The known inhibitory mechanism of the active drugs and the possible advantage of cycloheximide for clinical use are briefly mentioned.

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confidence: 99%

Inhibitory effect of various cytostatics and cycloheximide on acute experimental pancreatitis in rats.

Korbová¹,

Kohout²,

Maliś³

et al. 1977

Gut

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“…Considerable attention has been directed towards the study of factors involved in this maturation of the pancreas. Maturation in chicks (Cohen, Heller & Kulka, 1972;Yalovsky, Heller & Kulka, 1973;Cohen & Kulka, 1974;McEvoy, Hegre & Lazarow, 1975;Kumegawa, Takuma, Ikeda, Nakanishi & Hosoda, 1979), rats (Sasaki, Mura, Takeuchi, Furihata, Matsushima & Sugimura, 1976;Takeuchi, Ogawa & Sugimura, 1977) and mice (Takuma, Nakanishi, Takagj, Tanemura & Kumegawa, 1978) has been shown to be controlled by glucocorticoid hormones. However, since the levels of these hormones in the circulation do not change apppreciably between weeks 1 and 3 after birth (Daniels, Hardy & Malinowska, 1973;Diez, Sze & Ginsburg, 1976), it would appear that some hormones other than glucocorticoids may be involved in the maturation process.…”

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confidence: 99%

PERMISSIVE ROLE OF l-THYROXINE IN INDUCTION OF PANCREATIC AMYLASE BY CORTISOL IN NEONATAL RATS

Kumegawa¹,

Maeda²,

Yajima³

et al. 1980

Journal of Endocrinology

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The effect of L-thyroxine (T4) on amylase activity in the developing rat pancreas has been investigated. Administration of T4 (0.2 microgram/g body wt) alone to intact rats on days 5-10 after birth did not induce pancreatic amylase but the enzyme was induced significantly by daily injection of cortisol (10 microgram/g body wt) alone into intact rats over the same period. In thyroidectomized, adrenalectomized rats pancreatic amylase was not induced by the injection of cortisol alone but it was induced by the administration of cortisol plus T4. Increase in enzyme activity was much less in thyroidectomized animals than in intact animals. These results suggested that T4 does not have a direct effect in increasing pancreatic amylase activity but plays a permissive role in increasing enzyme activity.

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“…We also demonstrated that the administration of 0.25pmoVegg of cortisone or cortexolone had no effect on aniline hydroxylation and the elevation of TBARS levels in the liver and cataract formation. It is known that the C-1 1 positions of cortisone and cortexolone are hardly hydroxylated in chick liver (Moscona & Piddington 1967;Cohen & Kulka 1975), presumably because of lacking, or quite low activy of, 1 lp-hydroxysteroid dehydrogenase (type 1). Therefore, the phenomena described above could be caused by the biological actions of glucocorticoid since the C-11 p-hydroxyl group of the structure is known to be essential for the biological activities (Moscona & Piddington 1967;Cohen & Kulka 1975).…”

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confidence: 99%

“…It is known that the C-1 1 positions of cortisone and cortexolone are hardly hydroxylated in chick liver (Moscona & Piddington 1967;Cohen & Kulka 1975), presumably because of lacking, or quite low activy of, 1 lp-hydroxysteroid dehydrogenase (type 1). Therefore, the phenomena described above could be caused by the biological actions of glucocorticoid since the C-11 p-hydroxyl group of the structure is known to be essential for the biological activities (Moscona & Piddington 1967;Cohen & Kulka 1975). In addition, phenobarbital treatment, which stimulated hepatic hydroxylation activity of aniline in developing chick embryos at a similar rate to hydrocortisone treatment (Nishigori & Iwatsuru 1982), did not elevate TBARS in the liver and produce cataract (unpublished data).…”

mentioning

confidence: 99%

Alteration of Activities of Hepatic Antioxidant Defence Enzymes in Developing Chick Embryos After Glucocorticoid Administration - A Factor to Produce Some Adverse Effects?

Lee

Iwatsuru

Nishigori

1998

Journal of Pharmacy and Pharmacology

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Liver tissue is one of the principal targets of glucocorticoids, therefore changes in the balance between hepatic oxidative and reductive capacity may greatly influence adverse effects of glucocorticoid therapy. In this study, effects of glucocorticoid on the activities of hepatic antioxidant defence enzymes were examined by using developing chick embryos. After the administration of 0.25 micromol hydrocortisone sodium succinate, a typical glucocorticoid, to 15-day-old chick embryos, glutathione peroxidase, glutathione reductase, catalase and superoxide dismutase in the liver generally began to decrease at around 4 h, reaching 60-70% of control levels between 24 and 48 h. These changes were observed much earlier than the elevation of the hepatic thiobarbituric acid reacting substance (TBARS) level which began to increase from 20h, reaching about six times the control level at 48 h after hydrocortisone administration. Conversely, the elevated TBARS level decreased back to the normal level with the recoveries of these enzyme activities. Furthermore, it was found that the aniline hydroxylase activity, measured as a marker of oxidative activity, began to increase after around 12 h. These results suggested that TBARS levels were possibly produced by the suppression of antioxidant defence abilities and the significant induction of oxidative activity in the liver by glucocorticoid. As the elevated TBARS in the liver can be distributed to tissues, TBARS will be involved in the occurrence of some of the glucocorticoid-induced adverse effects such as cataract formation.

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Relationship of Steroid Structure to Induction of Chymotrypsinogen in Embryonic Chick Pancreas in Vitro

Cited by 15 publications

References 0 publications

Inhibitory effect of various cytostatics and cycloheximide on acute experimental pancreatitis in rats.

Inhibitory effect of various cytostatics and cycloheximide on acute experimental pancreatitis in rats.

PERMISSIVE ROLE OF l-THYROXINE IN INDUCTION OF PANCREATIC AMYLASE BY CORTISOL IN NEONATAL RATS

Alteration of Activities of Hepatic Antioxidant Defence Enzymes in Developing Chick Embryos After Glucocorticoid Administration - A Factor to Produce Some Adverse Effects?

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