Experimental Griseofulvin Porfhyria in Adult and Foetal Mice

Lochhead, Ann C.; and, J. H. Dago And; Goldberg, A.

doi:10.1111/j.1365-2133.1967.tb11463.x

Cited by 34 publications

(13 citation statements)

References 8 publications

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“…The carcinogenic activity of griseofulvin, as corroborated in this experiment, was formerly limited to mouse liver (DeMatteis et al, 1966;Lochhead et al, 1967). While previous reports in rats (Klein and Beall, 1972;Paget and Alcock, 1960) have yielded little information about carcinogenicity (perhaps owing to their brevity), our study records positive results in this species.…”

Section: Discussionsupporting

confidence: 78%

“…[WHO], 1966), with multiple malformations observed in cat offspring at therapeutic doses (Scott et al, 1975). Prolonged oral administration of griseofulvin to mice at elevated doses severely impaired hepatic porphyrin metabolism and caused hepatomegaly (DeMatteis, 1963;DeMatteis et al, 1966;Lochhead et al, 1967), extensive liver damage (Barich et al, 1961;Hurst and Paget, 1963) and hepatoma induction (DeMatteis et al, 1966;Hurst and Paget, 1963). Hepatoma induction by griseofulvin was also reported after s.c. administration of milligram quantities to infant mice (Epstein et al, 1967).…”

Section: Griseofulvin (Fulvicin Grisactin)mentioning

confidence: 99%

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Thyroid tumours in rats and hepatomas in mice after griseofulvin treatment

Rustia¹,

Shubik²

1978

Br J Cancer

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Summary.-Griseofulvin, an antibiotic used to treat dermatophytosis, was tested for carcinogenicity in mice, rats and hamsters. Three groups of mice and rats were given the drug in powdered diet in alternating 5-week periods for life, at dose levels of 3.000, 1-500 and 0-300 (mice) and 2.0%, 1-0% and 0-2% (rats). A group of mice and 3 groups of hamsters received continuous daily treatment for life with griseofulvin at 3-000, 1.5%, 0.300 and 0.1% dose levels respectively. A significant incidence of hepatic tumours was observed at the 2 higher treatment levels in mice. Also, statistically significant rates (P < 0.001 and/or P < 0.020) of thyroid tumours, indicating a dose-response, were recorded in male rats at the 2.00/ 1-0%0, and 0 2% dose levels, and in females at the 2.0°, and 1.0% dose levels. Hamsters did not develop neoplasms in response to treatment at any level.

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Section: Discussionsupporting

confidence: 78%

Section: Griseofulvin (Fulvicin Grisactin)mentioning

confidence: 99%

Thyroid tumours in rats and hepatomas in mice after griseofulvin treatment

Rustia¹,

Shubik²

1978

Br J Cancer

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“…The enzymatic abnormality in GF-induced protoporphyria is a decrease of hepatic heme synthetase activity (16). It is considered, therefore, that the pathogenesis of GF-induced protoporphyria has a hepatic origin (17).…”

Section: Commentsmentioning

confidence: 99%

The Synergistic Effect of Isonicotinic Acid Hydrazide (INH) and Griseofulvin (GF) on Porphyrin Metabolism

Watanabe

1991

The Journal of Dermatology

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Abnormal porphyrin metabolism can be induced by several chemicals. To investigate the synergistic effect on porphyrinopathy of isonicotinic acid hydrazide (INH) with a low concentration of griseofulvin (GF), the two chemicals were given to mice simultaneously. INH was added to drinking water at a concentration of 0.05%. GF was mixed with feed at a concentration of 0.1%. The mice (dd-y strain) were divided into four groups. Those in group A were fed normally. Group B received only 0.1% GF, group C received only 0.05% INH, and group D received both 0.1% GF and 0.05% INH. The treatment was continued for 13 to 30 weeks. After treatment, the mice were anesthetized and sacrificed. The liver and whole blood were taken for analysis of porphyrins. The results revealed a slight elevation of erythrocytic porphyrins in the groups treated with 0.1% GF or 0.05% INH alone and remarkable abnormalities in the hepatic and erythrocytic porphyrin levels of the group simultaneously treated with both chemicals. These results show that INH itself may have a small potential for the induction of porphyric abnormalities, and that the administration of INH with a low concentration of GF induces marked porphyrinopathy in dd-y strain mice.

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“…Griseofulvin (GF) is known to induce protoporphyria in mice (1), and GF-induced protoporphyric (GF-P) mice have been adopted as an experimental model for human erythropoietic protoporphyria (EPP) (2).…”

Section: Introductionmentioning

confidence: 99%

Relationship between N‐Acetyltransferase (NAT) Activity and Liver Protoporphyrin Level in Experimental Porphyria

Watanabe

Irifune

Ohgami

et al. 1996

The Journal of Dermatology

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The results of our previous studies demonstrated that isonicotinic acid hydrazide (INH) can aggravate griseofulvin (GF)-induced protoporphyria in mice. To elucidate this phenomenon, we studied the relationship between liver protoporphyrin (PP) levels and N-acetyltransferase (NAT) activity, which is known to be a major catabolic enzyme of INH metabolism in the liver. The results revealed a significant correlation between liver PP levels and NAT activity in the mice fed 0.1% GF and 0.05% INH. In this group, mice with high NAT activity developed severe protoporphyria. There was no correlation, however, between liver PP levels and NAT activity in the mice fed GF alone or INH alone. The result suggested that INH metabolites formed by NAT enhance the hepatotoxicity of GF in mice.

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Experimental Griseofulvin Porfhyria in Adult and Foetal Mice

Cited by 34 publications

References 8 publications

Thyroid tumours in rats and hepatomas in mice after griseofulvin treatment

Thyroid tumours in rats and hepatomas in mice after griseofulvin treatment

The Synergistic Effect of Isonicotinic Acid Hydrazide (INH) and Griseofulvin (GF) on Porphyrin Metabolism

Relationship between N‐Acetyltransferase (NAT) Activity and Liver Protoporphyrin Level in Experimental Porphyria

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