Prednisone is Not a Mouse Carcinogen

Dillberger, John E.; Cronin, Nancy S.; Carr, Gregory J.

doi:10.1177/019262339202000103

Cited by 12 publications

(10 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…About 20% of cells in the inner cortex showed cellular degeneration and the accumulation of rounded vacuolated cell debris, membranous material and pigment. 156 This was also characterized by the presence of degeneration and accumulation of large cells containing abundant golden brown pigment at the corticomedullary junction, i.e. Similar findings have been reported in dogs treated with other glucocorticoids for prolonged periods.…”

Section: Atrophy Of the Zona Fasciculata And Reticularissupporting

confidence: 71%

Endocrine Glands

Greaves¹

2012

Histopathology of Preclinical Toxicity Studies

View full text Add to dashboard Cite

Section: Atrophy Of the Zona Fasciculata And Reticularissupporting

confidence: 71%

Endocrine Glands

Greaves¹

2012

Histopathology of Preclinical Toxicity Studies

View full text Add to dashboard Cite

“…It has been reported that body weight loss in rodents treated with corticosteroids is caused by their systemic catabolic effects. 18 –20 Although systemic exposure to the TCSs was not measured in the present study, the body weight loss in the DF group was considered possibly related to a systemic effect of DF of very strong potency compared to PV (medium potency) and BV (strong potency). Difference in clinical efficacy/potency may explain why the body weight loss was seen only in the DF group.…”

Section: Discussionmentioning

confidence: 90%

“…It has been reported that body weight loss in rodents treated with corticosteroids is caused by their systemic catabolic effects. [18][19][20] Although systemic exposure to the TCSs was not measured in the present study, the body weight loss in the DF group was considered , and DF (F). Cldn-1 positivity was seen in the suprabasal layer in the epidermis (A).…”

Section: Discussionmentioning

confidence: 99%

Effects of Delgocitinib Ointment 0.5% on the Normal Mouse Skin and Epidermal Tight Junction Proteins in Comparison With Topical Corticosteroids

Anagawa-Nakamura¹,

Ryoke²,

Yasui³

et al. 2020

Toxicol Pathol

View full text Add to dashboard Cite

Delgocitinib ointment 0.5% is the world’s first topical Janus kinase inhibitor product and was approved for treatment of atopic dermatitis (AD) in Japan. Although topical corticosteroids (TCSs) have been the mainstay of pharmacotherapy in AD over the past decades, long-term use of TCSs causes skin atrophy and alteration of the epidermal tight junction (TJ) leading to epidermal barrier dysfunction. In this study, delgocitinib ointment 0.5% or representative TCSs of different potencies were applied dermally once daily to the ear pinna of normal ICR mice for 14 days, and ear pinna thickness, histopathology, and immunohistochemistry for epidermal TJ proteins claudin-1 and -4 were evaluated. All the TCSs caused decreases in ear pinna thickness with epidermal thinning, sebaceous gland atrophy, and atrophy/decreased number of the subcutaneous adipocytes and decreased immunohistochemical staining intensity for epidermal claudins. In contrast, delgocitinib ointment 0.5% did not cause any of those changes. In conclusion, once daily topical delgocitinib ointment 0.5% for 14 days did not cause skin atrophy or decreased immunohistochemical staining of epidermal claudins, which are common safety concerns associated with TCSs. These characteristics suggest that delgocitinib ointment 0.5% has an improved safety profile over currently available TCS therapies particular for the long-term AD treatment.

show abstract

“…This study highlights temporal changes in the adrenal glands of offspring and the emergence of specific abnormalities with ageing as evidenced by the fact that at 12 months of age, male offspring of Cort-exposed dams had an increased number of adrenal plaques. These deposits have been shown to be associated not only with ageing (Rosol et al 2001) but also elevated corticosteroid levels (Schardein et al 1967, Dunn 1970, Dillberger et al 1992.…”

Section: :1mentioning

confidence: 99%

Prenatal corticosterone exposure programs sex-specific adrenal adaptations in mouse offspring

Cuffe

Turton

Akison

et al. 2017

Journal of Endocrinology

View full text Add to dashboard Cite

Maternal stress can impair foetal development and program sex-specific disease outcomes in offspring through the actions of maternally produced glucocorticoids, predominantly corticosterone (Cort) in rodents. We have demonstrated in mice that male but not female offspring prenatally exposed to Cort (33 µg/kg/h for 60 h beginning at E12.5) develop cardiovascular/renal dysfunction at 12 months. At 6 months of age, renal function was normal but male offspring had increased plasma aldosterone concentrations, suggesting that altered adrenal function may precede disease. This study investigated the long-term impact of prenatal exposure to Cort on adrenal growth, morphology and steroidogenic capacity as well as plasma Cort concentrations in offspring at postnatal day 30 (PN30), 6 months and 12 months of age. Prenatal Cort exposure decreased adrenal volume, particularly of the zona fasciculata, in male offspring at PN30 but increased both relative and absolute adrenal weight at 6 months of age. By 12 months of age, male Cort-exposed offspring had reduced absolute adrenal weight in association with increased adrenal plaque deposition (lipogenic pigmentation). Plasma Cort concentrations were elevated in male 6-month offspring but not at other ages. mRNA expression of Mc2r (ACTH receptor) was increased in males at PN30, and Cyp11a1 expression was decreased at 6 and 12 months of age. There were no changes in the adrenals of female Cort-exposed offspring. This study demonstrates that prenatal Cort exposure induces offspring adrenal gland dysfunction in an age- and sex-specific manner, which may contribute to long-term programmed disease in male offspring after maternal stress.

show abstract

Prednisone is Not a Mouse Carcinogen

Cited by 12 publications

References 16 publications

Endocrine Glands

Endocrine Glands

Effects of Delgocitinib Ointment 0.5% on the Normal Mouse Skin and Epidermal Tight Junction Proteins in Comparison With Topical Corticosteroids

Prenatal corticosterone exposure programs sex-specific adrenal adaptations in mouse offspring

Contact Info

Product

Resources

About