Chronic stress decreases ornithine decarboxylase expression and protects against 1,2-dimethylhydrazine-induced colon car

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ORIGINAL ARTICLE

Chronic stress decreases ornithine decarboxylase expression and protects against 1,2‑dimethylhydrazine‑induced colon carcinogenesis Edgar Oswaldo Zamora‑González1   · Patricia Castro‑Félix2   · María del Rosario Huizar‑López2   · Josefina Casas‑Solís2   · María de la Luz Blanca Isabel Marques‑González2   · Martha Fabiola Martin del Campo‑Solís3   · Anne Santerre2  Received: 20 August 2020 / Accepted: 19 November 2020 © Springer Nature B.V. 2020

Abstract Biological response to stress depends on the type, timing, and severity of the stressor. Acute stressful environments may positively activate molecular and cellular mechanisms to favor adaptation; however, chronic stress is often associated with detrimental health effects. Colon cancer (CC) is one of the leading causes of death associated with cancer and has been mentioned as a stress-related disease. In the present work, the effect of chronic stress on the initial phase of CC was evaluated, and special emphasis was placed on ornithine decarboxylase (ODC) expression and polyamines for their role in hyperproliferative diseases. BALB/c mice (n = 5/group) were administered the pro-carcinogen 1,2-dimethylhydrazine (DMH) for 8 weeks (20 mg/kg body weight/week) to induce colon carcinogenesis, and then exposed for 4 weeks to two physical stressors: restraint and forced-swimming. Distal colon inflammatory lesions and histomorphological changes were evaluated by hematoxylin–eosin staining; plasma corticosterone levels, colon ODC expression, and urinary polyamines were determined by competitive ELISA, RT-qPCR, Western Blot, and HPLC, respectively. The short-term exposure to DMH triggered colon inflammation, initiated colon carcinogenesis and increased ODC expression; meanwhile, the exposure to chronic stress activated the hypothalamic–pituitary–adrenal (HPA) axis, elicited the production of plasmatic corticosterone, and decreased ODC expression. The exposure of DMH-treated mice to chronic stress counteracted the inflammatory effect of DMH and maintained ODC homeostasis. In early phase of carcinogenesis, the exposure of DMH-treated mice to chronic stress had a positive effect against colon inflammation and maintained ODC homeostasis. The cross-talk between corticosterone, ODC expression, and inflammation in a tumor environment is discussed. Keywords  Chronic stress · Corticosterone · Ornithine decarboxylase · Colon carcinogenesis · 1,2-Dimethylhydrazine

Introduction

* Anne Santerre [email protected] 1



Departamento de Bienestar y Desarrollo Sustentable, Centro Universitario del NORTE, Carretera Federal No. 23, Km 191, C.P. 46200 Colotlán, Jalisco, México

2



Departamento de Biología Celular y Molecular, Centro Universitario de Ciencias Biológicas y Agropecuarias, Carretera Guadalajara‑Nogales Km 15.5, Las Agujas, C.P. 45110 Zapopan, Jalisco, México

3

Departamento de Fundamentos del Conocimiento, Centro Universitario del NORTE, Carretera Federal No. 23, Km 191, C.P. 46200 Colotlán, Jalisco, México



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