Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet

Mammary gland epithelial dysfunction is one of the serious consequences of subchronic dietary vitamin A deficiency (VAD). However, the underlying mechanism of this process is incompletely known. Consequently, we utilized a virgin rat model of dietary VAD (3 and 6 months) and subsequently intervened with a vitamin A sufficient (VAS) diet (0.5 or 1 month) prior to treatment completion. This experimental model allowed us to investigate the underlying molecular mechanism of mammary gland tissue dysfunction caused by VAD. Dietary VAD for 3 and 6 months caused increased inflammatory cell infiltration in the mammary gland parenchyma and glandular cells, with increased inflammation and apoptosis and reduced cell proliferation. These changes can be reversed with a VAS diet. Imbalances between the NF-κB and retinoic acid (RA) signaling pathways underlie mammary gland dysfunction following subchronic VAD. Nulliparous rats fed a VAD diet experience mammary gland epithelial dysfunction because of inflammation, apoptosis, and impaired cell growth.

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Journal
Oxidative Medicine and Cellular Longevity
Published
2025-01-01
DOI
https://doi.org/10.1155/omcl/6334165
Primary Topic
Antioxidant Activity and Oxidative Stress
Type
article
Field-Weighted Citation Impact
0.00

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article

Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet

Graciela A. Jahn, Sandra Gomez-Mejiba, Verónica Filippa, Darío C. Ramírez et al.
Oxidative Medicine and Cellular Longevity
Antioxidant Activity and Oxidative Stress
article

Apoptosis in the Mammary Gland of Virgin Rats Subchronically Fed With a Vitamin A Deficient Diet

Graciela A. Jahn, Sandra Gomez-Mejiba, Verónica Filippa, Darío C. Ramírez, Fiorella Campo Verde Arboccó, Fabián Mohamed, María S. Giménez, Mariano Acosta, C Ferrari, M. Vasquez-Gomez
article en

Abstract

Mammary gland epithelial dysfunction is one of the serious consequences of subchronic dietary vitamin A deficiency (VAD). However, the underlying mechanism of this process is incompletely known. Consequently, we utilized a virgin rat model of dietary VAD (3 and 6 months) and subsequently intervened with a vitamin A sufficient (VAS) diet (0.5 or 1 month) prior to treatment completion. This experimental model allowed us to investigate the underlying molecular mechanism of mammary gland tissue dysfunction caused by VAD. Dietary VAD for 3 and 6 months caused increased inflammatory cell infiltration in the mammary gland parenchyma and glandular cells, with increased inflammation and apoptosis and reduced cell proliferation. These changes can be reversed with a VAS diet. Imbalances between the NF-κB and retinoic acid (RA) signaling pathways underlie mammary gland dysfunction following subchronic VAD. Nulliparous rats fed a VAD diet experience mammary gland epithelial dysfunction because of inflammation, apoptosis, and impaired cell growth.

Oxidative Medicine and Cellular LongevityVol. 2025(1)
University of Mendoza (AR), Centro Científico Tecnológico - San Luis (AR), Centro Científico Tecnológico - Mendoza (AR), National University of San Luis (AR)
Universidad Nacional de San Luis, Consejo Nacional de Investigaciones Científicas y Técnicas, Agencia Nacional de Promoción Científica y Tecnológica
Openalex Percentile: Top 84%
Antioxidant Activity and Oxidative Stress
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