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

## TL;DR

A vitamin A deficient diet in virgin rats causes mammary gland dysfunction through increased inflammation and cell death, which can be reversed with a vitamin A sufficient diet.

## Contribution

The study identifies imbalances between NF-κB and retinoic acid signaling as key mechanisms in mammary gland dysfunction due to vitamin A deficiency.

## Key findings

- Subchronic vitamin A deficiency increases inflammation and apoptosis in mammary gland cells.
- A vitamin A sufficient diet reverses the negative effects of vitamin A deficiency on mammary gland function.
- Imbalances in NF-κB and retinoic acid signaling underlie the observed mammary gland dysfunction.

## 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.