Aim: 

The Syrian hamster Harderian gland (HG) has been studied with regard to its strong sexual dimorphism not only in morphology but also in oxidative stress, which is moderate in male and extreme in female glands and alters the glandular structure showing gender-related differences in autophagic and invasive processes. So we hypothesize that redox-sensitive transcription factors, NF-kB and p53, could mediate in the gland physiology.

Methods: 

Syrian hamsters (n=24) Harderian glands were removed and stored until the experiments were performed: oxidative stress studies (protein carbonyl, lipid peroxidation and evaluation of NF-kB activation), cell adhesion studies (P-cadherin, cytokeratins, cathepsin H expression and matrix metalloproteinase-2 activity) and cell death studies (tunel assay, caspase-3, cathepsins B and D activities and expression of p53, cathepsin D, Lamp-2, Bcl-2, Beclin and LC3).

Results: 

Oxidative damage was higher in female than in male HGs but even so, NF-kB was activated in male glands. Female glands showed nuclear p53 expression, absence of classical apoptosis, alterations in the lysosomal pathway and presence of autophagic markers. Histological data showed, in female glands, a huge release of cellular debris and nuclei into the lumina. Moreover, cell adhesion studies revealed in female glands a downregulation in P-cadherin expression, changes in the cytoskeleton and promotion of some proteinases contributing to cell detachment that could be triggering autophagic cell death.

Conclusion: 

Our findings indicate that in Syrian hamster HG, oxidative stress orchestrates the glandular physiology through NF-kB and p53, modulating the autophagic cell death.