The rat vomeronasal organ is a vitamin D target

Rodewald, Andrea; Gebhart, V.M.; Oehring, H; Jirikowski, Gustav F.

doi:10.1016/j.jchemneu.2017.01.006

Cited by 2 publications

(1 citation statement)

References 36 publications

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“…In fact, if on one hand, small airborne molecules may interact with the olfactory epithelium [16], on the other hand, non-volatile substances such as steroids [17], peptides [18,19], and proteins [20] can be detected only by the vomeronasal organ (VNO) [21], a partially atrophic, even if functional in many subjects, organ that has been suspected to be the primary target of olfactory steroids [22]. In this light, the expression of sex hormone binding globulin, a transport protein for estradiol and testosterone, and vitamin D binding protein and receptor in the VNO has been recently observed [23][24][25]. Furthermore, biosynthesis and metabolism of these neuroactive steroids also occur within the brain [26,27] where they are involved in limbic functions [28,29].…”

Section: Introductionmentioning

confidence: 99%

Olfactory-Related Quality of Life in Multiple Chemical Sensitivity: A Genetic-Acquired Factors Model

Micarelli

Cormano²,

Caccamo³

et al. 2019

IJMS

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Genetic polymorphisms as well as environmental exposures to chemical compounds, iatrogenic, psychological, and physical trauma may play a pathophysiological role in multiple chemical sensitivity (MCS) olfactory complaints, given that xenobiotic metabolism is influenced by sequence variations in genes of metabolizing enzymes. Thus, the aim of the present study was to depict—by means of multiple regression analysis—how different genetic conditions, grouped according to their function as well as clinical background and environmental exposure may interfere with those olfactory complaints referred by MCS patients. Therefore, MCS patients after gene polymorphism sequencing, the olfactory-related quality of life score—calculated by means of the Questionnaire of Olfactory Disorder in forty-six MCS patients—have been found to significantly rely on the phase I and II enzymes score and exposure to previous compounds and surgical treatments. The present work—implementing for the first time a genetic-acquired factors model on a regression analysis—further reinforces those theories, positing MCS as a complex, multifactorial, disease in which the genetic risk related to phase I and II enzymes involved in xenobiotic detoxification, olfactory, and neurodegenerative diseases play a necessary, but probably not sufficient role, along the pathophysiological route of the disease.

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