4.2 Review

Food components and contaminants as (anti)androgenic molecules

Journal

GENES AND NUTRITION
Volume 12, Issue -, Pages -

Publisher

BMC
DOI: 10.1186/s12263-017-0555-5

Keywords

Androgen; Androgen receptor; Endocrine disruptors; Polyphenols; Pesticides; Plasticizers

Funding

  1. AIRC-Associazione Italiana Ricerca sul Cancro (IG) [15221]
  2. Italian Ministry of Health
  3. Rovereto town council (Healthy and sustainable agriculture)
  4. European LIFE-EDESIA project [LIFE12 ENV/IT/000633]

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Androgens, the main male sex steroids, are the critical factors responsible for the development of the male phenotype during embryogenesis and for the achievement of sexual maturation and puberty. In adulthood, androgens remain essential for the maintenance of male reproductive function and behavior. Androgens, acting through the androgen receptor (AR), regulate male sexual differentiation during development, sperm production beginning from puberty, and maintenance of prostate homeostasis. Several substances present in the environment, now classified as endocrine disruptors (EDCs), strongly interfere with androgen actions in reproductive and nonreproductive tissues. EDCs are a heterogeneous group of xenobiotics which include synthetic chemicals used as industrial solvents/lubricants, plasticizers, additives, agrochemicals, pharmaceutical agents, and polyphenols of plant origin. These compounds are even present in the food as components (polyphenols) or food/water contaminants (pesticides, plasticizers used as food packaging) rendering the diet as the main route of exposure to EDCs for humans. Although huge amount of literature reports the (anti) estrogenic effects of different EDCs, relatively scarce information is available on the (anti) androgenic effects of EDCs. Here, the effects and mechanism of action of phytochemicals and pesticides and plasticizers as possible modulators of AR activities will be reviewed taking into account that insight derived from principles of endocrinology are required to estimate EDC consequences on endocrine deregulation and disease.

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