Reproductive Toxicology 44 (2014) v–vi
Contents lists available at ScienceDirect
Reproductive Toxicology journal homepage: www.elsevier.com/locate/reprotox
Editorial
Environmental factors in dysregulation of puberty timing and progression
Keywords: Puberty timing Environmental contaminants Endocrine disrupting chemicals
Puberty has been described as the transitional stage from childhood to adulthood. The process of sexual maturation involves the hypothalamic-pituitary-gonadal system, and has its origin in fetal life. The neuroendocrine unit becomes suppressed during infancy and is reactivated at the onset of puberty. This includes reactivation of the hypothalamus and the pituitary, which initiate the sequence of changes leading to puberty. Studies from recent years have demonstrated a progressive decrease in age of onset of puberty in children around the world. Although the exact reason for this change is not completely understood, there is increasing evidence of a mutual dependency of genetic and environmental factors, directly or indirectly influencing puberty timing. The scope of this Special Issue is to discuss the role of exposure to environmental contaminants in dysregulation of puberty timing and progression. This volume of RTX encapsulates 3 reviews, 8 full length articles and one letter of correspondence. Data on both females and males, in humans, laboratory rodents and farm animals are presented. Different points of view are discussed, as evidenced by the letter of correspondence submitted in response to one of the reviews. Among environmental chemicals, endocrine and neuroendocrine disrupting chemicals (EDCs) have received growing attention. The roles of EDCs in dysregulation of puberty are deeply discussed in the reviews and original articles of this Special Issue. In vitro approaches show that EDCs alter the neuroendocrine GnRH regulatory network at all hierarchical levels. Furthermore, it is shown that the exposure to EDCs can alter genes involved in the modification of epigenetic marks. Although the scientific literature on altered onset of puberty predominantly involves studies on females, a comprehensive review is included on the role of environmental pollutants in dysregulation of male puberty in humans, laboratory rodents and farm animals. One of the important conclusions of the authors is that a more diversified methodology for determining the onset of male puberty in laboratory rodents is needed.
http://dx.doi.org/10.1016/S0890-6238(14)00037-9 0890-6238/© 2014 Published by Elsevier Inc.
Pre-puberty is presented as a critical window of increased susceptibility to the effects of environmental exposures. Peripubertal perturbations may have broad consequences that can be already visible during the pubertal phase as well as during later adult life. The original paper on delayed reproductive development in pubertal male rats exposed to statin since prepuberty covers this aspect. Moreover, postweaning exposure to genistein accelerates pubertal development, as shown by the acceleration in age of vaginal opening and mammary gland development, without negative consequences on early pregnancy in young female mice. In rats, the exposure to low levels of arsenic at prepuberty acted peripherally to suppress circulating levels of insulin-like growth factor (IGF-1) resulting in delayed sexual maturation. In view of these effects, arsenic was considered a “pubertal endocrine disruptor”. In female rats, short-term BPA exposure during the pre-pubertal period may have inhibitory effects on ovarian development and function, which were observed as developmental disorders in follicle growth and the inhibition of sex hormone secretion. Growing evidence has been documented in the lifelong consequences of perinatal influences. Herein, it is shown that in utero and lactational exposure to the anti-epiletic carbamazepin delays male rat puberty onset and affects steroidogenesis and sperm quality at late puberty. In another work, pubertal timing was altered in female rats after neonatal exposure to diethylstilbestrol (DES), in association with food restriction. Interestingly, alterations in pubertal timing due to neonatal exposure to DES are not unequivocally toward precocity, the level of exposure being critical. In humans, changes in steroid metabolism among girls with precocious puberty may not be associated with urinary levels of bisphenol A (BPA). Due to the complexity of the subject, important topics were not addressed in this Special Issue, and we hope this fact will serve to stimulate future research to unravel unanswered questions, and follow up submissions to RTX. I would like to thank Dr. Tom Knudsen for the opportunity to act as guest editor for this Special Issue of Reproductive Toxicology. My acknowledgements are also addressed for the authors of the reviews, original articles and the letter of correspondence. Some of them kindly accepted the invitation to submit their manuscripts for evaluation, while other submissions became part of the volume over time. In the name of Cindy Knudsen I would like to thank the editorial team of RTX for the constant support. This special volume
vi
Editorial / Reproductive Toxicology 44 (2014) v–vi
would not be possible without the honorable work of the reviewers that donated part of their busy time for the peer review of the manuscripts. To understand the role of exposure to environmental contaminants in dysregulation of puberty timing and progression is a puzzle. We hope we were able to put some parts together. Enjoy the reading. Your comments are welcome.
Wilma De Grava Kempinas (Ph.D.) ∗ Department of Morphology, Institute of Biosciences, UNESP – Univ Estadual Paulista, 18618-970 Botucatu, SP, Brazil ∗ Tel.: +55 14 3880 0476. E-mail address: [email protected]
Contents lists available at ScienceDirect
Reproductive Toxicology journal homepage: www.elsevier.com/locate/reprotox
Editorial
Environmental factors in dysregulation of puberty timing and progression
Keywords: Puberty timing Environmental contaminants Endocrine disrupting chemicals
Puberty has been described as the transitional stage from childhood to adulthood. The process of sexual maturation involves the hypothalamic-pituitary-gonadal system, and has its origin in fetal life. The neuroendocrine unit becomes suppressed during infancy and is reactivated at the onset of puberty. This includes reactivation of the hypothalamus and the pituitary, which initiate the sequence of changes leading to puberty. Studies from recent years have demonstrated a progressive decrease in age of onset of puberty in children around the world. Although the exact reason for this change is not completely understood, there is increasing evidence of a mutual dependency of genetic and environmental factors, directly or indirectly influencing puberty timing. The scope of this Special Issue is to discuss the role of exposure to environmental contaminants in dysregulation of puberty timing and progression. This volume of RTX encapsulates 3 reviews, 8 full length articles and one letter of correspondence. Data on both females and males, in humans, laboratory rodents and farm animals are presented. Different points of view are discussed, as evidenced by the letter of correspondence submitted in response to one of the reviews. Among environmental chemicals, endocrine and neuroendocrine disrupting chemicals (EDCs) have received growing attention. The roles of EDCs in dysregulation of puberty are deeply discussed in the reviews and original articles of this Special Issue. In vitro approaches show that EDCs alter the neuroendocrine GnRH regulatory network at all hierarchical levels. Furthermore, it is shown that the exposure to EDCs can alter genes involved in the modification of epigenetic marks. Although the scientific literature on altered onset of puberty predominantly involves studies on females, a comprehensive review is included on the role of environmental pollutants in dysregulation of male puberty in humans, laboratory rodents and farm animals. One of the important conclusions of the authors is that a more diversified methodology for determining the onset of male puberty in laboratory rodents is needed.
http://dx.doi.org/10.1016/S0890-6238(14)00037-9 0890-6238/© 2014 Published by Elsevier Inc.
Pre-puberty is presented as a critical window of increased susceptibility to the effects of environmental exposures. Peripubertal perturbations may have broad consequences that can be already visible during the pubertal phase as well as during later adult life. The original paper on delayed reproductive development in pubertal male rats exposed to statin since prepuberty covers this aspect. Moreover, postweaning exposure to genistein accelerates pubertal development, as shown by the acceleration in age of vaginal opening and mammary gland development, without negative consequences on early pregnancy in young female mice. In rats, the exposure to low levels of arsenic at prepuberty acted peripherally to suppress circulating levels of insulin-like growth factor (IGF-1) resulting in delayed sexual maturation. In view of these effects, arsenic was considered a “pubertal endocrine disruptor”. In female rats, short-term BPA exposure during the pre-pubertal period may have inhibitory effects on ovarian development and function, which were observed as developmental disorders in follicle growth and the inhibition of sex hormone secretion. Growing evidence has been documented in the lifelong consequences of perinatal influences. Herein, it is shown that in utero and lactational exposure to the anti-epiletic carbamazepin delays male rat puberty onset and affects steroidogenesis and sperm quality at late puberty. In another work, pubertal timing was altered in female rats after neonatal exposure to diethylstilbestrol (DES), in association with food restriction. Interestingly, alterations in pubertal timing due to neonatal exposure to DES are not unequivocally toward precocity, the level of exposure being critical. In humans, changes in steroid metabolism among girls with precocious puberty may not be associated with urinary levels of bisphenol A (BPA). Due to the complexity of the subject, important topics were not addressed in this Special Issue, and we hope this fact will serve to stimulate future research to unravel unanswered questions, and follow up submissions to RTX. I would like to thank Dr. Tom Knudsen for the opportunity to act as guest editor for this Special Issue of Reproductive Toxicology. My acknowledgements are also addressed for the authors of the reviews, original articles and the letter of correspondence. Some of them kindly accepted the invitation to submit their manuscripts for evaluation, while other submissions became part of the volume over time. In the name of Cindy Knudsen I would like to thank the editorial team of RTX for the constant support. This special volume
vi
Editorial / Reproductive Toxicology 44 (2014) v–vi
would not be possible without the honorable work of the reviewers that donated part of their busy time for the peer review of the manuscripts. To understand the role of exposure to environmental contaminants in dysregulation of puberty timing and progression is a puzzle. We hope we were able to put some parts together. Enjoy the reading. Your comments are welcome.
Wilma De Grava Kempinas (Ph.D.) ∗ Department of Morphology, Institute of Biosciences, UNESP – Univ Estadual Paulista, 18618-970 Botucatu, SP, Brazil ∗ Tel.: +55 14 3880 0476. E-mail address: [email protected]
