Exposure of rodents to phthalates is associated with developmental and reproductive anomalies, and there is concern that these compounds may be causing adverse effects on human reproductive health. Testosterone (T), secreted almost exclusively by Leydig cells in the testis, is the primary steroid hormone that maintains male fertility. Leydig cell T biosynthesis is regulated by the pituitary gonadotropin LH. Herein, experiments were conducted to investigate the ability of di(2-ethylhexyl)phthalate (DEHP) to affect Leydig cell androgen biosynthesis. Pregnant dams were gavaged with 100 mg(-1) kg(-1) day(-1) DEHP from Gestation Days 12 to 21. Serum T and LH levels were significantly reduced in male offspring, compared to control, at 21 and 35 days of age. However, these inhibitory effects were no longer apparent at 90 days. In a second set of experiments, prepubertal rats, from 21 or 35 days of age, were gavaged with 0, 1, 10, 100, or 200 mg(-1) kg(-1) day(-1) DEHP for 14 days. This exposure paradigm affected Leydig cell steroidogenesis. For example, exposure of rats to 200 mg(-1) kg(-1) day(-1) DEHP caused a 77% decrease in the activity of the steroidogenic enzyme 17beta-hydroxysteroid dehydrogenase, and reduced Leydig cell T production to 50% of control. Paradoxically, extending the period of DEHP exposure to 28 days (Postnatal Days 21-48) resulted in significant increases in Leydig cell T production capacity and in serum LH levels. The no-observed-effect-level and lowest-observed-effect-level were determined to be 1 mg(-1) kg(-1) day(-1) and 10 mg(-1) kg(-1) day(-1), respectively. In contrast to observations in prepubertal rats, exposure of young adult rats by gavage to 0, 1, 10, 100, or 200 mg(-1) kg(-1) day(-1) DEHP for 28 days (Postnatal Days 62-89) induced no detectable changes in androgen biosynthesis. In conclusion, data from this study show that DEHP effects on Leydig cell steroidogenesis are influenced by the stage of development at exposure and may occur through modulation of T-biosynthetic enzyme activity and serum LH levels.
The current review sought to describe the published literature relative to addressing trauma in schools. Through a systematic review of peer-reviewed publications as well as gray literature, we identified a total of 91 publications that were coded for study rigor as well as a number of intervention characteristics. Publications included in the review mentioned a variety of intervention components, most notably an emphasis on counseling services, skill development, psychoeducation related to trauma, and parent engagement. We identified a relative lack of empirical evaluation of whole-school approaches and interventions intended to be delivered by non-clinical staff. We also found that less rigorous publications were more likely to highlight the needs of particularly vulnerable groups of youth and to emphasize cultural competence and community engagement in efforts to address trauma in schools. We call for more rigorous evaluation of practices and policies that take a whole-school approach and can be implemented by non-clinical staff. In particular, we highlight the need to evaluate professional development strategies that can help school staff acquire knowledge and skills that can translate into improved outcomes for students-especially students from historically marginalized groups. We also emphasize the importance of ensuring that high-quality research be made accessible to policymakers and school staff to ensure that clear, evidence-based guidance is available to avoid programs, practices, and policies that may inadvertently traumatize students or exacerbate symptoms among students who have already experienced trauma.
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