Exposure to phthalates and female reproductive health: A literature review.

Endocrine-disrupting chemicals (EDCs) are exogenous compounds that have been known for their ability to interfere with the action of hormones and affect endocrine pathways, including the ones involved in the development and function of both male and female reproductive systems. EDCs comprise a wide class of compounds, such as pesticides, bisphenol A, phthalates and, parabens, that are present in the environment and in several daily use products. Phthalate esters, compounds commonly used as plasticizers and additives in many industrial applications, have attracted special attention because of the widespread human exposure and the potential for disruption of androgen-dependent development in males. Although phthalates are rapidly metabolized and excreted, their ubiquitous presence ensures continuous exposures throughout different life stages from conception to adult life, as documented by a number of human biomonitoring studies worldwide. Although most research efforts have been placed on the impact of phthalates on male reproductive development and functions, there is a large body of recent experimental and observational data indicating that phthalates can negatively affect female reproductive health, and in particular alter ovarian and uterine functions, potentially contributing to disorders like polycystic ovarian syndrome, endometriosis, and other common female reproductive problems. This review summarizes the most recent experimental and epidemiologic literature on the potential effects of phthalate exposures on female reproductive health and their impact on female fertility.

Correlation Between Inflammatory and Epigenetic Marks With Aerobic Performance in 10-km Runners.

Purpose: Our goals were to evaluate the effect of a 10-km running trial on inflammatory and epigenetic markers of 10-km runners and correlate the biochemical findings with anthropometric variables and performance. Methods: Twenty trained 10-km runners and seven sedentary male volunteers were recruited. Venous blood samples were collected at different times: under resting conditions, before the 10 Km race, and immediately after the finish. Inflammatory markers (IL-6, IL-10, and IL-ß) and cortisol levels were evaluated in plasma, while DNA methyltransferases (DNMT1 and DNMT3b) contents were measured in peripheral blood mononuclear cells (PBMCs). Results: Higher levels of plasma IL-6 levels were observed in 10-km runners compared to the sedentary group. After the trial, the runners had a significant increase on IL-6, IL-10, and cortisol plasma levels compared to baseline. Conclusion: Our findings suggest that inflammatory profile, but not DNMT content, influences aerobic performance in 10-km runners.

The endocrine disrupting effects of sodium arsenite in the rat testis is not mediated through macrophage activation.

Arsenic (As) is an endocrine disrupting chemical that can disturb the male reproductive system. In a previous study, it was suggested that testicular macrophages could display a role in endocrine disruption induced by As exposure. This work aimed to evaluate the effects of chronic As exposure in the testis function of Wistar rats and examine the participation of macrophage activation and inflammatory response in these processes. We examined gene expression of steroidogenic machinery and immunological markers by RT-QPCR, plasma testosterone concentrations, sperm count and morphology, and histomorphometrical parameters after 60-days exposure to 1 or 5 mg.kg-1.day-1 of sodium arsenite, combined or not with 50 µg.kg-1 of LPS administered one day before euthanasia. We have demonstrated that As exposure reduced the weight of androgen-dependent organs and induced changes in spermatogenesis, in particular at the highest dose. LPS and As co-exposure promoted a decrease in testosterone synthesis, but did not increase the overexpression of markers of macrophage activation seen in LPS-only rats. Our results suggest that As does not alter the testicular macrophage function, but under immunological challenges LPS and As can display a complex interaction, which could lead to endocrine disruption.

Treadmill exercise induces age and protocol-dependent epigenetic changes in prefrontal cortex of Wistar rats.

Some studies have linked age-related beneficial effects of exercise and epigenetic mechanisms. Although, the impact of treadmill exercise on histone acetylation, histone and DNA methylation marks in aged cortices yet remains poorly understood. Considering the role of frontal cortex on brain functions, we investigated the potential of different exercise protocols, single session and daily exercise, to modulate epigenetic marks, namely global H4 acetylation, histone methyltransferase activity (HMT H3K27) and levels of DNA methytransferase (DNMT1 and DNMT3b) in prefrontal cortices from 3 and 21-months aged Wistar rats. The animals were submitted to two treadmill exercise protocols, single session (20min) or daily moderate (20min/day during 14days). The daily exercise protocol induced an increased in histone H4 acetylation levels in prefrontal cortices of 21-months-old rats, without any effects in young adult group. DNMT3b levels were increased in aged cortices of animals submitted to single session of exercise. These results indicate that prefrontal cortex is susceptible to epigenetic changes in a protocol dependent-manner and that H4 acetylation levels and DNMT3b content changes might be linked at least in part to exercise-induced effects on brain functions.

Long-term effects of pre and post-ischemic exercise following global cerebral ischemia on astrocyte and microglia functions in hippocampus from Wistar rats.

Persistent effects of pre- and postischemic exercise on glial cells activation after global cerebral ischemia remains poorly understood. Here, we investigated the effect of both pre and postischemic treadmill exercise protocols (20min/day during 2 weeks) on glial cells immunostaining in the hippocampus of Wistar rats submitted to global ischemia. A synergistic effect between ischemia and postischemic exercise on the astrocytic area was demonstrated. Postischemic exercise partially reversed the ischemia-induced increase on the area occupied by microglia, without any effect of pre-ischemic protocol. In conclusion, postischemic exercise distinctly modulates astrocyte and microglia immunostaining in the hippocampal dentate gyrus following global cerebral ischemia in Wistar rats.