Perinatal androgenic exposure and reproductive health effects female rat offspring.

Environmental contaminants known as endocrine-disrupting chemicals (EDC) have been associated with adverse effects on reproductive processes. These chemicals may mimic or antagonize endogenous hormones, disrupting reproductive functions. Although preliminary studies focused on environmental estrogens, the presence of compounds with androgenic activity has also been described. This study examines exposure of female pregnant and lactating rats to low doses of androgens and assesses potential effects on female offspring. Pregnant Wistar rats were exposed to testosterone propionate (TP) at doses of 0.05, 0.1, or 0.2 mg/kg or corn oil (vehicle), subcutaneously, to determine influence on reproductive health of female offspring. There were two exposure groups: (1) rats treated from gestational day (GD) 12 until GD 20; and (2) animals treated from GD 12 until the end of lactation. Perinatal exposure to TP produced increased anogenital distance after birth and diminished height of uterine glandular epithelium at puberty in animals exposed to 0.2 mg/kg. However, these alterations were not sufficient to impair sexual differentiation and normal physiology of the female rat reproductive tract.

Effect of smoking on the DNA methylation pattern of the SOCS1 promoter in epithelial cells from the saliva of patients with chronic periodontitis.

BACKGROUND: The aim of the present study was to evaluate the methylation pattern in the suppressor of cytokine signaling 1 (SOCS1) gene in smokers and non-smokers with chronic periodontitis (CP). METHODS: Methylation-specific polymerase chain reaction (PCR) was performed to determine the methylation status of the SOCS1 promoter in 45 saliva samples from smokers and non-smokers with CP. RESULTS: Cells from the saliva of CP patients who smoked were 7.08 times more likely to have a methylated SOCS1 promoter than cells from the saliva of non-smoking patients. CONCLUSIONS: SOCS1 gene promoter methylation, with its potential effects on the expression of this gene, seems to be a consequence of exposure to tobacco and not to periodontal disease. Further studies are needed to elucidate the relationship between the epigenetic control of immune response gene expression, exposure to environmental factors, and the development, progression, and prognosis of CP.

Skewed X-chromosome inactivation and shorter telomeres associate with idiopathic premature ovarian insufficiency.

OBJECTIVE: To analyze whether telomere length, X-chromosome inactivation (XCI), and androgen receptor (AR) GAG polymorphism are related to idiopathic premature ovarian insufficiency (POI). DESIGN: Case-control study. SETTING: University hospital. PATIENT(S): A total of 121 women, including 46 nonsyndromic POI and 75 controls. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Age, weight, height, body mass index (BMI), systolic and diastolic arterial pressure, E2, androstenedione, T, and C-reactive protein were assessed. Telomere length was estimated by quantitative real-time polymerase chain reaction, XCI was measured using the Human Androgen Receptor and X-linked retinitis pigmentosa 2 (RP2) methylation assays. AR and FMR1 polymorphism was assessed by quantitative fluorescent polymerase chain reaction and sequencing. RESULT(S): Premature ovarian insufficiency women had a higher mean age, weighed less, and exhibited lower C-reactive protein, E2, and androstenedione levels. The AR polymorphism did not differ between the groups. Four patients had premutation (55-200 CGG repeats), and none displayed a full mutation in the FMR1 gene. However, patients with POI showed shorter telomere length and higher frequency of skewed XCI. Extreme skewing (≥90%) was observed in 15% of women with POI, and shorter telomeres correlated with XCI skewing in both groups. CONCLUSION(S): Skewed XCI and shortened telomere length were associated with idiopathic POI, despite no alterations in the AR and FMR1 genes. Additionally, there is a tendency for women with short telomeres to exhibit skewed XCI.

Cervicovaginal bacterial count and failure of metronidazole therapy for bacterial vaginosis.

OBJECTIVE: To evaluate whether total bacterial count in cervicovaginal fluid is associated with failure of metronidazole therapy for bacterial vaginosis. METHODS: In a cross-sectional study, women attending a primary health center in Botucatu, São Paulo, Brazil, for routine cervical screening between September 2012 and October 2013 were enrolled. Women who tested positive for bacterial vaginosis (Nugent classification) were offered oral metronidazole. Women who completed metronidazole treatment and an equal number of control women with normal vaginal flora at initial screening were included in analyses of total bacterial count, assessed by flow cytometry of cervicovaginal fluid samples. RESULTS: Of 287 women who enrolled, 49 were excluded because they tested positive for trichomoniasis, chlamydial endocervicitis, gonorrhea, or candidiasis. Among the remaining 238, 85 (35.7%) had bacterial vaginosis. Among 36 women evaluated at follow-up, 23 (63.9%) had successfully restored lactobacilli-dominant flora, 12 (33.3%) had persistent bacterial vaginosis, and 1 (2.8%) had vaginal candidiasis (excluded from flow cytometry). Total bacterial count did not differ between 35 women with bacterial vaginosis and 35 with normal vaginal flora (P=0.62). Total bacterial count did not differ at enrollment between women who went on to have persistent bacterial vaginosis and those who had successful treatment (P=0.78). CONCLUSION: Failure of oral metronidazole therapy for bacterial vaginosis was not associated with total bacterial count in cervicovaginal fluid.