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The main objective of this work is to analyze the perinatal protective effects of curcumin (Cur) on the toxicity of inorganic mercury (mercuric chloride – HgCl 2) in the developing mice offspring on their behavioral and biochemical changes. Six groups of pregnant mice (consisting of ten animals in each) were allocated in a way that Group I consuming tap water was used as control. Groups II to VI were the experimentally treated groups in which Group II and III received 150 and 300 ppm of curcumin, respectively; Group IV was given 10 ppm of HgCl 2 ; and Group V and VI were also exposed to 10 ppm of HgCl 2 but concurrently they were also treated with 150 and 300 ppm of curcumin, respectively. Appearance of vaginal plug was considered as the first day of pregnancy and all treatment started from day one of pregnancy until post-natal day 15 (PD 15) and the mothers were switched to plain tap water thereafter. At the age of PD 40, the male pups were subjected to measuring the depression in the light-dark chambers, forced swimming and tail suspension tests and to measuring their anxiety in plus-maze and open-field tests. Subsequently, after behavioral tests, the levels of corticosterone and cortisol hormones were estimated in the plasma of the experimental offspring. Behavioral tests were measured in the HgCl 2 treated offspring for the light-dark chambers; forced swimming test; tail suspension test; plus-maze test; and open –field test showed significant alterations in their depression, anxiety and locomotory activities. Biochemical estimation of corticosterone and cortisol hormones in the plasma of these offspring showed significant depletion in their levels. Treatment of these offspring with curcumin significantly and dose dependently ameliorated all the behavioral and biochemical disruptive effects in the offspring due to HgCl 2 toxicity. In conclusion, curcumin ameliorates the toxic effects of HgCl 2 in the offspring during gestation and lactation periods. Thus, exposure to HgCl 2 to mothers during pregnancy needs careful monitoring for minimizing its toxicity. Curcumin appears to be a promising ameliorating agent for such HgCl 2 toxicity; however, further studies are needed for establishing these preliminary findings. [ABSTRACT FROM AUTHOR]

Prolonged exposure to low levels of dietary contaminants is a context in modern life that could alter organ physiology gradually. Here, we aimed to investigate the impact of continuous exposure to acceptable daily intake (ADI) and non-observable adverse effect level (NOAEL) of glyphosate from gestation to adulthood using C57BL/6J mice and incorporating these levels into their food pellets. From adulthood, we analyzed neurophysiological and neuro-glia cellular adaptations in male and female animals. Using ex-vivo hippocampal slice electrophysiology, we found a reduced efficacy of Schaffer collateral-to-CA1 excitatory synapses in glyphosate-exposed dietary conditions, with ADI and NOAEL dose-dependent effects. Short-term facilitation of excitatory synaptic transmission was specifically increased in NOAEL conditions, with a predominant influence in males, suggesting a reduced probability of neurotransmitter release. Long-term synaptic potentiation (LTP) was decreased in NOAEL-exposed mice. Next, we explore whether these neurophysiological modifications are associated with neuro-glia changes in the somatosensory cortex and hippocampus. High-resolution confocal microscopy analyses unveil a dose-dependent increased density of excitatory Vglut1+ Homer1+ synapses. Microglial Iba1+ cells displayed a shortening of their ramifications, a sign of cellular reactivity that was more pronounced in males at NOAEL levels. The morphology of GFAP+ astrocytes was generally not modified. Finally, we asked whether mouse-specific cross-correlations exist among all data sets generated. This examination included the novel object recognition (NOR) test performed before ex vivo functional and immunohistochemical examinations. We report a negative linear regression between the number of synapses and NOR or LTP maintenance when plotting ADI and NOAEL datasets. These results outline synaptic and microglial cell adaptations resulting from prenatal and continuous dietary low levels of glyphosate, discernible in, but not limited to, adult males exposed to the NOAEL. We discuss the potential significance of these findings to real-world consumer situations and long-term brain resilience. [Display omitted] • Dietary exposure to low glyphosate levels from prenatal to adulthood prompts neuro-glial adjustments. • In adults, synaptic function and number are modified mainly at NOAEL glyphosate compared to ADI. • Reduced microglial cell ramifications hint at activation, mainly at NOAEL dose. • These results support a framework highlighting a long-term risk of brain frailty due to continuous contaminant exposure. [ABSTRACT FROM AUTHOR]

Objective: To examine the associations of in utero exposure to maternal diabetes with surrogate measures of offspring pubertal timing (age at peak height velocity [APHV]) and speed of pubertal growth (peak height velocity [PHV]).Study Design: Data from 77 exposed and 340 unexposed youth followed from age 2 to 19 years (51% non-Hispanic white, 50% female) were analyzed using the Exploring Perinatal Outcomes among Children study, a historical prospective cohort. Maternal diabetes status was collected from obstetric records, and child heights from 2 years to current age from pediatric records. Other covariates were collected during research visits. The superimposition by translation and rotation method, using height measurements (4-52 per participant), modeled APHV and PHV. Accelerated failure time analyses were used to test whether exposure to maternal diabetes was associated with younger APHV and faster PHV.Results: Adjusting for child's sex, race/ethnicity, and socioeconomic status, median APHV was reached ~3 months earlier in youth exposed to maternal diabetes compared with unexposed youth (P < .03). Youth exposed to maternal diabetes had a faster PHV than unexposed youth: exposed girls had 10.5% greater median PHV compared with unexposed girls and exposed boys had a 4.0% greater median PHV compared with unexposed boys (P < .001 for exposure by sex interaction).Conclusions: Our findings provide evidence that exposure to maternal diabetes in utero is associated with earlier pubertal timing and faster pubertal growth. Whether earlier puberty or faster speed of pubertal growth mediates the association between maternal diabetes exposure and later chronic disease risk remains to be studied. [ABSTRACT FROM AUTHOR]

Organophosphorus flame retardants (OPFRs), including 2-ethylhexyl diphenyl phosphate (EHDPHP), are prevalent in everyday life due to their broad usage in fields such as healthcare, electronics, industry, and sports. These compounds, added to polymers through physical mixing, can leach into the environment, posing a risk to humans through direct contact or the food chain. Despite known associations with health issues like endocrine disruption, neurotoxicity, and reproductive toxicity, the implications of perinatal EHDPHP exposure on both mothers and offspring are still unclear. This study aimed to investigate the neuroinflammatory effects of EHDPHP and the potential mitigating role of inulin. Pregnant C57 mice were administered either a corn oil control or an EHDPHP solution (300 μg/kg bw/d) from gestation day 7 (GD7) to postnatal day 21 (PND21). Concurrently, mice were provided either regular drinking water or water supplemented with 1% inulin. We found that EHDPHP significantly increased the serum levels of IL-1β, IL-6, and MDA, but decreased SOD levels in both mothers and pups. These effects were reversed by inulin supplementation. RNA-sequencing revealed that EHDPHP induced inflammation and oxidative stress through the TLR4/NF-κB pathway, which was mitigated by inulin. In conclusion, inulin ameliorated EHDPHP-induced neuroinflammation and oxidative stress in both mothers and offspring, highlighting its potential therapeutic role. [Display omitted] • Perinatal exposure to EHDPHP led to neuroinflammation and oxidative stress in dams and pups. • EHDPHP upregulated the expressions of inflammation and oxidative stress related biomarkers. • Inulin attenuated EHDPHP-associated oxidative stress and neuroinflammation in both dams and pups. [ABSTRACT FROM AUTHOR]

Zamzam water is well documented for plenty of medicinal value for curing illness. In the present study, the effects of perinatal consumption of Zamzam and normal drinking water by the pregnant mice on their offspring’s physical parameters, early sensory motor reflexes, locomotor activities, acetylcholinesterase (AChE) activity in the homogenize brain tissue and blood parameters were compared. To achieve that; Zamzam water was given to female Swiss-Webster strain mice as the only source of drinking fluid and the control animals were administered plain tap water. Treatment started from the first day of pregnancy and continued until the postnatal day fifteen of delivery. All offspring were subjected to various tests. The rate of body weight gain remained relatively unaffected until the second week of weaning period, however; in the last week the offspring exposed to Zamzam water gained significant body weight as compared to their control offspring. Furthermore, the opening of eyes and appearance of body hairs in Zamzam exposed pups remained unaffected as compared to the controls. The sensory motor reflexes in Zamzam exposed pups after birth and during the first two weeks of weaning period were significantly increased. Locomotor Activity Test performed in the male and female offspring after weaning period showed a significant decrease in the male and increase in the female on most of the elements of this test due to Zamzam exposure. AChE activity in the homogenized brain tissue and blood parameters were unaffected as compared to the controls, the present Zamzam effects in the offspring are possibly via in utero action and/or via mother’s milk. [ABSTRACT FROM AUTHOR]

The present study compares concentrations and chemical profiles of an extended range of persistent organic pollutants (dioxins, polychlorobiphenyls, brominated flame retardants and organochlorine pesticides) in breast milk samples from French (n = 96), Danish (n = 438) and Finnish (n = 22) women. Median exposure levels observed in French women (WHO-TEQ 2005 PCDD/F = 6.1 pg/g l.w., WHO-TEQ 2005 dl-PCB = 4.3 pg/g l.w., sum of 6 ndl-PCB = 85.2 ng/g l.w., sum of 7 i-PBDE = 1.5 ng/g l.w.) appeared overall lower than in Danish and Finnish women for all examined POPs, except for α-HBCD (2-fold higher level at 0.6 ng/g l.w.). Furthermore, the observed exposure levels of dioxins and PCBs were higher in Danish women (WHO-TEQ 2005 PCDD/F = 13.2 pg/g l.w., WHO-TEQ 2005 dl-PCB = 6.6 pg/g l.w., sum of 6 ndl-PCB = 162.8 ng/g l.w.) compared to Finnish women (WHO-TEQ 2005 PCDD/F = 9.0 pg/g l.w., WHO-TEQ 2005 dl-PCB = 4.6 pg/g l.w., sum of 6 ndl-PCB = 104.0 ng/g l.w.), whereas the concentrations of PBDEs were similar for Danish and Finnish women (sum of 7 i-PBDE = 4.9 and 5.2 ng/g l.w. respectively). The organochlorine (OC) pesticide contamination profile, determined in a subset of French samples, was dominated by p,p’-DDE (56.6%), followed by β-HCH (14.2%), HCB (9.7%) and dieldrin (5.2%), while other compounds were only minor contributors (<5%). The three countries appeared to be discriminated by the observed contamination patterns of the PCDD/F versus PCB, and the 1,2,3,6,7,8-HxCDD versus 1,2,3,4,7,8-HxCDD ratios, in addition to the relative contributions of specific congeners to the contamination profile (PCBs #118 and #156, PBDEs #28, #47, #99 and #153). In conclusion, unique chemical signatures were observed for each country on the basis of some POP congeners. Future biomonitoring studies will need to consider the high variability of individual exposure profiles in relation to multiple exposure sources but also physiological and metabolic differences. [ABSTRACT FROM AUTHOR]

Associations between early-life exposure to perinatal dampness problems and health effects among 2917 children (3–6 years) were evaluated in this study. After adjusted for gender, age, family history of asthma or allergies, environmental tobacco smoke exposure, gestation age and house location in the logistic regression models, perinatal exposure to dampness indicators was observed to be strongly associated with some respiratory and allergic symptoms in the last 12 months, including wheezing, cough at night, rhinitis and eczema. The prevalence of theses respiratory and allergic symptoms in the last 12 months was significantly increased with perinatal-only exposure to most dampness indicators and was further increased with continuous exposure (perinatal plus current exposure). There was almost no such significant increase with current-only exposure. This study found less association between perinatal-only exposure and doctor-diagnosed diseases, and these associations may be explained by recall bias. Early-life exposure to perinatal dampness reported by parents was significantly associated with some current respiratory and allergic symptoms among children in Chongqing, China. Hence, it is necessary to pay attention to early living environment, especially home dampness, although the mechanisms are still unclear. [ABSTRACT FROM AUTHOR]

Perinatal exposure to deltamethrin (DM) causes attention-deficit/ hyperactivity disorder-like behaviors. However, the vulnerable time window to DM exposure and the possible mechanism are obscure. We aimed to identify the critical window(s) at perinatal stages for DM exposure and the possible mechanism. Pregnant mice were exposed to DM (0.5 mg/kg) at three different prenatal stages [gestational day (GD) 0–5, 6–15 and 16-birth (16-B)] and early postnatal stage (PD 0–10). Locomotor activity, learning and memory were evaluated using open field and Y-maze test, respectively. Nissl staining and western blots were used to examine the neuronal loss and the protein expression, respectively. Perinatal exposures to DM had no effect on reproductive and growth index of offspring. However, mice receiving DM exposure during GD 16-B displayed significantly higher mortality suggesting GD 16-B is the most vulnerable time window to DM exposure. Prenatal but not early postnatal DM exposure impaired locomotor activity, learning and memory, and caused neuron loss in the dentate gyrus of male offspring. However, neither prenatal nor postnatal DM exposure affected mouse behavior of female offspring. Prenatal DM exposures decreased the protein levels of NR2A and NR2B in both hippocampi and cerebral cortices of male offspring. However, female mice receiving DM exposure at GD 16-B but not other stages displayed increased expression levels of NR2A and NR2B in hippocampi. Prenatal but not early postnatal DM exposure impairs the neuron development in male but not female mice. Altered NMDA receptor expression may correlate to DM-induced behavioral deficits. • Perinatal exposure to low dose of deltamethrin (DM) causes neural development deficits. • Male mice are more susceptible to perinatal DM exposure than female mice. • Gestational day 16-Birth (GD16-B) is the most vulnerable time window to DM exposure. • Altered NMDA receptor expression may correlate to DM-induced behavioral deficits. [ABSTRACT FROM AUTHOR]

Background: Epidemiologic studies associate environmental tobacco smoke (ETS) exposure with childhood asthma. Objective: To investigate whether specific pathophysiological alterations that contribute to asthma development in human beings can be induced in infant monkeys after perinatal ETS exposure. Methods: Rhesus macaque fetuses/infants were exposed to ETS at 1 mg/m3 of total suspended particulate matter from 50 days gestational age to 2.5 months postnatal age. Inflammatory and neural responses to ETS exposure were measured in the infant monkeys. Results: Perinatal ETS exposure could induce systemic and local responses, which include significant elevation of plasma levels of C5a and brain-derived neurotrophic factor, as well as significant increases in pulmonary expression of proinflammatory cytokine TNF-α and TH2 cytokine IL-5, chemokine monocyte chemoattractant protein 1, and the density of substance P–positive nerves along the bronchial epithelium. Perinatal ETS exposure also significantly increased the numbers of mast cells, eosinophils, monocytes, and lymphocytes in the lungs of infant monkeys. In addition, ex vivo measurements showed significantly increased levels of IL-4 and brain-derived neurotrophic factor in the culture supernatant of PBMCs. Interestingly, as an important component of cigarette smoke, LPS was detected in the plasma of infant monkeys subjected to perinatal exposure to ETS. In contrast, an inhibitory effect of perinatal ETS exposure was also observed, which is associated with decreased phagocytic activity of alveolar macrophages and a significantly decreased level of nerve growth factor in the bronchoalveolar lavage fluid. Conclusion: Perinatal ETS exposure can induce a TH2-biased inflammatory response and alter airway innervation in infant monkeys. [Copyright &y& Elsevier]

The article focuses on a study to show the effects of bisphenol A (BPA) on female rat offsprings during pregnancy. The doses of bisphenol A were orally administered to rats and the neurotransmitters such as dopamine (DA) and serotonin (5HT) were taken out of the brains of dams and female offspring. After somedays, the rats died. The study showed that quantity of DA and 5HT was increased in 3 week old offspring and dams. It was found in the study that BPA has a very weak estrogenic activity.

Abstract: Metabolites of the commonly used imidazole fungicide prochloraz are androgen receptor antagonists. They have been shown to block androgen-driven development and compromise reproductive function. We tested the effect of prochloraz on cognitive behavior following exposure to this fungicide during the perinatal period. Pregnant Wistar rats were administered a 200mg/kg dose of prochloraz on gestational day (GD) 7, GD11, and GD15. The social recognition test (SRT) was performed on 7-week-old male rat offspring. We found an increase in pregnancy length and a significantly reduced pup weight on PND15 and PND40 but no effect of prenatal prochloraz exposure on social investigation or acquisition of social-olfactory memory. [Copyright &y& Elsevier]

Comment on "Maternal exposure to air pollution and risk of autism in children: A systematic review and meta-analysis". Some points and/or limitations of their review and meta-analysis should be discussed. [ABSTRACT FROM AUTHOR]