scholarly journals Maternal exposure to trace cadmium affects gonadal differentiation and development in male offspring rats though a star pathway

2021 ◽  
Author(s):  
Yan LIU ◽  
Xiaohong WEN ◽  
Dan WANG ◽  
Xiaogang LIAO
Keyword(s):  
Maternal Exposure ◽  
Male Offspring ◽  
Gonadal Differentiation ◽  
Trace Cadmium

Maternal exposure to cadmium impairs cognitive development of male offspring by targeting the Coronin-1a signaling pathway

Chemosphere ◽  
2019 ◽  
Vol 225 ◽  
pp. 765-774 ◽  
Author(s):  
Jianfeng Feng ◽  
Shaomin Chen ◽  
Youjin Wang ◽  
Qunxing Liu ◽  
Mengqi Yang ◽  
...  
Keyword(s):  
Cognitive Development ◽  
Signaling Pathway ◽  
Maternal Exposure ◽  
Male Offspring

MATERNAL EXPOSURE TO POLYBROMINATED BIPHENYLS AND GENITOURINARY CONDITIONS IN MALE OFFSPRING

2008 ◽  
Vol 179 (4S) ◽  
pp. 97-98
Author(s):  
John J DeCaro ◽  
Chanley M Small ◽  
Metrecia L Terrell ◽  
Celia E Dominguez ◽  
Lorraine L Cameron ◽  
...  
Keyword(s):  
Maternal Exposure ◽  
Male Offspring ◽  
Polybrominated Biphenyls

Maternal exposure to mixtures of dienestrol, linuron and flutamide. Part II: Endocrine-related gene expression assessment on male offspring rat testes

2020 ◽  
Vol 144 ◽  
pp. 111603 ◽  
Author(s):  
Efrosini S. Katsanou ◽  
Petros Batakis ◽  
Anastasia Spyropoulou ◽  
Elga Schreiber ◽  
Toine Bovee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Maternal Exposure ◽  
Male Offspring ◽  
Related Gene

Maternal exposure to low doses of bisphenol A affects learning and memory in male rat offspring with abnormal N-methyl-d-aspartate receptors in the hippocampus

2021 ◽  
pp. 074823372098462
Author(s):  
Chong Wang ◽  
Yao Shu ◽  
Li Xu ◽  
Qiling Liu ◽  
Bei Zhang ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Learning And Memory ◽  
Maternal Exposure ◽  
Male Offspring ◽  
Male Rat ◽  
Control Group ◽  
Sprague Dawley ◽  
Expression Levels ◽  
Rat Offspring ◽  
Sprague Dawley Rats

Bisphenol A (BPA), a component of polycarbonate and epoxy resins, has been reported to induce learning and memory deficits. However, the mechanisms have not been fully elucidated. Growing evidence has suggested that N-methyl-d-aspartate receptors (NMDARs) are involved in cognitive impairments. In this study, BPA was administered to female Sprague–Dawley rats (six per dose group) at concentrations of 0 (control), 4, 40, and 400 μg/kg·body weight/day from gestation day 1 through lactation day 21. Spatial learning was evaluated using the Morris water maze on postnatal day 22. Expression levels of NMDARs were determined using real-time polymerase chain reaction and Western blot. The results showed that male offspring exposed to BPA exhibited increased latency in reaching the platform and reduced time in the target quadrant, and the number of crossing the platform was less, as compared with the control group. The mRNA and protein expression levels of NMDARs in the hippocampus were significantly downregulated when compared with the control group of male offspring. The data showed that maternal exposure to BPA at low dosage can cause cognitive deficits in male rat offspring, probably due to a decrease in NMDARs in the hippocampus.

scholarly journals Effects of Maternal Exposure to Di-(2-ethylhexyl) Phthalate during Fetal and/or Neonatal Periods on Atopic Dermatitis in Male Offspring

2008 ◽  
Vol 116 (9) ◽  
pp. 1136-1141 ◽  
Author(s):  
Rie Yanagisawa ◽  
Hirohisa Takano ◽  
Ken-ichiro Inoue ◽  
Eiko Koike ◽  
Kaori Sadakane ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Maternal Exposure ◽  
Male Offspring ◽  
Ethylhexyl Phthalate

Maternal exposure to diets containing flaxseed flour or flaxseed oil during pregnancy and lactation protects the aortic remodeling in adult male offspring of diabetic rat dams

2015 ◽  
Vol 95 (14) ◽  
pp. 2973-2980 ◽  
Author(s):  
Gabriela Câmara Vicente ◽  
André Manoel Correia-Santos ◽  
Akemi Suzuki ◽  
Luis Guillermo Coca Velarde ◽  
Maurício Alves Chagas ◽  
...  
Keyword(s):  
Adult Male ◽  
Flaxseed Oil ◽  
Maternal Exposure ◽  
Male Offspring ◽  
Diabetic Rat ◽  
Flaxseed Flour ◽  
Pregnancy And Lactation ◽  
Aortic Remodeling

scholarly journals Prenatal exposure to diesel exhaust PM2.5 causes offspring β cell dysfunction in adulthood

2018 ◽  
Vol 315 (1) ◽  
pp. E72-E80 ◽  
Author(s):  
Minjie Chen ◽  
Shuai Liang ◽  
Xiaobo Qin ◽  
Li Zhang ◽  
Lianglin Qiu ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Adult Male ◽  
Diesel Exhaust ◽  
Maternal Exposure ◽  
Male Offspring ◽  
Β Cells ◽  
Β Cell

Environmental stressors that encounter in early-life and cause abnormal fetal and/or neonatal development may increase susceptibility to non-communicable diseases such as diabetes. Maternal exposure to ambient fine particulate matter (PM2.5) is associated with various fetal abnormalities, suggesting that it may program offspring’s susceptibility to diabetes. In the present study, we therefore examined whether maternal exposure to diesel exhaust PM2.5 (DEP), one of the major sources of ambient PM2.5 in urban areas, programs adult offspring’s glucose metabolism. Female C57Bl/6J mice were intratracheally instilled with DEP or vehicle throughout a 7-wk preconceptional period, gestation, and lactation, and the glucose homeostasis of their adult male offspring was assessed. Intraperitoneal glucose tolerance test (IPGTT) revealed that the maternal exposure to DEP significantly impaired adult male offspring’s glucose tolerance. Unexpectedly, it did not influence their insulin sensitivity, whereas it significantly decreased their glucose-induced insulin secretion (GIIS). This deficit in insulin secretion was corroborated by their significant decrease in arginine-induced insulin secretion. Histological analysis demonstrated that the deficit in insulin secretion was accompanied by the decrease in pancreatic islet and β cell sizes. To differentiate the effects of maternal exposure to DEP before birth and during lactation, some offspring were cross-fostered once born. We did not observe any significant effect of cross-fostering on the glucose homeostasis of adult male offspring and the function and morphology of their β cells. Prenatal exposure to DEP programs the morphology and function of β cells and thus homeostatic regulation of glucose metabolism in adult male offspring.

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