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题名:Transmaternal bisphenol A exposure accelerates diabetes type 1 development in NOD mice.
作者:BODIN J; KOCBACH BOLLING A; BECHER R; KUPER F; LOVIK M; NYGAARD UC;
来源:Toxicol Sci. 2013 Nov 6. [ IF= 0.00 ] ]
URL :10.1093/toxsci/kft242
日期:20131203
摘要:Diabetes mellitus type 1 (T1DM) is an autoimmune disease with a genetic
predisposition that is triggered by environmental factors during early life.
Epidemiological studies show that bisphenol A (BPA), an endocrine disruptor, has
been detected in about 90% of all analysed human urine samples. In this study,
BPA was found to increase the severity of insulitis and the incidence of diabetes
in female non obese diabetic (NOD) mice offspring after transmaternal exposure
through the dams' drinking water (0, 0.1, 1 and 10mg/l). Both the severity of
insulitis in the pancreatic islets at 11 weeks of age and the diabetes prevalence
at 20 weeks were significantly increased for female offspring in the highest
exposure group compared to the control group. Increased numbers of apoptotic
cells, a reduction in tissue resident macrophages and an increase in regulatory T
cells were observed in islets prior to insulitis development in transmaternally
exposed offspring. The detectable apoptotic cells were identified as mostly
glucagon producing alpha-cells but also tissue resident macrophages and
beta-cells. In the local (pancreatic) lymph node neither regulatory T cell nor
NKT cell populations were affected by maternal BPA exposure. Maternal BPA
exposure may have induced systemic immune changes in offspring, as evidenced by
alterations in LPS- and ConA-induced cytokine secretion in splenocytes. In
conclusion, transmaternal BPA exposure, in utero and through lactation,
accelerated the spontaneous diabetes development in NOD mice. This acceleration
appeared to be related to early life modulatory effects on the immune system,
resulting in adverse effects later in life.

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