ABSTRACT
OBJECTIVE Study the role of estrogen receptor (ER)in the inhibition of cell viability and differentiation induced by bisphenol A (BPA)in micro mass culture of rat e mbryonic midbrain(MB) cells.METHODS Micro mass cultures of MB were prepared fro m rat e mbryonic midbrain on gestation day 13.MB cells were exposed to BPA (10 -4 ,10 -6 ,10 -8 ,10 -10 ,10 -12 mol·L -1 )for 5 d.Cell viability was assessed by neutral red uptake test.MB differentiation was detected by he matoxylin staining and i mage analysis.In order to observe the role of ER pathway in the toxicity induced by BPA,cell cultures were co-treated with ICI182780 0.1 n mol·L -1 ,ta moxifen 1 n mol·L -1 and BPA 0.1 mmol·L -1 for 5 d, the cell viability and foci differentiation were detected.Moreover,the protein expression levels of ER in normal e mbryonic brain of gestation day 18,testis tissue fro m adult rats and midbrain cells untreated with BPA were investigated by Western blot.The mRNA expression levels of ER in normal e mbryonic brain of gestation day 13 and gestation day 18,ovary and testis tissue fro m adult rats,and midbrain cells un-treated with BPA were investigated by real-ti me PCR.The mRNA expression levels of Notch1 and Hes1 in MB cells treated with BPA 0.1 mmol·L -1 were also detected by real-ti me PCR.RESULTS BPA 0.1 mmol·L -1 could inhibited MB cell viability and foci differentiation.However,this effect could not be reversed by ER antagonist.The protein and mRNA expression levels of ER in e mbryonic brain and MB cells untreated with BPA were found to be extre mly low.In addition,BPA 0.1 mmol·L -1 could inhibited the mRNA expression levels of Notch1 and Hes1 .CONCLUSION BPA could inhibited MB cell viability and foci differentiation.ER pathway might be not involved in this effect.Instead,Notch-Hes pathway might be involved for this effect.
ABSTRACT
<p><b>OBJECTIVE</b>To study the changes of immune function in mice offspring whose mothers were exposed to Rare Earth (RE)(NO(3))(3).</p><p><b>METHODS</b>RE(NO(3))(3) was administered to mother mice after giving birth by gavage at dosages of 2, 20 and 200 mg/kg bw during breast-feeding period. The weights of spleen and thymus, the spleen plaque forming cells (PFC), the delayed type hypersensitivity (DTH) and the charcoal clearance of the offspring were determined.</p><p><b>RESULTS</b>The results obtained from the offspring after weaning showed that the body weight of offspring treated with 200 mg/kg RE(NO(3))(3) was 18.8% lower than that of the control group; at the dosage of 2 mg/kg, the number of IgM-PFC was increased by 82.7%; and at the dosage of 20 mg/kg the rate of clearance and clearance index were significantly higher than that of the control group. No difference in DTH was found in any treated group as compared to the control group. The results of offspring at three weeks after weaning showed that the number of IgM-PFC of the 20 and 200 mg/kg bw dose groups were 47.0% and 44.7% lower than that of control group respectively; the rate of clearance and clearance index of the 200 mg/kg group were significantly lower than that of the control group. No significant changes in DTH were observed in each exposed group.</p><p><b>CONCLUSION</b>RE(NO(3))(3) treatment affected the immune function of mice offspring which may caused by breast milk.</p>
Subject(s)
Animals , Female , Mice , Pregnancy , Immunity , Immunoglobulin M , Metals, Rare Earth , Pharmacokinetics , Toxicity , Milk , Metabolism , Organ SizeABSTRACT
<p><b>OBJECTIVE</b>To study the immunotoxicity induced by 9,10-dimethyl-1,2-benzathrancene (DMBA) in metallothionein gene-knocked-out mice [MT(-/-)] as compared with that in wild-type mice [(MT(+/+)].</p><p><b>METHODS</b>Female mice were treated with 25 mg/kg and 50 mg/kg of DMBA i.p., respectively and immunized with sheep red blood cells (SRBC) i.v. on the following day and rechallenged by injection of SRBC via footpad s.c. on the fourth day post-immunization. Humoral and cell-mediated immune function was assessed by the number of spleen IgM antibody plaque formation cells (PFC) to SRBC and cell-mediated delayed-type hypersensitivity (DTH) measured by footpad swelling thickness.</p><p><b>RESULTS</b>After treatment with 25 mg/kg DMBA, a decrease in weight of their spleen and thymus and PFC/spleen were observed in MT(-/-) mice, while only decrease in thymus weight of MT(+/+) mice. The humoral function was suppressed by 72% in MT(-/-) mice. No obvious change in cell-mediated immune function was observed both in MT(-/-) and MT(+/+) mice. Both humoral and cell-mediated immune function were suppressed more severe (91%) in MT(-/-) mice treated with 50 mg/kg DMBA than those treated with 25 mg/kg DMBA (72%). DTH was not altered by DMBA in MT(+/+) mice. The weight of their spleen and thymus decreased and humoral immune function suppressed in MT(+/+) mice, but these changes were significantly less severe. No obvious suppression of cell-mediated immune function was observed in MT(+/+) mice.</p><p><b>CONCLUSION</b>Their humoral and cell-mediated immune function was more susceptible to being suppressed by DMBA in MT(-/-) mice, indicating that MT could protect their immune function from damage caused by DMBA.</p>