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1.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 92-95, 2013.
Article in Chinese | WPRIM | ID: wpr-343699

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the changes in the expression of DNA methyltransferases (DNMTs) and activities of histone acetyltransferase (HAT) and histone deacetylase (HDAC) in the testis of male rats exposed to bromopropanes (BPs).</p><p><b>METHODS</b>Twenty-seven male rats were randomly divided into three groups to be intraperitoneally injected with 1-BP,2-BP, or corn oil (as a control) for two weeks. The sperm count and morphology in the epididymis were evaluated. The mRNA expression of DNMT1, DNMT3a, and DNMT3b and activities of HAT and HDAC in the testis were measured by quantitative real-time PCR and ELISA.</p><p><b>RESULTS</b>Compared with the control group, the BP exposure groups showed significant decreased absolute and relative sperm counts; the proportion of tailless sperm increased in the 1-BP exposure group, while the proportion of sperm with abnormal heads increased in the 2-BP exposure group. The 2-BP exposure group had significantly lower mRNA expression of DNMT1, DNMT3a, and DNMT3b than the control group (P < 0.05). There were no significant differences in the activities of HAT and HDAC between the control group and 1-BP exposure group; the 2-BP exposure group showed significantly higher HAT activity than the control group (P < 0.05), but no significant difference was found in HDAC activity between them.</p><p><b>CONCLUSION</b>Exposure to 2-BP might induce abnormal DNA methylation and histone acetylation, and epigenetic regulation might play an important role in the reproductive toxicity of 2-BP.</p>


Subject(s)
Animals , Male , Rats , Acetylation , DNA (Cytosine-5-)-Methyltransferase 1 , DNA (Cytosine-5-)-Methyltransferases , Metabolism , DNA Methylation , Histones , Metabolism , Hydrocarbons, Brominated , Toxicity , Rats, Sprague-Dawley , Sperm Count , Testis , Metabolism
2.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 289-292, 2012.
Article in Chinese | WPRIM | ID: wpr-273502

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effects of rat maternal exposure to fenvalerate during lactation on behaviors development in rat pubertal female offspring.</p><p><b>METHODS</b>Twelve ICR maternal mice were randomly divided into 7.5 and 30.0 mg/kg fenvalerate exposure groups and control group (four dams each group, ten pups each dam, half male half female, twenty female pups each group). The exposure groups were orally exposed to fenvalerate at the doses of 7.5 and 30 mg/kg a day from postnatal day 1 (PND1) to PND21. The control group was exposed to corn oil. The effects of maternal fenvalerate exposure during lactation on motor and species-typical behaviors in female offspring were observed on the PND 35.</p><p><b>RESULTS</b>The peripheral time and standing frequency of 30.0 mg/kg exposure group were (263.4 ± 54.8) s and (47.3 ± 16.2) times, which were significantly higher than those [(203.4 ± 53.0) s and (30.9 ± 17.3) times] of control group (P < 0.05). The scores in 7.5 mg/kg and 30.0 mg/kg exposure groups were 56.50 ± 50.79 and 54.73 ± 53.91, respectively, which were significantly lower than that (114.53 ± 53.87) in control group (P < 0.05). However, no significant differences in beam walking scores, food hoarding quantity, food digging quantity, and nest construction scores between two exposure groups were found (P > 0.05).</p><p><b>CONCLUSION</b>The rat maternal exposure to fenvalerate during lactation could decrease the ability of exploration and motor condition and increase the anxiety but not affect life habit in rat pubertal female offspring.</p>


Subject(s)
Animals , Female , Male , Mice , Pregnancy , Behavior, Animal , Maternal Exposure , Mice, Inbred ICR , Nitriles , Toxicity , Prenatal Exposure Delayed Effects , Pyrethrins , Toxicity
3.
Chinese Pharmacological Bulletin ; (12): 1610-1614, 2009.
Article in Chinese | WPRIM | ID: wpr-405081

ABSTRACT

Aim To investigate the effects of pyrrolidine dithiocarbamate (PDTC) on D-galactosamine/lipopolysaccharides (GalN/LPS)-induced acute apoptotic liver injury and its mechanism.Methods All mice were randomly divided into four groups.Mice in GalN/LPS group were co-injected with GalN (600 mg·kg~(-1),ip) and LPS (20 μg·kg~(-1), ip). Mice in PDTC+GalN/LPS group were injected with two doses of PDTC,one (100 mg·kg~(-1), ip) at 24 h before LPS and the other at 2 h before LPS (20 μg·kg~(-1), ip).Mice in control groups were treated with PDTC (100 mg·kg~(-1), ip) or saline. Ten mice in each group were observed for animal survival within 72 h after LPS treatment. Six mice in each group were sacrificed 1.5 h after LPS for collecting blood and isolating livers. The expression of hepatic TNF-α mRNA was determined by reverse transcription and polymerase chain reaction (RT-PCR). Hepatic nuclear factor-κB (NF-κB) binding activity was measured with electrophoretic mobility shift assay (EMSA).Twelve mice in each group were sacrificed 8 h after LPS treatment. Serum was collected for measurement of alanine aminotransferase (ALT) and hepatocellular apoptosis and histological examination.Results Co-injection of GalN and LPS markedly increased serum ALT activity. Histopathological examination of liver sections revealed that GalN/LPS induced hepatic congestion, necrosis and massive macrophages infiltration, and increased the number of TUNEL-positive cells in mouse liver.GalN/LPS treatments, led to 90% mortality within 72 h with severe congestion and necrosis in the liver of all the dead mice. PDTC pretreatment significantly inhibited GalN/LPS-induced hepatic NF-κB activation and TNF-α expression. In contrast, PDTC aggravated GalN/LPS-triggered hepatocellular apoptosis, increased serum ALT activity, exacerbated hepatic hemorrhage and necrosis, and accelerated death.Conclusion PDTC aggravates GalN/LPS-induced acute apoptotic liver injury via inhibiting NF-κB-mediated anti-apoptotic effects.

4.
Journal of Environment and Health ; (12)1989.
Article in Chinese | WPRIM | ID: wpr-547638

ABSTRACT

Objective To explore the effects of maternal cypermethrin exposure during lactation on testicle development and steroidogenesis of weaning offspring, and to provide a theoretical basis for the toxicity study of cypermethrin on reproduction.Methods Twenty-one healthy pregnant mice(clean animal) were randomly divided into three groups.Maternal mice were orally administered with different doses of cypermethrin [0,6.25 and 25 mg(/kg?d),10 ml/kg] dissolved in corn oil daily from postnatal day 1(PND1) to PND21.Fifteen male pups were randomly selected from each group and sacrificed at PND21 after exposure.The testicle organ coefficients were calculated.Serum testosterone(T) and estrogen(E2),testicle T were measured by radioimmunoassay(RIA).Histopathological changes in the testicle tissues were observed by HE stain.Testicle cells apoptosis was detected by TdT-mediated dUTP nick end labeling(TUNEL).Results A significant decrease was observed in body weight and the testicle organ coefficients in cypermethrin-treated group was in a dose-dependent manner(P0.05).Histological examination showed that maternal cypermethrin exposure markedly decreased the number and layers of spermatogenic cells,increased the inside diameter(ID) of seminiferous tubules,and disturbed the array of spermatogenic cells in testicle sections of pups at PND21.No significant effect on apoptosis of testicle cells was seen.Conclusion Maternal cypermethrin exposure during lactation may damage testicles and steroidogenesis of weaning offspring.

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