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Objective To establish mouse poisoning model by inhaling benzene, and to investigate the induction effect of benzene on the apoptosis of mouse bone marrow cells and its mechanism, and to provide an experimental basis for study on bone marrow toxicity mechanism.Methods 24 male mice were randomly divided into four groups (n=6).The mice in one group were exposed to ambient air (control group)and the mice in the other three groups were exposed to different doses (400,800,1 600 mg·m-3 )of benzene (low,middle and high doses of benzene groups)for 1 5 d in the respective inhalation chambers. At the end of the experiment, the mice were killed. The bone marrow of the mice was obtained. The pathological changes of the bone marrow cells of the mice in various groups were observed under light microscope with HE staining.The apoptotic rates and mitochondrial membrane potential (MMP ) of the mice in various groups were detected by flow cytometry, and the expressions of mitochondrial-deperdent apoptosis related gene proteins were determined with immunohistochemistry method. Results The number of distal and central cells in different doses of benzene groups were significantly reduced,and accompanied by blood sinus expansion in high dose of benzene group.The apoptotic rates of the cells in middle and high doses of benzene groups were obviously higher than that in control group (Ρ<0.01),and there were also significant differences between high dose group and low,middle doses of benzene groups (Ρ<0.05).The MMP was significantly decreased with the increasing of benzene doses, and there were significant differences between middle,high doses of benzene groups and control group (Ρ<0.05).The number of Bax,CytC positive cells in different doses of benzene groups and the number of Caspase-9,Caspase-3 positive cells in middle and high doses of benzene groups were significantly increased compared with control group(Ρ<0.05);the number of Bcl-2 positive cells in different doses of benzene groups was decreased(Ρ<0.05),and number of Bcl-2 positive cells in middle and high doses of benzene groups was decreased compared with low dose of benzene group (P<0.05). Conclusion Benzene with certain dose can induce the apoptosis of mouse bone marrow cells, and promote the expressions of mitochondrial apoptosis related gene proteins. Benzene-induced apoptosis through mitochondrial-dependent apoptosis pathway may be an important mechanism of bone marrow toxicity induced by benzene.
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Objective To explore the reproductive toxicity of 2,4-D butylate to the testis in male mice.Methods Forty-eight ICR male mice were randomly divided into four groups : the control group, and three 2,4-D butylate experimental groups (10, 20, 40 mg/kg), 12 mice in each group.2,4-D butylate was intragastrically administered once a day and six days per week for five weeks .At the end of the exposure, the activities of total antioxidant capacity (T-AOC), Na+ K+-ATPase, Ca+ + Mg+ +-ATPase, lactate dehydrogenase (LDH) and succinate dehydrogenase (SDH) in testis homogenate were measured by spectrophotometry .Results The activity of T-AOC was gradually decreased with the increase of doses, with a significant difference between the high dose group and other groups .The activities of LDH in the moderate and high dose groups were significantly lower than those of the low dose group and control group , and there was a significant difference between the high dose group and moderate dose group .The activities of SDH in the testis was gradually decreased with the increase of the 2,4-D butylate dose, showing significant differences between the high dose group and the moderate dose and control groups , and between the high and moderate dose groups and the low dose group . The activities of Na +K +-ATPase in the moderate and high dose groups were significantly lower than that of the control and low dose group.The activities of Ca++Mg++-ATPase was significantly lower in the experimental groups than that in the control group.Conclusion Exposure to 2,4-D butylate has certain toxic effect on the testicular tissue in male mice .
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Objective To probe the influence of electron beam radiotherapy in different manners using different tissue equivalent boluses on skin and lung.Methods Adult female cavia cobayas were randomly divided into four groups as control group,fuU-time with bolus group,half-time with bolus group and without bolus group.Acute-irradiation animal models were established using electron beam in different manners with or without 0.5 cm tissue equivalent bolus.Pathological changes in lung,hair vesicle and fibroblast cell count were analyzed 40 clays after irradiation.Results The radiation dermatitis in the group with bolus was slighter than that of the group without bolus,but the radiation pneumonia was reverse.With bolus,the radiation dermatitis of haft-time group was slighter than that of full-time group.The injury repair of half-time group was more active than full-time group.Conclusions The treatment of haft-time bolus could protect lung without serious skin complications.
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Objective To explore the anti-tumor effects of Egr-IFNγ gene therapy combined with 125I-UdR radionuclide therapy in mice bearing H22 hepatocarcinoma and its mechanism. Methods The recombinant plasmid pcDNAEgr-IFNγ mixed with liposome was injected into tumor. 48 h later, 370 kBq 125I-UdR was injected into tumor. The tumor growth rates at different times were observed. After 3 d gene-radionuclide therapy, the concentration of IFNγ in cytoplasm of H22 cells and cytotoxic activities of splenic CTL of the mice in different groups were examined. Results The tumor growth rates of pcDNAEgr-IFNγ +125 I-UdR group were obviously lower than those of control group, 125I-UdR group and pcDNAEgr-1 +125I-UdR group 6-15 d after gene-radionuclide therapy. IFNγ protein was found in cytoplasm of H22 cells in PcDNAEgr-1FNγ+125I-UdR group after 3 d gene-radionuclide therapy. Cytotoxic activity of splenic CTL in pcDNAEgr-IFN7 + 125I-UdR group was significantly higher than that in the other groups (P<0.01). Conclusions The anti-tumor effects in vivo of pcDNAEgr-IFNγ gene therapy combined with 125I-UdR radionuclide therapy are better than those of 125I-UdR therapy.