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The Effect Of Environmental Hormone Bisphenol A On The Expression Of P450scc And3β-HSD Protein In Adult SD Rat Testis

Posted on:2013-12-14Degree:MasterType:Thesis
Country:ChinaCandidate:J H JiaFull Text:PDF
GTID:2234330374958718Subject:Surgery
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Objective: Environmental pollution is getting heavier and heavier, thedamage of the environment on human more and more powerful, especially inthe production and use of a large number of chemical materials, making theenvironment pollution has never been higher by humans pay attention to it,Because it has been deeply harmful to human health, even against humanitynext generation. In a large number of environmental pollutants in the systemthat environmental hormones particularly fetching attention. A very importantone pollutant is environmental hormone substances bisphenol A, Bisphenol Acan be found in plastic products everywhere in our daily life, the wide range ofuses, the half-life is long, difficult degradation of biological naturalenvironment. In recent years, male fertility is getting worse, compared withfifty or sixty years of the last century, the sperm density decreased more thandoubled,that reality caused the attention of scientists. After a lot of researchand analysis found that environmental pollution is one of the main factorscausing decline in male fertility. Environmental hormone bisphenol A on malefertility influence research to become scientists research focus.This experiment is to study the environmental hormone bisphenol A effectstestosterone synthesis in rat testis after gavage male SD rats.And to explorethe effect of the protein of P450scc and3beta HSD expression on Leydig cellafter the rats were given intragastrically bisphenol A.In the cell protein levelresearch the influence mechanism of bisphenol A on male rats testosteronesynthesis. In order to be able to ascertain the specific mechanisms thatenvironmental hormone bisphenol A affects male fertility. Thus from thesource to prevent and solve the environmental hormone bisphenol A on humanfertility in male rats. Materials and methods:1Experimental animal and material: Select the clean8-weeks-old adult maleSD rats as the laboratory animal, weighing180―200g and all rats dividedequally cages in the animal room after a week for experiment. Daily simulatenatural lighting12hours, were fed ad libitum the full price of feed pellets, tapwater, regular daily exposure, exposure5times a week. Exposed to eightweeks for the experiment. Bisphenol A in each dose group was diluted withcorn oil.2Experimental animals grouped and exposed:48rats were randomly dividedinto four groups, control group, low-dose group, middle dose group and highdose group (n=12).Each experimental group were formulated with corn oilinto a different dose levels of BPA, daily low-dose group given2mg/kg BPAgavage, the middle dose group give20mg/kg BPA gavage, daily high dosegroup give200mg/kg BPA gavage the control group, daily filling the sameamount of corn oil.3Experimental specimen processing: after the end of the exposed ratsweighing, the execution of heart blood, at rest and after centrifugation serum,enzyme-linked immunosorbent method to detect the concentration of serumtestosterone, testis epididymis weighed to calculate the organ coefficient oftestes neutral formaldehyde embedded sections of HE staining andimmunohistochemical staining, the comparative analysis of the exposed groupand control group differences, the results were analyzed using SPSS softwaresystem.Results:1Daily activity changes in rats: rats exposed to high dose group showed suchas hair messy, less activity, and soft stools and other symptoms of poisoning,while the slow weight gain. The remaining rats in other groups the normalstate showed no abnormal activities.2Body weight and testicular changes in rats after Bisphenol A exposure: Withthe increase of BPA exposure doses, the body weight of rats, testicular organcoefficient decreased, the middle dose group and high dose group comparedwith the control group organs indicators were statistically significant (P <0.05), and the ratsweight, testis coefficient associated with BPA exposure doses andexposure doses greater the slower the growth.3Difference of serum testosterone levels: low-dose group, serum testosteroneconcentration slightly higher, but the difference was not statisticallysignificant; testosterone concentration in the high dose group lower than thecontrol group, with increasing exposure dose is reducedThe difference wasstatistically significant.4Testicular changes in organizational structure: the control group rat testisstructure shows good testicular development, Seminiferous tubules arranged indense, spermatogonia, primary spermatocytes, secondary spermatocytes, andsperm cells in turn arranged in neat rows, a large number of sperm in thelumen.The middle dose group and high dose group testes were poorlydeveloped. Fine tubules arranged in loose, sparse interstitial cells, the smalllumen of some seminiferous germ cell derangement. Slice of low-dose groupwere no obvious abnormalities.5P450scc expression in rat Leydig cells:Mesenchymal cells more positive inthe control group and low dose group,Cells are dark colored, close to theabsorbance, the difference was not statistically significant;The middle dosegroup and high dose group P450scc-positive cells expressed weak, lightstaining, small absorbance difference was statistically significant.63βHSD expression in rat Leydig cells:The number of3βHSD positive cellsin the middle dose group and high dose group to be higher than that in thecontrol group.No significant difference between control group and low-doseexposure group, the positive cells, stained dark.Conclusion:Environmental hormone bisphenol A can cause reproductivetoxicity in male rats by oral intake. Reaches a certain concentration can affectthe body weight of rats and testicular weight changes, and higher doses caninhibit the testes to produce testosterone,Mechanism may be that bisphenol Ainhibits testosterone synthesis key enzyme (P450scc and3βHSD) expression.
Keywords/Search Tags:Environmental hormones, Bisphenol A, Testosterone, 3β-HSD, P450scc
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