鉛鎘聯(lián)合對(duì)大鼠腎臟的毒性研究一、本文概述Overviewofthisarticle本文旨在探討鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟的毒性作用。鉛和鎘是兩種常見的重金屬污染物，廣泛存在于工業(yè)廢水、廢氣以及城市環(huán)境中。這些重金屬可通過食物鏈進(jìn)入人體，并在腎臟等器官中積累，從而引發(fā)一系列毒性反應(yīng)。本文采用大鼠作為實(shí)驗(yàn)動(dòng)物，通過染毒實(shí)驗(yàn)，觀察鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟組織結(jié)構(gòu)和功能的影響，以期為預(yù)防和治療重金屬污染引起的腎臟損傷提供理論依據(jù)。Thisarticleaimstoexplorethetoxiceffectsofcombinedexposuretoleadandcadmiumonthekidneysofrats.Leadandcadmiumaretwocommonheavymetalpollutants,widelypresentinindustrialwastewater,exhaustgas,andurbanenvironments.Theseheavymetalscanenterthehumanbodythroughthefoodchainandaccumulateinorganssuchasthekidneys,triggeringaseriesoftoxicreactions.Thisarticleusesratsasexperimentalanimalstoobservetheeffectsofcombinedexposuretoleadandcadmiumonthestructureandfunctionofratkidneytissuethroughtoxicityexperiments,inordertoprovidetheoreticalbasisforthepreventionandtreatmentofkidneydamagecausedbyheavymetalpollution.實(shí)驗(yàn)過程中，我們將大鼠分為不同組別，分別暴露于不同濃度的鉛和鎘環(huán)境中。通過對(duì)比各組大鼠腎臟組織的病理學(xué)變化、腎功能指標(biāo)以及氧化應(yīng)激水平等指標(biāo)，全面評(píng)估鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟的毒性作用。我們還將探討鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟毒性的可能機(jī)制，為進(jìn)一步揭示重金屬污染的健康風(fēng)險(xiǎn)提供科學(xué)依據(jù)。Duringtheexperiment,wedividedtheratsintodifferentgroupsandexposedthemtodifferentconcentrationsofleadandcadmiumenvironments.Bycomparingthepathologicalchanges,renalfunctionindicators,andoxidativestresslevelsofkidneytissueindifferentgroupsofrats,acomprehensiveevaluationofthetoxiceffectsofleadandcadmiumcombinedexposureonratkidneyswasconducted.Wewillalsoexplorethepossiblemechanismsofcombinedexposureofleadandcadmiumonrenaltoxicityinrats,providingscientificbasisforfurtherrevealingthehealthrisksofheavymetalpollution.通過本文的研究，我們期望能夠?yàn)橹亟饘傥廴痉揽睾湍I臟疾病防治提供新的思路和方法，為保障人類健康和環(huán)境安全做出貢獻(xiàn)。Throughtheresearchinthisarticle,wehopetoprovidenewideasandmethodsforthepreventionandcontrolofheavymetalpollutionandkidneydisease,andcontributetoensuringhumanhealthandenvironmentalsafety.二、文獻(xiàn)綜述Literaturereview鉛和鎘是兩種常見的重金屬，廣泛存在于工業(yè)、農(nóng)業(yè)和日常生活中。由于人類活動(dòng)的影響，這兩種重金屬經(jīng)常通過食物鏈進(jìn)入生物體，對(duì)機(jī)體產(chǎn)生多種毒性作用。腎臟作為人體重要的排泄器官，對(duì)重金屬的毒性作用尤為敏感。近年來，鉛和鎘對(duì)腎臟的聯(lián)合毒性作用逐漸受到學(xué)者們的關(guān)注。Leadandcadmiumaretwocommonheavymetalsthatarewidelypresentinindustry,agriculture,anddailylife.Duetotheinfluenceofhumanactivities,thesetwoheavymetalsoftenenterorganismsthroughthefoodchain,causingvarioustoxiceffectsonthebody.Asanimportantexcretoryorganinthehumanbody,thekidneysareparticularlysensitivetothetoxiceffectsofheavymetals.Inrecentyears,thecombinedtoxiceffectsofleadandcadmiumonthekidneyshavegraduallyattractedtheattentionofscholars.在文獻(xiàn)中，有大量關(guān)于鉛和鎘單獨(dú)對(duì)腎臟毒性作用的研究。鉛進(jìn)入體內(nèi)后，主要通過血液循環(huán)到達(dá)腎臟，與腎臟中的蛋白質(zhì)結(jié)合，導(dǎo)致腎小管損傷、腎小球?yàn)V過率下降等腎功能障礙。而鎘則主要通過呼吸道和消化道進(jìn)入體內(nèi)，積累在腎臟中，引起腎小管上皮細(xì)胞壞死、腎間質(zhì)纖維化等病變。Therearenumerousstudiesintheliteratureonthenephrotoxiceffectsofleadandcadmiumalone.Afterenteringthebody,leadmainlyreachesthekidneysthroughbloodcirculationandbindswithproteinsinthekidneys,leadingtorenaldysfunctionsuchastubularinjuryanddecreasedglomerularfiltrationrate.Cadmium,ontheotherhand,mainlyentersthebodythroughtherespiratoryanddigestivetractsandaccumulatesinthekidneys,causingnecrosisofrenaltubularepithelialcellsandinterstitialfibrosis.然而，鉛和鎘在環(huán)境中的共存現(xiàn)象使得它們的聯(lián)合毒性作用不容忽視。研究表明，鉛和鎘在腎臟中的聯(lián)合作用可能導(dǎo)致更嚴(yán)重的腎臟損傷。這種聯(lián)合毒性作用可能與兩者之間的相互作用有關(guān)，如競(jìng)爭(zhēng)性地與腎臟中的某些蛋白質(zhì)結(jié)合，或者通過共同的代謝途徑產(chǎn)生協(xié)同效應(yīng)。However,thecoexistenceofleadandcadmiumintheenvironmentmakestheircombinedtoxiceffectsundeniable.Researchhasshownthatthecombinedeffectofleadandcadmiuminthekidneysmayleadtomoreseverekidneydamage.Thiscombinedtoxiceffectmayberelatedtotheinteractionbetweenthetwo,suchascompetitivelybindingtocertainproteinsinthekidneys,orproducingsynergisticeffectsthroughacommonmetabolicpathway.鉛和鎘的聯(lián)合毒性作用還受到多種因素的影響，如暴露劑量、暴露時(shí)間、暴露途徑以及機(jī)體的個(gè)體差異等。因此，在研究鉛和鎘對(duì)腎臟的聯(lián)合毒性作用時(shí)，需要綜合考慮這些因素的影響。Thecombinedtoxicityofleadandcadmiumisalsoinfluencedbyvariousfactors,suchasexposuredose,exposuretime,exposurepathway,andindividualdifferencesinthebody.Therefore,whenstudyingthecombinedtoxiceffectsofleadandcadmiumonthekidneys,itisnecessarytocomprehensivelyconsidertheeffectsofthesefactors.鉛和鎘對(duì)腎臟的聯(lián)合毒性作用是一個(gè)復(fù)雜的研究領(lǐng)域。為了更好地了解這兩種重金屬對(duì)腎臟的毒性作用機(jī)制，需要進(jìn)一步開展深入的研究，以期為預(yù)防和治療相關(guān)腎臟疾病提供理論依據(jù)。Thecombinedtoxiceffectsofleadandcadmiumonthekidneysisacomplexresearchfield.Inordertobetterunderstandthetoxicmechanismsofthesetwoheavymetalsonthekidneys,furtherin-depthresearchisneededtoprovidetheoreticalbasisforthepreventionandtreatmentofrelatedkidneydiseases.三、材料與方法MaterialsandMethods選用健康成年雄性Sprague-Dawley大鼠，體重約200-250g，購(gòu)自[動(dòng)物實(shí)驗(yàn)中心名稱]，所有動(dòng)物均飼養(yǎng)在恒溫（22±2℃）、恒濕（55±5%）和12小時(shí)光照/黑暗循環(huán)的環(huán)境中，并自由獲取標(biāo)準(zhǔn)飼料和飲用水。HealthyadultmaleSpragueDawleyratsweighingapproximately200-250gwereselectedandpurchasedfrom[AnimalExperimentCenterName].Allanimalswerekeptinaconstanttemperature(22±2℃),constanthumidity(55±5%),anda12hourlight/darkcycleenvironment,withfreeaccesstostandardfeedanddrinkingwater.鉛（Pb）和鎘（Cd）溶液購(gòu)自[試劑供應(yīng)商名稱]，純度均大于9%。所有溶液均用去離子水配制。實(shí)驗(yàn)所用儀器包括[列出主要儀器名稱和型號(hào)]，所有儀器均在使用前進(jìn)行校準(zhǔn)，以確保實(shí)驗(yàn)結(jié)果的準(zhǔn)確性。Lead(Pb)andcadmium(Cd)solutionswerepurchasedfrom[reagentsuppliername],withpuritygreaterthan9%.Allsolutionsarepreparedwithdeionizedwater.Theinstrumentsusedintheexperimentinclude[listthemaininstrumentnamesandmodels],andallinstrumentsarecalibratedbeforeusetoensuretheaccuracyoftheexperimentalresults.大鼠隨機(jī)分為四組：對(duì)照組、鉛暴露組、鎘暴露組和鉛鎘聯(lián)合暴露組。每組10只大鼠。對(duì)照組大鼠給予去離子水，鉛暴露組大鼠給予不同濃度的鉛溶液，鎘暴露組大鼠給予不同濃度的鎘溶液，鉛鎘聯(lián)合暴露組大鼠則同時(shí)給予相應(yīng)濃度的鉛和鎘溶液。暴露周期為[暴露周期，如“6周”]。Ratswererandomlydividedintofourgroups:controlgroup,leadexposuregroup,cadmiumexposuregroup,andleadcadmiumcombinedexposuregroup.10ratspergroup.Thecontrolgroupratsweregivendeionizedwater,theleadexposuregroupratsweregivendifferentconcentrationsofleadsolutions,thecadmiumexposuregroupratsweregivendifferentconcentrationsofcadmiumsolutions,andtheleadcadmiumcombinedexposuregroupratsweregivencorrespondingconcentrationsofleadandcadmiumsolutionssimultaneously.Theexposureperiodis[exposureperiod,suchas"6weeks"].暴露結(jié)束后，所有大鼠進(jìn)行麻醉并處死。迅速取出腎臟，用生理鹽水清洗，去除多余血液，然后用濾紙吸干表面水分，稱重并記錄。一部分腎臟組織用于生化指標(biāo)檢測(cè)，另一部分腎臟組織用10%中性福爾馬林固定，用于后續(xù)的組織病理學(xué)檢查。Afterexposure,allratswereanesthetizedandeuthanized.Quicklyremovethekidney,washwithphysiologicalsalinetoremoveexcessblood,thenusefilterpapertoabsorbsurfacemoisture,weighandrecord.Partofthekidneytissueisusedforbiochemicalindicatordetection,whiletheotherpartisfixedwith10%neutralformalinforsubsequenthistopathologicalexamination.取腎臟組織勻漿，采用[生化指標(biāo)檢測(cè)方法，如“酶聯(lián)免疫吸附法（ELISA）”]測(cè)定相關(guān)生化指標(biāo)，包括[列出具體指標(biāo)，如“肌酐（Cr）、尿素氮（BUN）”]等，以評(píng)估腎臟功能。Takekidneytissuehomogenateandusebiochemicalindicatordetectionmethodssuchasenzyme-linkedimmunosorbentassay(ELISA)tomeasurerelevantbiochemicalindicators,includinglistingspecificindicatorssuchascreatinine(Cr)andureanitrogen(BUN),toevaluatekidneyfunction.固定后的腎臟組織進(jìn)行石蠟包埋、切片，然后進(jìn)行[染色方法，如“蘇木精-伊紅（HE）染色”]。染色后的切片在光鏡下觀察，記錄腎臟組織的病理變化，并進(jìn)行半定量分析。Thefixedkidneytissueisembeddedinparaffin,sliced,andthensubjectedtostainingmethodssuchashematoxylineosin(HE)staining.Thestainedsectionsareobservedunderalightmicroscopetorecordthepathologicalchangesofrenaltissueandundergosemiquantitativeanalysis.所有數(shù)據(jù)均以均數(shù)±標(biāo)準(zhǔn)差（mean±SD）表示。采用SPSS軟件進(jìn)行數(shù)據(jù)分析，多組間的比較采用單因素方差分析（ANOVA），以P<05為差異有統(tǒng)計(jì)學(xué)意義。Alldataareexpressedasmean±standarddeviation(mean±SD).SPSSsoftwarewasusedfordataanalysis,andone-wayanalysisofvariance(ANOVA)wasusedforcomparisonbetweenmultiplegroups,withP<05indicatingstatisticalsignificance.以上即為本次《鉛鎘聯(lián)合對(duì)大鼠腎臟的毒性研究》的材料與方法部分，詳細(xì)描述了實(shí)驗(yàn)動(dòng)物的選擇、試劑與儀器的準(zhǔn)備、實(shí)驗(yàn)設(shè)計(jì)、樣品收集與處理、生化指標(biāo)檢測(cè)、組織病理學(xué)檢查以及數(shù)據(jù)處理與分析的過程，為后續(xù)實(shí)驗(yàn)結(jié)果的解讀提供了堅(jiān)實(shí)的基礎(chǔ)。TheaboveistheMaterialsandMethodssectionofthisstudyonthetoxicityofleadcadmiumcombinationonratkidneys.Itprovidesadetaileddescriptionoftheselectionofexperimentalanimals,preparationofreagentsandinstruments,experimentaldesign,samplecollectionandprocessing,biochemicalindexdetection,histopathologicalexamination,anddataprocessingandanalysis,providingasolidfoundationfortheinterpretationofsubsequentexperimentalresults.四、結(jié)果Result本研究通過對(duì)大鼠進(jìn)行鉛鎘聯(lián)合暴露，觀察其對(duì)腎臟的毒性作用，得到了以下主要結(jié)果。Thisstudyobservedthetoxiceffectsofleadandcadmiumcombinedexposureonthekidneysinrats,andobtainedthefollowingmainresults.在生理指標(biāo)方面，暴露于鉛鎘聯(lián)合處理的大鼠，其血尿素氮（BUN）和血清肌酐（SCr）水平均顯著升高，這提示我們腎臟功能可能受到了損害。同時(shí)，聯(lián)合暴露組大鼠的腎臟指數(shù)也顯著高于對(duì)照組，這進(jìn)一步證實(shí)了腎臟發(fā)生了病理變化。Intermsofphysiologicalindicators,ratsexposedtoleadcadmiumcombinedtreatmentshowedsignificantincreasesinbloodureanitrogen(BUN)andserumcreatinine(SCr)levels,suggestingthatourrenalfunctionmayhavebeenimpaired.Meanwhile,therenalindexofthecombinedexposuregroupratswassignificantlyhigherthanthatofthecontrolgroup,furtherconfirmingthepathologicalchangesinthekidneys.在組織病理學(xué)觀察中，我們發(fā)現(xiàn)聯(lián)合暴露組大鼠的腎臟組織出現(xiàn)了明顯的腎小管上皮細(xì)胞變性、壞死，以及腎小管管腔內(nèi)有大量蛋白管型，這些都是腎臟受損的典型病理表現(xiàn)。腎小球也出現(xiàn)了腫脹、炎性細(xì)胞浸潤(rùn)等現(xiàn)象，表明腎小球也受到了損害。Inhistopathologicalobservation,wefoundthattherenaltissueofratsinthecombinedexposuregroupexhibitedsignificantdegenerationandnecrosisofrenaltubularepithelialcells,aswellasalargenumberofproteintubulesintherenaltubularlumen,whicharetypicalpathologicalmanifestationsofkidneydamage.Theglomerulusalsoshowedswellingandinflammatorycellinfiltration,indicatingthattheglomeruluswasalsodamaged.在氧化應(yīng)激方面，聯(lián)合暴露組大鼠腎臟組織的MDA含量顯著升高，而SOD和GSH-Px活性則顯著降低。這表明鉛鎘聯(lián)合暴露導(dǎo)致了大鼠腎臟組織發(fā)生了氧化應(yīng)激反應(yīng)，抗氧化能力下降，進(jìn)一步加重了腎臟損傷。Intermsofoxidativestress,theMDAcontentinthekidneytissueofratsinthecombinedexposuregroupsignificantlyincreased,whileSODandGSHPxactivitysignificantlydecreased.Thisindicatesthatcombinedexposuretoleadandcadmiumresultedinoxidativestressresponseinratkidneytissue,decreasedantioxidantcapacity,andfurtheraggravatedkidneydamage.在凋亡相關(guān)蛋白表達(dá)方面，我們發(fā)現(xiàn)聯(lián)合暴露組大鼠腎臟組織的Bax蛋白表達(dá)顯著增加，而Bcl-2蛋白表達(dá)則顯著減少。Caspase-3的活性也顯著升高。這些結(jié)果表明鉛鎘聯(lián)合暴露促進(jìn)了腎臟組織細(xì)胞的凋亡過程。Intermsofapoptosisrelatedproteinexpression,wefoundthattheexpressionofBaxproteininthekidneytissueofratsexposedtocombinedexposurewassignificantlyincreased,whiletheexpressionofBcl-2proteinwassignificantlyreduced.TheactivityofCaspase-3alsosignificantlyincreased.Theseresultsindicatethatcombinedexposuretoleadandcadmiumpromotestheapoptosisprocessofrenaltissuecells.鉛鎘聯(lián)合暴露對(duì)大鼠腎臟具有明顯的毒性作用，可導(dǎo)致腎臟功能損傷、組織病理學(xué)改變、氧化應(yīng)激反應(yīng)以及細(xì)胞凋亡等。這些結(jié)果為進(jìn)一步探討鉛鎘聯(lián)合暴露的腎臟毒性機(jī)制提供了重要依據(jù)。Thecombinedexposureofleadandcadmiumhasasignificanttoxiceffectonthekidneysofrats,whichcanleadtorenalfunctiondamage,histopathologicalchanges,oxidativestressresponse,andcellapoptosis.Theseresultsprovideimportantevidenceforfurtherexploringtherenaltoxicitymechanismofleadcadmiumcombinedexposure.五、討論Discussion本研究旨在探討鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟的毒性作用，為預(yù)防和治療相關(guān)腎臟疾病提供理論依據(jù)。實(shí)驗(yàn)結(jié)果表明，鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟產(chǎn)生了明顯的毒性作用，其機(jī)制可能與氧化應(yīng)激、炎癥反應(yīng)和細(xì)胞凋亡等多種生物學(xué)過程有關(guān)。Theaimofthisstudyistoexplorethetoxiceffectsofcombinedexposuretoleadandcadmiumonthekidneysofrats,providingatheoreticalbasisforthepreventionandtreatmentofrelatedkidneydiseases.Theexperimentalresultsindicatethatthecombinedexposureofleadandcadmiumhasasignificanttoxiceffectonthekidneysofrats,anditsmechanismmayberelatedtovariousbiologicalprocessessuchasoxidativestress,inflammatoryresponse,andcellapoptosis.從氧化應(yīng)激的角度來看，鉛和鎘聯(lián)合暴露可導(dǎo)致大鼠腎臟組織中的活性氧（ROS）水平顯著升高，同時(shí)抗氧化酶活性降低。這一結(jié)果提示我們，鉛和鎘聯(lián)合暴露可能通過誘導(dǎo)氧化應(yīng)激反應(yīng)，破壞腎臟細(xì)胞的氧化還原平衡，進(jìn)而導(dǎo)致腎臟損傷。因此，抗氧化治療可能成為緩解鉛和鎘聯(lián)合暴露引起腎臟毒性的有效手段。Fromtheperspectiveofoxidativestress,combinedexposuretoleadandcadmiumcanleadtoasignificantincreaseinreactiveoxygenspecies(ROS)levelsinratkidneytissue,whilereducingantioxidantenzymeactivity.Thisresultsuggeststhatcombinedexposuretoleadandcadmiummayinduceoxidativestressresponse,disrupttheredoxbalanceofkidneycells,andultimatelyleadtokidneydamage.Therefore,antioxidanttherapymaybecomeaneffectivemeansofalleviatingrenaltoxicitycausedbycombinedexposuretoleadandcadmium.炎癥反應(yīng)在鉛和鎘聯(lián)合暴露引起的腎臟損傷中也發(fā)揮了重要作用。實(shí)驗(yàn)結(jié)果顯示，聯(lián)合暴露后大鼠腎臟組織中炎性細(xì)胞因子表達(dá)水平顯著升高，提示炎癥反應(yīng)可能參與了腎臟損傷的過程。這一發(fā)現(xiàn)為我們提供了新的思路，即通過抑制炎癥反應(yīng)來減輕腎臟損傷。Inflammatoryreactionsalsoplayanimportantroleinkidneydamagecausedbycombinedexposuretoleadandcadmium.Theexperimentalresultsshowedthattheexpressionlevelsofinflammatorycytokinesinthekidneytissueofratssignificantlyincreasedaftercombinedexposure,indicatingthatinflammatoryresponsemaybeinvolvedintheprocessofkidneyinjury.Thisdiscoveryprovidesuswithanewapproachtoalleviatekidneydamagebyinhibitinginflammatoryresponses.細(xì)胞凋亡也可能是鉛和鎘聯(lián)合暴露導(dǎo)致腎臟損傷的重要機(jī)制之一。實(shí)驗(yàn)結(jié)果顯示，聯(lián)合暴露后大鼠腎臟細(xì)胞凋亡率顯著增加。這表明鉛和鎘聯(lián)合暴露可能通過誘導(dǎo)腎臟細(xì)胞凋亡，導(dǎo)致腎臟功能受損。因此，尋找能夠抑制細(xì)胞凋亡的藥物或方法，可能成為治療鉛和鎘聯(lián)合暴露引起腎臟損傷的有效途徑。Apoptosismayalsobeoneoftheimportantmechanismsofkidneydamagecausedbycombinedexposuretoleadandcadmium.Theexperimentalresultsshowedthattheapoptosisrateofratkidneycellssignificantlyincreasedaftercombinedexposure.Thisindicatesthatcombinedexposuretoleadandcadmiummayinducerenalcellapoptosis,leadingtoimpairedrenalfunction.Therefore,searchingfordrugsormethodsthatcaninhibitcellapoptosismaybecomeaneffectivewaytotreatkidneydamagecausedbycombinedexposuretoleadandcadmium.鉛和鎘聯(lián)合暴露對(duì)大鼠腎臟產(chǎn)生了明顯的毒性作用，其機(jī)制涉及氧化應(yīng)激、炎癥反應(yīng)和細(xì)胞凋亡等多種生物學(xué)過程。未來研究可進(jìn)一步探討這些機(jī)制的具體作用途徑，以及尋找有效的干預(yù)措施來減輕或預(yù)防鉛和鎘聯(lián)合暴露引起的腎臟損傷。對(duì)于人類而言，加強(qiáng)環(huán)境保護(hù)和減少重金屬污染，也是預(yù)防腎臟疾病的重要措施之一。Thecombinedexposureofleadandcadmiumhasasignificanttoxiceffectonthekidneysofrats,involvingvariousbiologicalprocessessuchasoxidativestress,inflammatoryresponse,andcellapoptosis.Futureresearchcanfurtherexplorethespecificpathwaysofthesemechanismsandfindeffectiveinterventionmeasurestoreduceorpreventkidneydamagecausedbycombinedexposuretoleadandcadmium.Forhumans,strengtheningenvironmentalprotectionandreducingheavymetalpollutionarealsoimportantmeasurestopreventkidneydisease.六、結(jié)論Conclusion本研究對(duì)鉛鎘聯(lián)合暴露對(duì)大鼠腎臟的毒性進(jìn)行了深入探討，通過一系列的實(shí)驗(yàn)設(shè)計(jì)和結(jié)果分析，得出了一些有意義的結(jié)論。Thisstudyconductedanin-depthexplorationofthetoxicityofcombinedexposuretoleadandcadmiumonthekidneysofrats.Throughaseriesofexperimentaldesignsandresultanalysis,somemeaningfulconclusionsweredrawn.實(shí)驗(yàn)結(jié)果顯示，鉛鎘聯(lián)合暴露對(duì)大鼠腎臟產(chǎn)生了明顯的毒性作用。這表現(xiàn)在大鼠腎臟功能的降低，腎組織結(jié)構(gòu)的破壞，以及腎細(xì)胞凋亡的增加等方面。這些結(jié)果提示我們，鉛鎘聯(lián)合暴露對(duì)腎臟健康的危害不容忽視。Theexperimentalresultsshowedthatthecombinedexposureofleadandcadmiumhadasignificanttoxiceffectonthekidneysofrats.Thisismanifestedinthedecreaseofrenalfunctioninrats,thedestructionofrenaltissuestructure,andtheincreaseofrenalcellapoptosis.Theseresultssuggestthattheharmofcombinedexp