







摘要:水土環(huán)境中的新污染物嚴(yán)重威脅生態(tài)安全與人類健康,食物鏈?zhǔn)瞧湟l(fā)風(fēng)險(xiǎn)的關(guān)鍵途徑。本文對(duì)水土環(huán)境食物鏈中新污染物遷移相關(guān)研究進(jìn)展進(jìn)行了總結(jié)與歸納。水環(huán)境中微塑料、抗生素與持久性有機(jī)污染物的遷移呈現(xiàn)顯著差異:微塑料因水生生物的吸收、選擇性攝食與排泄行為的動(dòng)態(tài)平衡,在食物鏈中表現(xiàn)出富集與消減并存的雙向趨勢(shì);抗生素則因生物代謝活動(dòng)的逐級(jí)強(qiáng)化,其濃度沿營(yíng)養(yǎng)級(jí)呈現(xiàn)衰減特征;與之相反,高疏水性的持久性有機(jī)污染物通過脂質(zhì)分配機(jī)制在生物體內(nèi)持續(xù)積累,表現(xiàn)出典型的生物放大效應(yīng);低脂溶性的內(nèi)分泌干擾物依賴蛋白質(zhì)結(jié)合在高營(yíng)養(yǎng)級(jí)蓄積,高脂溶性的內(nèi)分泌干擾物則通過脂質(zhì)介導(dǎo)的生物放大沿食物鏈富集。土壤環(huán)境中,抗生素抗性基因的遷移更具復(fù)雜性,其通過植物水分吸收、動(dòng)物攝食、空氣沉降等多途徑傳遞,并借助水平基因轉(zhuǎn)移在土壤-蔬菜-昆蟲食物鏈中跨物種擴(kuò)散,顯著增加了健康風(fēng)險(xiǎn)。本文通過分析新污染物的遷移機(jī)制,深化了對(duì)新污染物生態(tài)毒性效應(yīng)理解,并為新污染物控制提供科學(xué)依據(jù)。
關(guān)鍵詞:新污染物;水土食物鏈;積累與排出;遷移機(jī)制
中圖分類號(hào):X50 文獻(xiàn)標(biāo)志碼:A 文章編號(hào):1672-2043(2025)03-0617-13 doi:10.11654/jaes.2025-0150
新污染物是指排放到環(huán)境中的,具有生物毒性、環(huán)境持久性、生物累積性等特征,對(duì)生態(tài)環(huán)境或人體健康存在較大風(fēng)險(xiǎn),但尚未納入管理或現(xiàn)有管理措施不足的有毒有害化學(xué)物質(zhì),其廣泛存在于環(huán)境中,對(duì)人體健康構(gòu)成潛在威脅[1]。新污染物并不僅指新的化學(xué)物質(zhì),其在人類生活環(huán)境中已經(jīng)存在較長(zhǎng)時(shí)間,往往是人類生產(chǎn)生活中經(jīng)常使用的物品的組成成分,不當(dāng)使用與回收便會(huì)造成環(huán)境污染[2]。當(dāng)前,新污染物主要包括藥物及個(gè)人護(hù)理產(chǎn)品[3]、內(nèi)分泌干擾物[4]、微塑料[5]、抗生素抗性基因[6]等類型,我國(guó)通過《重點(diǎn)管控新污染物清單(2023年版)》已對(duì)全氟化合物、抗生素、內(nèi)分泌干擾物等14類物質(zhì)實(shí)施管控,但面對(duì)污染物種類的持續(xù)新增,現(xiàn)有清單在覆蓋范圍與動(dòng)態(tài)更新機(jī)制方面仍存在不足。新污染物的來源多種多樣,主要分為點(diǎn)源和非點(diǎn)源。城市污水處理廠是新污染物排放的重要點(diǎn)源,因?yàn)槠錈o法完全去除復(fù)雜的有機(jī)化合物而成為污染擴(kuò)散的關(guān)鍵環(huán)節(jié)[7]。非點(diǎn)源污染則包括農(nóng)業(yè)徑流、大氣沉降和廢棄物泄漏,這些途徑能夠?qū)⒋罅啃挛廴疚镙斔椭梁恿骱秃矗瑢?dǎo)致水體污染[8]。此外,廢棄藥品的不當(dāng)處理和工業(yè)廢水的直接排放也是不可忽視的污染來源[9]。
近年來,因?qū)ι鷳B(tài)環(huán)境和人類健康的不利影響已得到充分證實(shí),新污染物已成為人們關(guān)注的焦點(diǎn),其易對(duì)人類和動(dòng)物的生殖、神經(jīng)、發(fā)育和免疫系統(tǒng)等產(chǎn)生負(fù)面影響[10]。經(jīng)口攝食是環(huán)境中新污染物暴露于生物體與人體的關(guān)鍵環(huán)節(jié)[11]。研究發(fā)現(xiàn),持久性有機(jī)污染物多氯聯(lián)苯(PCBs)和多環(huán)芳烴(PAHs)因其高脂溶性與化學(xué)穩(wěn)定性易在水生生物體內(nèi)積累,并通過食物鏈傳遞到魚類和海洋哺乳動(dòng)物,最終進(jìn)入人體,引發(fā)癌癥風(fēng)險(xiǎn)與生殖毒性[12]。全氟化合物(PFASs)廣泛應(yīng)用于工業(yè)和消費(fèi)品中,具有顯著的環(huán)境殘留性,近年來受到熱點(diǎn)關(guān)注,其可大量累積于蔬菜和貝類,被攝食后進(jìn)入人體,引發(fā)甲狀腺疾病和免疫功能失調(diào)、增加癌癥風(fēng)險(xiǎn)、影響胎兒發(fā)育[13]。傳統(tǒng)污染物通常具有簡(jiǎn)單的環(huán)狀或直鏈結(jié)構(gòu),功能基團(tuán)單一,疏水性強(qiáng),易富集于生物脂肪或沉積物;而新污染物結(jié)構(gòu)復(fù)雜,含多樣功能基團(tuán),極性差異顯著:部分高親水性易擴(kuò)散,部分兼具水溶性與生物蓄積性。傳統(tǒng)污染物降解路徑明確,而新污染物常生成穩(wěn)定且高毒的轉(zhuǎn)化產(chǎn)物,其環(huán)境行為與毒性更具不確定性。由此可見,新污染物嚴(yán)重威脅著人類健康,而食物鏈?zhǔn)墙閷?dǎo)環(huán)境中新污染物暴露于人體的關(guān)鍵途徑之一[14]。
新污染物對(duì)農(nóng)業(yè)環(huán)境及農(nóng)業(yè)生產(chǎn)的潛在危害也不容忽視,農(nóng)業(yè)生態(tài)系統(tǒng)作為人類食物供給的核心載體,其土壤、水體及生物群落極易受到新污染物的侵襲。微塑料在農(nóng)田土壤中的長(zhǎng)期累積可改變土壤孔隙結(jié)構(gòu),阻礙根系發(fā)育與水分滲透,進(jìn)而抑制作物生長(zhǎng)并降低產(chǎn)量[15]。抗生素抗性基因在土壤-蔬菜-昆蟲食物鏈中的水平基因轉(zhuǎn)移可能加速“超級(jí)細(xì)菌”的擴(kuò)散,加劇農(nóng)業(yè)環(huán)境中病原微生物的耐藥性問題,進(jìn)一步威脅農(nóng)業(yè)生態(tài)系統(tǒng)的穩(wěn)定性[16]。
食物鏈錯(cuò)綜復(fù)雜,涵蓋了植物、動(dòng)物等多種生命體(圖1),這些生命體間相互依存、相互影響,對(duì)污染物均具累積與代謝作用。因此,食物鏈對(duì)污染物的傳遞與累積是一個(gè)十分復(fù)雜的過程[17]。目前,新污染物在食物鏈中各營(yíng)養(yǎng)級(jí)中的積累及其毒性效應(yīng)已有大量的研究,但對(duì)遷移過程中的關(guān)鍵環(huán)境因素與生物學(xué)過程聯(lián)動(dòng)機(jī)制揭示不足,生態(tài)風(fēng)險(xiǎn)評(píng)估的系統(tǒng)性和預(yù)測(cè)性仍然欠缺。基于此,本文聚焦了環(huán)境分布廣、健康威脅大的典型新污染物:微塑料、內(nèi)分泌干擾物、抗生素、抗生素抗性基因、持久性有機(jī)污染物,深入分析其在食物鏈中的遷移行為,解析了其遷移與累積的關(guān)鍵影響因子與驅(qū)動(dòng)機(jī)制,揭示了新污染物的差異化遷移規(guī)律,為突破單一污染物研究局限、推動(dòng)全鏈條風(fēng)險(xiǎn)評(píng)估提供關(guān)鍵科學(xué)支撐。通過系統(tǒng)總結(jié),可提升關(guān)于新污染物生態(tài)毒性效應(yīng)的相關(guān)認(rèn)識(shí),以期為新污染物控制提供科學(xué)依據(jù)。
1 新污染物在水環(huán)境食物鏈中的遷移行為
新污染物通過復(fù)雜的生物積累和生物放大機(jī)制在水生食物鏈中遷移,其影響貫穿整個(gè)生態(tài)系統(tǒng),對(duì)水生生物多樣性、生態(tài)服務(wù)功能及人類健康構(gòu)成多重威脅,并加劇全球環(huán)境治理的復(fù)雜性[18]。近年來,關(guān)于新污染物在水生食物鏈中的遷移行為受到了學(xué)者關(guān)注,相關(guān)研究涉及的新污染物包括微塑料、抗生素、持久性有機(jī)污染物等(表1)。
1.1 微塑料在水生食物鏈中的遷移行為
由表1數(shù)據(jù)可知,隨食物鏈傳遞,微塑料含量呈現(xiàn)升高或降低兩種趨勢(shì)。生產(chǎn)者(藻類)對(duì)水環(huán)境中微塑料的累積作用、無脊椎動(dòng)物的選擇性進(jìn)食行為以及魚對(duì)微塑料的積累與排出機(jī)制共同驅(qū)動(dòng)了其歸趨(圖2)。
1.1.1 藻類對(duì)微塑料的吸附作用
吸附作用是微塑料從水環(huán)境中向藻類遷移的關(guān)鍵途徑之一,該過程與微塑料表面物理特性密切相關(guān)。其中,靜電吸附是微塑料與藻類相互作用的關(guān)鍵機(jī)制之一,其是指藻類細(xì)胞表面和微塑料顆粒表面所帶的電荷不同而產(chǎn)生的互相吸引[19]。例如,綠藻(Chlorella vulgaris)細(xì)胞壁中含有羧基和硫酸根基團(tuán),從而帶有較多的負(fù)電荷,其與帶有正電荷的脒乳膠聚苯乙烯微塑料顆粒間形成強(qiáng)烈靜電吸附,進(jìn)而使微塑料累積于綠藻表面[20]。高鹽度環(huán)境下,水中較多的陽離子會(huì)屏蔽藻類細(xì)胞表面和微塑料顆粒表面的電荷,減弱靜電吸附作用;而在低鹽度的環(huán)境下,靜電吸附作用則比較強(qiáng)烈[21]。
當(dāng)藻類與微塑料發(fā)生吸附作用時(shí),其表面常伴隨細(xì)菌及其他污染物的附著,形成復(fù)雜的生物膜復(fù)合體[22]。藻類和細(xì)菌在微塑料表面的增殖顯著改變了其物理行為:低密度生物膜通過增加微塑料浮力使其懸浮于水體表層,易被浮游動(dòng)物誤食;而高密度生物膜則通過重力效應(yīng)促使微塑料沉降至底泥,成為底棲生物的潛在食物來源[23]。更為關(guān)鍵的是,生物膜內(nèi)微生物可通過分泌降解酶將微塑料作為碳源分解,主動(dòng)誘導(dǎo)其表面開裂并破碎為納米級(jí)顆粒,納米級(jí)微塑料可借助藻類主動(dòng)吸收或被動(dòng)運(yùn)輸污染物的過程侵入細(xì)胞內(nèi),并隨食物鏈逐級(jí)遷移,最終通過生物放大作用加劇生態(tài)與健康風(fēng)險(xiǎn)[24]。
1.1.2 水中無脊椎動(dòng)物的選擇性進(jìn)食行為
無脊椎動(dòng)物是水生生態(tài)系統(tǒng)中的重要組成部分,其進(jìn)食行為驅(qū)動(dòng)了食物鏈中微塑料從生產(chǎn)者向第一營(yíng)養(yǎng)級(jí)生物中的遷移。無脊椎動(dòng)物對(duì)微塑料的攝食首先受到顆粒物理特性的驅(qū)動(dòng),包括大小、形狀和表面特征。顆粒大小是決定其能否進(jìn)入無脊椎動(dòng)物口器的關(guān)鍵因素。Prata等[25]發(fā)現(xiàn)無脊椎動(dòng)物的口器結(jié)構(gòu)(如濾食器和觸須)對(duì)顆粒的尺寸有一定選擇性,濾食器濾網(wǎng)間隙決定了能夠進(jìn)入口器的顆粒尺寸范圍,直徑在50~500 μm的微塑料顆粒最易被攝入。顆粒形狀對(duì)無脊椎動(dòng)物攝入微塑料的效率也有顯著影響。纖維狀顆粒由于形狀接近藻絲,更容易引發(fā)捕食性無脊椎動(dòng)物(如螃蟹和蝦類)的攝食行為[26]。此外,微塑料的表面粗糙程度與顆粒柔軟性也影響著部分依靠觸覺捕食的無脊椎動(dòng)物對(duì)其的攝入。測(cè)試牡蠣(Crassostrea virginica)對(duì)不同柔軟性的微塑料的吸收程度,發(fā)現(xiàn)柔性橡膠顆粒的積累速度與最終積累濃度均大于剛性尼龍碎片[27]。Porter 等[28]研究發(fā)現(xiàn),水蚤(Daphnia magna)通過觸須感知微塑料顆粒的物理特性,當(dāng)顆粒的粗糙度或柔性接近藻類時(shí),觸覺感知系統(tǒng)會(huì)誤認(rèn)為其為食物,從而將其攝食。
此外,微塑料表面的附著物進(jìn)一步影響了無脊椎動(dòng)物對(duì)其的選擇性進(jìn)食。比如,微塑料表面覆蓋的有機(jī)物或生物膜會(huì)釋放誘食信號(hào),使無脊椎動(dòng)物認(rèn)為其是天然食物[29],進(jìn)而將其誤食。研究發(fā)現(xiàn),相較于表面無生物膜的單分散聚甲基丙烯酸甲酯微球,表面包裹大腸桿菌生物膜的微球在牡蠣(Ostrea edulis)體內(nèi)的累積量提升了約10倍[30]。
不同水層深度中的無脊椎動(dòng)物吸收微塑料的尺寸閾值也存在差異。生活在水體上層的濾食性小型浮游甲殼動(dòng)物喜食細(xì)菌與藻類,因此相似尺寸的、直徑為1~10 μm 的微塑料顆粒較易被其攝入[31],而底棲片足類物種則對(duì)粒徑小于90 nm的顆粒攝入量最高[32]。
由此可見,因不同環(huán)境中微塑料種類與尺寸等有所不同,并且不同環(huán)境中的無脊椎動(dòng)物物種組成也不一致,這些因素共同導(dǎo)致了微塑料在不同水生食物鏈中富集或消減的不同歸趨。
1.1.3 魚類對(duì)微塑料的積累與排出
(1)魚類對(duì)微塑料的積累。魚類通常處于食物鏈第二營(yíng)養(yǎng)層級(jí)及以上,因此在同一生態(tài)系統(tǒng)中更容易接受微塑料的二次或多次轉(zhuǎn)移;其可直接攝入水中的懸浮微塑料,也可通過捕食其他污染生物間接攝入顯著量的微塑料顆粒[33]。此外,由于體型較大且新陳代謝率較高,魚類往往需要消耗更多食物,因而也更易攝入微塑料顆粒[34]。攝食后,魚類腸道在處理微塑料時(shí)也展現(xiàn)了復(fù)雜的生物學(xué)機(jī)制,這些機(jī)制受腸道環(huán)境條件與微塑料顆粒尺寸等共同調(diào)控。一方面,部分魚類的消化道較長(zhǎng)且復(fù)雜,為微塑料的存留提供了更多機(jī)會(huì)。部分魚類如泥鰍(Paramisgurnus dabryanus)則可通過分泌黏液來降低自身排泄速率,這也導(dǎo)致微塑料在其體內(nèi)的滯留時(shí)間延長(zhǎng)[35]。另一方面,相較于大尺寸微塑料顆粒,粒徑處于10 μm以下的微塑料可穿透腸道黏膜屏障,進(jìn)入腸組織甚至血液循環(huán)系統(tǒng)中,進(jìn)而導(dǎo)致了微塑料在魚類體內(nèi)的長(zhǎng)久累積,該現(xiàn)象被稱為微塑料的“跨腸道屏障遷移”[36]。
(2)魚類對(duì)微塑料的排出與降解。微塑料可隨魚類糞便排出,這一過程受到微塑料顆粒的大小和形狀以及魚類腸道蠕動(dòng)速率等多因素共同影響。粒徑較大的微塑料顆粒易引發(fā)魚類腸道的頻繁蠕動(dòng),從而加速其排泄,這一現(xiàn)象是魚類為減少機(jī)械性損傷而采取的一種自我保護(hù)措施[37]。相比之下,粒徑小于50 μm的小型微塑料顆粒在腸道內(nèi)的排出速度較慢,其原因在于直徑小的微塑料顆粒更容易附著在魚類腸道黏膜上,并可能與食物殘?jiān)Y(jié)合形成較難排泄的團(tuán)塊[38]。此外,Xiao等[39]發(fā)現(xiàn)纖維狀的微塑料顆粒由于容易嵌入腸道褶皺中,可能滯留更長(zhǎng)時(shí)間,從而降低其排出效率。Lu等[40]研究發(fā)現(xiàn)草食性魚類的腸道較長(zhǎng)且蠕動(dòng)頻率更高,微塑料在其體內(nèi)的滯留時(shí)間通常短于肉食性魚類。
雖然微塑料化學(xué)穩(wěn)定性較強(qiáng),但魚類腸道的酸性環(huán)境在一定程度上能夠改變其表面化學(xué)結(jié)構(gòu)。胃部的強(qiáng)酸性環(huán)境可破壞某些聚合物的表面涂層,使微塑料更易被分解[41]。比如,聚氨酯和聚碳酸酯顆粒在魚類腸道中出現(xiàn)粒徑減小和表面粗糙度增加的情況,這可能是在胃液作用下其表面部分化學(xué)鍵發(fā)生了斷裂[42]。此外,部分水生生物產(chǎn)生的酶對(duì)微塑料有顯著的降解效果。比如,斑馬魚的腸道微生物能夠分泌脂酶和氧化酶,這些酶類可將聚酰胺類微塑料顆粒降解為小分子聚合物,并被斑馬魚腸道分泌的黏液包裹,隨糞便排出[43]。
1.2 抗生素在食物鏈中的遷移行為
抗生素化學(xué)性質(zhì)較穩(wěn)定且生物活性強(qiáng),因此在水體中具有較高的持久性,并易于通過生物攝取進(jìn)入生物體內(nèi)。如表1所示,抗生素在水生食物鏈中均呈現(xiàn)濃度逐級(jí)降低的趨勢(shì),這主要是由于生物體內(nèi)擁有一系列復(fù)雜的代謝機(jī)制,可改變抗生素分子結(jié)構(gòu),從而減少其毒性并促進(jìn)其從生物體內(nèi)排出。低營(yíng)養(yǎng)級(jí)生物通常會(huì)對(duì)抗生素進(jìn)行初步代謝,當(dāng)抗生素及其初級(jí)代謝產(chǎn)物進(jìn)入更高營(yíng)養(yǎng)級(jí)生物(如魚類)后,高級(jí)生物體內(nèi)更為復(fù)雜的酶促反應(yīng)會(huì)對(duì)抗生素進(jìn)行更為深入的轉(zhuǎn)化與降解(圖3)。
1.2.1 藻類對(duì)抗生素的吸收與降解
抗生素主要通過被動(dòng)擴(kuò)散、被動(dòng)促進(jìn)擴(kuò)散和主動(dòng)運(yùn)輸?shù)确绞奖辉孱惣?xì)胞吸收。抗生素的被動(dòng)擴(kuò)散無需能量,主要通過濃度差驅(qū)動(dòng),從細(xì)胞膜外部擴(kuò)散至內(nèi)部,外部抗生素濃度越高,其遷移到藻類細(xì)胞內(nèi)的速度和效率越高[63];被動(dòng)促進(jìn)擴(kuò)散是抗生素在轉(zhuǎn)運(yùn)蛋白的幫助下穿過細(xì)胞膜;而主動(dòng)運(yùn)輸則是通過消耗能量使抗生素逆濃度梯度移動(dòng)[64]。研究發(fā)現(xiàn),當(dāng)胞外氯霉素濃度達(dá)10 mg·L-1時(shí),被動(dòng)擴(kuò)散和轉(zhuǎn)運(yùn)蛋白是其進(jìn)入綠藻(Chlorella vulgaris)細(xì)胞內(nèi)的主要方式。然而,抗生素也會(huì)對(duì)藻細(xì)胞產(chǎn)生毒性效應(yīng),進(jìn)而導(dǎo)致其累積濃度降低。例如,暴露48 h內(nèi),藻細(xì)胞內(nèi)部氯霉素含量持續(xù)上升,但隨暴露時(shí)間延長(zhǎng)至96 h,細(xì)胞內(nèi)部氯霉素濃度反而開始下降,這一現(xiàn)象主要是由于藻類細(xì)胞膜在高濃度氯霉素長(zhǎng)時(shí)間暴露下受到損傷,導(dǎo)致胞內(nèi)抗生素流出[65]。
藻類對(duì)抗生素的代謝降解主要包括酶促降解和光降解兩種類型。在酶促降解過程中,藻類通過分泌過氧化物酶和胞外蛋白酶等特定酶,將抗生素分子轉(zhuǎn)化為毒性較低的代謝產(chǎn)物[66]。光降解過程在藻類抗生素降解中也占有重要地位。藻類光合作用中釋放的活性氧分子(如超氧化物陰離子、氫氧自由基等)可使抗生素分子鍵斷裂,進(jìn)而促進(jìn)其分解[67]。
1.2.2 無脊椎動(dòng)物細(xì)胞色素酶對(duì)抗生素的代謝
作為生產(chǎn)者之后的第一營(yíng)養(yǎng)級(jí),無脊椎動(dòng)物體內(nèi)積累的抗生素濃度反而低于藻類細(xì)胞(表1),這主要是由于其體內(nèi)的細(xì)胞色素P450(CYP450)對(duì)抗生素具有顯著降解作用。CYP450能夠作為一種高效的氧化酶參與氧化反應(yīng)、脫甲基反應(yīng)以及芳香環(huán)裂解等化學(xué)轉(zhuǎn)化過程,催化多種抗生素(如磺胺類、四環(huán)素類、氟喹諾酮類等)的降解,降低了抗生素在水生生物中的累積及危害。
CYP450的中心有一個(gè)鐵原子,這個(gè)鐵原子能夠與氧分子結(jié)合形成高活性的氧化鐵(FeO3+)中間體,氧化鐵中間體能夠?qū)⒀踉硬迦肟股胤肿又校裳趸a(chǎn)物,改變抗生素分子結(jié)構(gòu),進(jìn)而減少其生物活性[68]。在磺胺類抗生素磺胺甲惡唑的降解過程中,CYP450首先通過氧化反應(yīng)在抗生素氨基或芳香環(huán)結(jié)構(gòu)上插入氧原子,從而形成氨基氧化物或羥基化產(chǎn)物,進(jìn)而改變抗生素結(jié)構(gòu)及其生物活性[69]。
去甲基化是CYP450降解四環(huán)素類抗生素的關(guān)鍵機(jī)制。在這一過程中,其發(fā)生氧化還原反應(yīng),消耗煙酰胺腺嘌呤二核苷酸磷酸(NADPH)提供的電子,進(jìn)而促進(jìn)氧分子活化并導(dǎo)致四環(huán)素中的甲基基團(tuán)被去除,生成去甲基四環(huán)素,后續(xù)經(jīng)進(jìn)一步的氧化反應(yīng),去甲基四環(huán)素分子中的芳香環(huán)被羥基化,產(chǎn)生更多極性較強(qiáng)的代謝產(chǎn)物,這些產(chǎn)物可以通過肝臟代謝或直接排泄被無脊椎動(dòng)物排出[70]。
對(duì)于氟喹諾酮類抗生素,CYP450的降解機(jī)制主要涉及去氟反應(yīng)。環(huán)丙沙星等氟喹諾酮類抗生素會(huì)與CYP450 酶反應(yīng)進(jìn)而導(dǎo)致其分子中的氟原子被去除,具體反應(yīng)過程如下:由FeO3+中間體啟動(dòng),將氧分子插入環(huán)丙沙星的氟原子中,導(dǎo)致氟原子脫去,生成去氟中間體。隨著去氟反應(yīng)的發(fā)生,環(huán)丙沙星的親脂性會(huì)降低,容易被水解和排出生物體外。此外,去氟后的環(huán)丙沙星分子也會(huì)在生物體內(nèi)繼續(xù)發(fā)生芳香環(huán)氧化反應(yīng)和環(huán)裂解反應(yīng),最終生成醛類和羧酸類低毒性小分子產(chǎn)物[71]。CYP450 降解抗生素的過程通常需要其他酶和輔因子的協(xié)同作用,例如輔助因子細(xì)胞色素c作為電子傳遞體,可將NADPH 氧化還原酶產(chǎn)生的電子傳遞給CYP450,這一電子轉(zhuǎn)移對(duì)于氧氣的活化和后續(xù)抗生素的降解至關(guān)重要,如果這些輔因子供應(yīng)不足,CYP450 的降解效率將極大降低[72]。
1.2.3 魚類肝臟對(duì)抗生素的代謝
魚類肝臟功能比無脊椎動(dòng)物更發(fā)達(dá),能夠進(jìn)行與哺乳動(dòng)物相似的抗生素代謝過程。首先,抗生素會(huì)在魚類肝臟發(fā)生葡萄糖醛酸化反應(yīng),使其水溶性增強(qiáng)。隨后發(fā)生的芳香環(huán)羥基化反應(yīng)進(jìn)一步提高了抗生素極性,使其更易被魚類機(jī)體代謝和排出。此外,側(cè)鏈N-去異丙化反應(yīng)可降低抗生素親脂性,減少其在脂肪組織中的積累,從而降低其毒性。
側(cè)鏈葡萄糖醛酸化是一種常見的生物轉(zhuǎn)化反應(yīng),依賴葡萄糖醛酸轉(zhuǎn)移酶催化,葡萄糖醛酸與抗生素側(cè)鏈反應(yīng)生成水溶性增強(qiáng)的葡萄糖醛酸化合物,便于通過腎臟排出,減少體內(nèi)積累[73]。芳香環(huán)羥基化反應(yīng)通常由CYP450酶系統(tǒng)催化,尤其是鯽魚(Carassius au?ratus)肝臟中的CYP1A和CYP3A亞型酶在該反應(yīng)中起關(guān)鍵作用。此過程中抗生素分子結(jié)構(gòu)中的芳香環(huán)被酶氧化,并插入了分子氧形成羥基化產(chǎn)物,這改變了抗生素的分子結(jié)構(gòu),提高了其水溶性[74]。側(cè)鏈N-去異丙化是另一個(gè)關(guān)鍵代謝步驟,抗生素分子中的N-異丙基基團(tuán)在CYP450酶系統(tǒng)催化下發(fā)生氧化還原反應(yīng),生成去異丙基產(chǎn)物,之后被氨基氧化為較小的分子。該過程顯著降低了抗生素的親脂性,使其易于排出[75]。
1.3 持久性有機(jī)污染物在食物鏈中的遷移行為
持久性有機(jī)污染物(POPs)在食物鏈中的遷移行為受其疏水性調(diào)控。辛醇-水分配系數(shù)(lgKow)是衡量化學(xué)物質(zhì)親水性與親油性之間平衡的一個(gè)重要指標(biāo),是判斷持久性有機(jī)污染物疏水或親水程度的關(guān)鍵參數(shù)。這一系數(shù)在許多污染物的生物積累模型中扮演著關(guān)鍵角色,尤其對(duì)于脂溶性污染物,其決定了污染物能否在生物體內(nèi)積累以及可否在食物鏈中傳遞(圖4)。
對(duì)于lg Kow較高的污染物,較強(qiáng)的親脂性使其易在水生生物的脂肪組織中積累[76]。全氟辛烷磺酰基化合物(PFOS)、全氟辛酸(PFOA)和短鏈氯化石蠟(SCCPs)進(jìn)入水體后,與水中有機(jī)物和懸浮固體相互作用,形成聚合物,并被水生生物攝食[77]。進(jìn)入生物體內(nèi)后,疏水性驅(qū)動(dòng)POPs的體內(nèi)分配,高親脂性污染物優(yōu)先在脂肪組織中積累,其濃度通常高于水環(huán)境中[78]。在“藻類-無脊椎動(dòng)物-魚類”食物鏈中,lg Kow值較高的POPs濃度逐級(jí)上升[79];這是由于魚類的脂質(zhì)含量通常遠(yuǎn)大于無脊椎動(dòng)物和藻類,因此POPs在較高營(yíng)養(yǎng)級(jí)的魚類體內(nèi)濃度顯著增加,呈現(xiàn)生物放大效應(yīng)[80]。
1.4 內(nèi)分泌干擾物
內(nèi)分泌干擾物(EDCs)是一類可通過干擾生物體內(nèi)分泌系統(tǒng)影響激素合成、釋放及信號(hào)傳導(dǎo)的化學(xué)物質(zhì),可能引發(fā)生殖、發(fā)育和免疫功能異常。這類物質(zhì)在水生食物鏈中的遷移機(jī)制主要涉及直接水體暴露、食物鏈傳遞以及生物累積過程。
以雙酚A(BPA)為例,其作為食品包裝和瓶罐涂層的常見原料,雖具有較低的lg Kow,在脂肪組織中的蓄積能力較弱,但表現(xiàn)出強(qiáng)蛋白質(zhì)結(jié)合特性,可通過與血清白蛋白、轉(zhuǎn)運(yùn)蛋白等結(jié)合,在高營(yíng)養(yǎng)級(jí)生物體內(nèi)形成穩(wěn)定復(fù)合物,顯著延緩其代謝排出速度,從而在食物鏈中持久存在[60]。
相比之下,四溴雙酚A(TBBPA)及其衍生物四溴雙酚A-二(烯丙基醚)(TBBPA-DAE)等阻燃型EDCs,因具有較高的lg Kow 值,其環(huán)境行為與典型POPs相似[61]。這類物質(zhì)更易在生物體脂肪組織中富集,并通過脂質(zhì)介導(dǎo)的生物放大效應(yīng)沿食物鏈傳遞,導(dǎo)致其在高營(yíng)養(yǎng)級(jí)生物體內(nèi)濃度顯著升高[62]。
2 新污染物在土壤食物鏈中的遷移行為
相較于水環(huán)境,學(xué)者們對(duì)于土壤食物鏈中新污染物的遷移關(guān)注較少,僅涉及較少種類的污染物;在這些研究中,微塑料和抗生素抗性基因(ARGs)較受關(guān)注。
土壤中的納米微塑料可通過植物根系水分吸收過程侵入植物組織,值得注意的是,微塑料的粒徑對(duì)其遷移路徑具有顯著篩選作用:直徑超過100 nm的顆粒因空間位阻被根系細(xì)胞壁攔截;而20~40 nm的納米微塑料則可穿透細(xì)胞膜屏障,甚至通過共質(zhì)體或質(zhì)外體途徑轉(zhuǎn)運(yùn)至莖葉等地上部分。這一過程不僅導(dǎo)致微塑料在植物體內(nèi)的累積,還可能通過干擾細(xì)胞代謝影響作物生長(zhǎng)與品質(zhì)[15]。
土壤中的持久性有機(jī)污染物(POPs)通過植物吸收和土壤動(dòng)物傳遞兩條路徑進(jìn)入食物鏈:在植物系統(tǒng)中,POPs首先通過土壤水相的溶解或吸附于溶解性有機(jī)質(zhì)進(jìn)入根際區(qū)域,而部分POPs能夠穿過通道蛋白或者通過必需營(yíng)養(yǎng)元素的共轉(zhuǎn)運(yùn)系統(tǒng)進(jìn)入植物維管束,隨蒸騰流向上運(yùn)輸至莖葉,其中高脂溶性的POPs 會(huì)優(yōu)先分配至植物表皮蠟質(zhì)層或細(xì)胞膜脂質(zhì)中[81]。蚯蚓等土壤動(dòng)物通過吞食含POPs的土壤顆粒或腐殖質(zhì)直接攝入污染物,POPs通過被動(dòng)擴(kuò)散進(jìn)入脂肪組織,在動(dòng)物體內(nèi)轉(zhuǎn)化為更持久或毒性更強(qiáng)的產(chǎn)物[82]。植物和動(dòng)物的吸收過程共同構(gòu)成陸生食物鏈中POPs的遷移行為。
從表2中可以看出,土壤環(huán)境中的ARGs會(huì)進(jìn)一步在植物及后續(xù)營(yíng)養(yǎng)級(jí)中累積。ARGs從土壤介質(zhì)向食物鏈中的遷移以及其后續(xù)在食物鏈中的傳遞過程主要涉及兩種機(jī)制,一是含有ARGs的抗生素耐藥微生物可以由水分吸收、動(dòng)物攝食、空氣沉降等途徑介導(dǎo)在食物鏈中傳遞,二是這些ARGs可以通過基因水平轉(zhuǎn)移(HGT)方式在食物鏈不同種、不同生境微生物間傳遞(圖5)。
2.1 ARGs從土壤向生產(chǎn)者(蔬菜)中的遷移行為
ARGs 可以隨植物吸收水分的過程從土壤遷移進(jìn)入植物體內(nèi)[83]。蔬菜的根系通過毛細(xì)管作用從土壤中吸收水分,水分會(huì)攜帶著微生物一同進(jìn)入植物體內(nèi)[84]。根際環(huán)境為耐藥菌進(jìn)入蔬菜體內(nèi)提供了通道,根毛表面的吸附作用使這些細(xì)菌能夠通過毛細(xì)管進(jìn)入蔬菜組織。例如,使用含有ARGs的污染水灌溉菠菜,其根部與地上部分均可檢出相應(yīng)類型的ARGs[85]。
2.2 ARGs在蔬菜-昆蟲以及昆蟲-昆蟲環(huán)節(jié)的遷移行為
ARGs通常以質(zhì)粒為載體通過HGT在蔬菜-昆蟲和昆蟲-昆蟲之間遷移。昆蟲在攝食含有ARGs的食物時(shí),ARGs會(huì)隨食物消化被釋放進(jìn)其消化系統(tǒng)中[86]。昆蟲腸道內(nèi)繁多的微生物為HGT提供了有利條件,促進(jìn)了ARGs的傳播過程[87]。植物內(nèi)生菌可通過接合的方式直接將其攜帶的ARGs 轉(zhuǎn)移給昆蟲腸道內(nèi)的其他細(xì)菌種群[88]。不同細(xì)菌對(duì)于ARGs的接納程度不同,因此昆蟲腸道微生物群落組成是影響ARGs遷移的關(guān)鍵因素之一。昆蟲腸道內(nèi)的微生物群體和宿主之間存在著共生關(guān)系[89],當(dāng)高營(yíng)養(yǎng)級(jí)昆蟲捕食低營(yíng)養(yǎng)級(jí)昆蟲后,高營(yíng)養(yǎng)級(jí)昆蟲腸道內(nèi)的細(xì)菌會(huì)接納被捕食昆蟲腸道中攜帶ARGs 的同門細(xì)菌,這些細(xì)菌中的ARGs可進(jìn)一步通過HGT 侵染高營(yíng)養(yǎng)級(jí)昆蟲腸道中的其他微生物,從而導(dǎo)致ARGs豐度增加[90]。
2.3 空氣沉降的媒介作用
空氣顆粒不僅能夠在環(huán)境中長(zhǎng)時(shí)間穩(wěn)定存在,其還可作為載體攜帶和傳播ARGs。據(jù)報(bào)道,養(yǎng)雞場(chǎng)以及奶牛舍等養(yǎng)殖點(diǎn)內(nèi)空氣中ARGs 豐度明顯高于周圍空氣,并且離養(yǎng)殖點(diǎn)越近,ARGs豐度越高[91]。進(jìn)一步研究發(fā)現(xiàn),空氣顆粒,如工業(yè)排放或農(nóng)業(yè)活動(dòng)產(chǎn)生的微細(xì)灰塵顆粒,能夠攜帶ARGs,通過沉降被植物葉片吸附,其攜帶的ARGs 便可通過氣孔進(jìn)入植物體內(nèi)。此外,昆蟲在攝食植物時(shí),也可將這些含有ARGs的空氣顆粒一并攝入[16]。
2.4 ARGs在土壤-蔬菜-昆蟲間的水平基因轉(zhuǎn)移
HGT是ARGs在土壤-蔬菜-昆蟲食物鏈中遷移的重要途徑,ARGs通過不同的HGT機(jī)制(轉(zhuǎn)化、轉(zhuǎn)導(dǎo)和接合)在土壤微生物之間傳播。
轉(zhuǎn)化是指細(xì)菌吸收來自外界環(huán)境的游離DNA片段,并將其整合進(jìn)基因組中的過程。該過程需要細(xì)菌具備接收外源DNA的能力,這一機(jī)制對(duì)ARGs的傳播較為重要,因?yàn)檗D(zhuǎn)化不依賴于細(xì)菌間的直接接觸,這使得ARGs 可以直接從土壤環(huán)境介質(zhì)遷移到細(xì)菌群體中[92]。轉(zhuǎn)導(dǎo)是通過病毒介導(dǎo)的基因轉(zhuǎn)移。在轉(zhuǎn)導(dǎo)過程中,ARGs 存在于噬菌體中,當(dāng)噬菌體侵染細(xì)菌時(shí),ARGs便被轉(zhuǎn)移到新的宿主中[93]。接合則是通過兩個(gè)細(xì)菌之間的接觸使ARGs在兩株菌間傳遞,供體細(xì)菌會(huì)將質(zhì)粒中的ARGs 傳遞給受體細(xì)菌。這種方式是ARGs傳播關(guān)鍵途徑,可以使一個(gè)細(xì)菌種群中的ARGs迅速擴(kuò)展至其他細(xì)菌種群中,尤其在同一生境的不同種類細(xì)菌之間[94]。
3 總結(jié)與展望
近年來,隨著新污染物對(duì)生態(tài)環(huán)境及人類健康的潛在威脅日益顯現(xiàn),其在環(huán)境中的遷移、積累、生物毒性效應(yīng)等受到了學(xué)者廣泛關(guān)注。特別是食物鏈作為環(huán)境污染暴露于生物體與人體的關(guān)鍵媒介,新污染物在其中的遷移行為逐漸被聚焦,相關(guān)研究取得了一些進(jìn)展。
微塑料、抗生素、POPs、ARGs是目前關(guān)注較多的新污染物類型。受藻類對(duì)微塑料的吸附作用、無脊椎動(dòng)物的選擇性進(jìn)食行為以及魚類對(duì)微塑料的積累與排出機(jī)制等復(fù)雜因素的共同作用,微塑料在水生食物鏈“藻類-無脊椎動(dòng)物-魚類”中呈現(xiàn)累積與消減兩種趨勢(shì)。而抗生素在水生食物鏈中的濃度則逐級(jí)降低,這主要是由于不同營(yíng)養(yǎng)層級(jí)生物均可對(duì)抗生素進(jìn)行代謝、轉(zhuǎn)化與降解。與之相反,POPs的疏水性驅(qū)動(dòng)了其在食物鏈中的逐級(jí)富集,呈現(xiàn)顯著的生物放大效應(yīng)。脂溶性低的EDCs借助蛋白質(zhì)結(jié)合在高營(yíng)養(yǎng)級(jí)生物中持久蓄積,而高脂溶性的EDCs能夠通過生物放大效應(yīng)沿食物鏈富集。土壤環(huán)境中,ARGs通過植物水分吸收、動(dòng)物攝食、空氣沉降以及基因水平轉(zhuǎn)移等途徑在食物鏈中傳遞。
盡管目前新污染物在食物鏈中的遷移行為已被關(guān)注,但仍存在一些未被探索的領(lǐng)域。關(guān)于食物鏈中多污染物的同步遷移行為仍需加強(qiáng)研究,特別是微塑料作為吸附載體,已被報(bào)道可與其他新污染物如抗生素、POPs等相互作用,當(dāng)其與其他新污染物共同存在于水土食物鏈時(shí),多種污染的遷移行為是否有別于單一污染仍需更多探索。再者,一些新污染物在食物鏈中遷移的關(guān)鍵驅(qū)動(dòng)機(jī)制還有待更深入的挖掘,比如,ARGs在昆蟲腸道細(xì)菌中的遷移行為以及其利用空氣顆粒作為載體從植物氣孔進(jìn)入植物體內(nèi)的具體機(jī)制尚未完全明確,仍需更多探索。
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