Ua rau lub raum tsis ua haujlwm: Heavy Hlau raug

PART Ⅰ: Lub raum Laus—Raws li cuam tshuam los ntawm Hnyav Hlau raug thiab Selenium Supplementation

Yog xav paub ntxiv:ali.ma@wecistanche.com

Jan Aaseth, Jan Alexander, Urban Alehagen, Alexey Tinkov, Anatoly Skalny, Anders Larsson, Guido Crisponi thiab Valeria Marina Nurchi

1. Taw qhia

Covraumzoo nkaus li yog qhov chaw loj ntawm kev hloov pauv hnub nyoog, ntxiv rau ua lub hom phiaj rau ntau qhov chaw ib puag ncig [1]. Ntev ntev raug raucov hlau hnyavxws li mercury, lead, thiab cadmium tuaj yeem ua rau muaj hnub nyoog txog lub raum tsis zoo, uas nyob rau hauv ib feem tuaj yeem ua rau muaj kev cuam tshuam ntawm kev txuam nrog.cov hlau hnyavhauvlub raumthaum lub sij hawm ua cov zis thawj. Vim lub neej expectancy ntawm tib neeg nyob rau hauv lub ntiaj teb niaj hnub no, nrog rau kev nce qib ntawm ib puag ncig cov pa phem hlau nrog kev tshem tawm ntev ib nrab-lub neej, nws zoo li tias cov neeg laus niaj hnub no tau nce qib ntawm cov tshuaj lom ntau dua li cov tib neeg tau ntau xyoo dhau los. . Tsis tas li ntawd, cov neeg laus coob zuj zus tuaj. Thoob plaws ntiaj teb, ntau dua 10 feem pua ​​​​ntawm cov neeg muaj hnub nyoog tshaj 60 xyoo, thiab qhov feem pua ​​​​yuav tau kwv yees tias yuav nce siab los ntawm 2050 [2]. Kev nkag siab zoo txog qhov cuam tshuam ntawm lub hnub nyoog ntawm ntau lub cev, nrog rau covlub raum, yog qhov tseem ceeb thaum tswj kev saib xyuas kev noj qab haus huv dav dav txij li cov neeg laus ua ib feem tseem ceeb ntawm cov neeg mob kho mob.

Ntau yam kev hloov pauv ntawm lub cev tshwm sim hauv cov lauslub raum, tshwj xeeb tshaj yog tom qab muaj hnub nyoog 70. Txawm hais tias cov neeg laus noj qab haus huv zoo li muaj peev xwm tswj tau lub raum ua haujlwm txawm tias muaj kev hloov pauv ntawm lub cev thiab lub cev, qhov no tau ua tiav ntawm tus nqi ntawm lub raum kev ua haujlwm cia. Txawm li cas los xij, thaum lub luag haujlwm cia poob lawm, lub raum muaj peev xwm txo qis los teb rau cov kev cov nyom sab nraud, suav nrog txo qis peev xwm tshem tawm cov tshuaj lom. Yog li ntawd, cov neeg laus tej zaum yuav raug ntau dua li cov hluas thaum raugtshuaj lomhlaulos ntawm ib puag ncig.

Cov txheej txheem kev laus ua rau muaj kev hloov pauv ntau ntawm cov qib cellular thiab molecular. Ib qho ntawm cov kev hloov pauv no suav nrog txo qis peev xwm kho cov hlwb raug mob [3]. Concomitantly, mob theem reactants xws li, piv txwv li, C-reactive protein (CRP), qog necrosis factor-alpha (TNF-ax), thiab interleukin -6 (IL-6) yog qhia nyob rau theem siab dua [ 4].

Mitochondrial raug mob zoo li yog ib qho tseem ceeb hauv cellular senescence. Cov dawb radical txoj kev xav ntawm kev laus [5] hais tias tiam thiab to ntawm ROS (reactive oxygen hom) los ntawm mitochondrial respiratory saw nce nrog hnub nyoog thiab ua rau intracellular oxidative puas. Deterioration ntawm mitochondrial DNA yuav ua rau kev ua haujlwm ntawm cov kab mob ua pa, uas yog nrog los ntawm kev tsim ROS ntxiv thiab kev raug mob DNA. Cov xwm txheej no tau pom zoo los koom nrog lub voj voog txuas ntxiv ntawm kev tsim tawm radical uas tuaj yeem ua rau muaj kev laus sai [6]. Ntau qhov kev tshawb fawb tau qhia tias kev laus muaj feem cuam tshuam nrog kev poob qis ntawm ntau yam kev tiv thaiv oxidative kev ntxhov siab ntsig txog enzymes xws li superoxide dismutases (SOD1 thiab SOD2), catalase, thiab glutathione peroxidases (GPXs) [7]. Kev txo qis hauv cov dej num ntawm cov enzymes tiv thaiv no yuav ua rau muaj kev nce ntxiv hauv oxidative kev nyuaj siab thiab kev laus ntawm cellular. Kev cuam tshuam rau mercury, cadmium, lossis txhuas, txawm tias nyob rau qib qis, paub tias cuam tshuam rau kev tiv thaiv oxidative enzyme systems [8,9] thiab tej zaum yuav txhawb nqa lub hnub nyoog hloov pauv hauv nruab nrog cev, tshwj xeeb tshaj yog nyob rau hauv lub cev.lub raum[10]. Lub hom phiaj ntawm qhov kev tshuaj xyuas tam sim no yog los tham txog lub raum toxicity ntawm mercury, cadmium, thiab lead compounds hauv cov neeg laus, thiab lub luag haujlwm tiv thaiv ntawm sulfur thiab selenium compounds.

Cov hlau hnyav npaum li cas cuam tshuam rau lub raum

Nyem rau cistanche hmoov cov txiaj ntsig kev noj qab haus huv thiab cov khoom Cistanche

2. Mercury, Cadmium, thiab Lead-Nephrotoxic Environmental Pollutants

Tshuaj lomhlaumuaj ntau nyob rau hauv ib puag ncig, thiab nyob rau theem siab dua hauv qee qhov chaw ua haujlwm, txhais tau hais tias tib neeg raug rau cov nohlauyog inevitable. Kev sib xyaw ua ke ntawm cov neeg laus rau cov kab mob nephrotoxic no tuaj yeem txhawb kev muaj hnub nyoog raws li kev loj hlob ntawm lub raum tsis zoo [11]. Vim lawv txoj haujlwm ua txoj haujlwm tseem ceeb ntawm kev tawm ntawm lub cev,lub raumnyob rau hauv cov neeg laus yog tshwj xeeb tshaj yog yooj yim rauhlau hnyavtoxicity [10], feem ntau rau mercury (Hg), cadmium (Cd), thiab lead (Pb). Raws li mercury, txawm tias me me los ntawm kev siv hauv kev kho hniav, tshuaj tiv thaiv, qhov muag te, thiab hauv cov tshuaj pej xeem cov tshuaj yuav ua rau muaj kev cuam tshuam nephrotoxic, uas tej zaum yuav nyuaj rau kev ntsuam xyuas vim tias feem ntau tshwm sim ntau lub hlis lossis xyoo tom qab raug qis lossis nruab nrab. [12, 13]. Mercury paub tias cuam tshuam rau tib neeg cov txheej txheem biochemical los ntawm kev cuam tshuam nrog cov tshuab redox nyuaj siv los tswj cov cell ciaj sia taus thiab mitochondrial muaj nuj nqi [14]. Cells uas muaj zog oxidative kev nyuaj siab, piv txwv li, vim yog ib tug inflammatory txheej txheem nyob rau hauv ib tug neeg laus, yog presumed yuav muaj ntau rhiab heev rau Hg toxicity tshaj cov hlwb noj qab haus huv nyob rau hauv kev tswj tej yam kev mob. Mercury tshwm sim nyob rau hauv peb lub ntsiab, viz. elemental mercury (Hg), organic mercury (piv txwv li, CH3Hgt, ntawm no qhia MeHg), thiab inorganic mercury (Hg2 ntxiv , Hg), cov ntaub ntawv tom kawg feem ntau tshwm sim raws li ntsev (piv txwv li, HgCl2) [15]. Tag nrho cov ntaub ntawv no muaj kev cuam tshuam raulub raum[16]. Thaum inorganic Hg tebchaw yog cov paub zoo nephrotoxic cov neeg ua haujlwm, raug rau cov ntsiab lus mercury vapor lossis cov organic mercury kuj tseem cuam tshuam rau nephrotoxicity ntxiv rau lawv cov neurotoxicity. Elemental mercury (Hg") yog cov kua hnyav nyob rau hauv chav tsev kub; nws yog volatile heev thiab nyob rau hauv saturation, ntawm 25 degree ib m3 ntawm cov huab cua muaj 20 mg Hg" uas tuaj yeem nqus sai sai thaum nqus tau [17]. Tom qab noj, ib feem ntawm Hg" yog oxidized rau nephrotoxic Hg2 ntxiv rau daim ntawv [18].

Kev tshawb fawb txog kab mob kis tau muab pov thawj ntawm lub raum raug mob tom qab tsis yog mob hnyav nkaus xwb tab sis kuj kis tau mus rau ntau hom mercury [19,20]. Qhov mob hnyav tshaj plaws ntawm nephropathy yog tshwm sim tom qab raug cov ntsev inorganic ntawm Hg2 ntxiv rau [16,21]. Kev sib sau ntawm mercury nyob rau hauv cov tubular cov hlwb tau pom tias muaj kev cuam tshuam tsis zoo rau cov enzymes antioxidative [22]. Yog li, kev raug mercury mus sij hawm ntev tau raug tshaj tawm los txo lub raum qhia cov enzymes koom nrog kev tiv thaiv xws li NADPH-quinone oxidoreductase thiab glutathione S-transferase [23]. Hauv kev sim nrog cov nas noj qab haus huv raug rau HgCl, lub raum theem ntawm SOD, catalase, thiab glutathione (GSH) tau qis dua, qhia txog cov teebmeem oxidative ntawm Hg2 ntxiv [24]. Pom tau tias, ntau qhov kev raug mob ntawm tes raug mob los ntawm kev raug mercury mus sij hawm ntev, txawm tias tsawg dua, zoo ib yam li cov neeg raug ntxias los ntawm kev laus.

Raws li rau cadmium (Cd), muaj kuab paug hnyav nrog cov hlau no yog thawj zaug lees paub los ntawm nws cov pob txha tshwm sim hu ua Itai Itai kab mob hauv Nyiv [25]. Ob peb xyoos tom qab, cov kev tshawb fawb soj ntsuam tau qhia txog qhov teeb meem ntawm Cd ntxiv nrog rau kev puas tsuaj loj thiab kev hloov pauv hauv histological.lub raum, nrog rau lub raum tsis ua haujlwm [25]

Nyob rau hauv daim siab thiab lwm cov ntaub so ntswg, Cd2 ntxiv rau tsim ib tug complex nrog cov uas tsis muaj molecular hnyav protein metallothionein (MT), uas yuav raug thauj mus rau thiab lim los ntawm glomeruli, ua raws li los ntawm reabsorption mus rau lub proximal tubulin. Intracellularly, nyob rau hauv tubular hlwb, MT-complex tso tawm dawb Cd2 ntxiv rau thaum overloading, yog li ua rau lub raum puas, ia. Los ntawm perturbing calcium homeostasis, inducing oxidative kev nyuaj siab, thiab downregulating mitochondrial enzymes [26,27l. Qhov Cd-ntxiv-induced kev puas tsuaj rau proximal tubulin, txheeb xyuas raws li ib tug reabsorptive dysfunction, yog tshwm sim los ntawm cov yam ntxwv proteinuria uas tej zaum yuav muaj xws li albumin, tab sis lwm yam yog dominated los ntawm tsawg molecular yuag proteins uas 2-microglobulin thiab N-acetyl{{ 9}}D-glucosaminidase yog siv los ua cov cim [28]. Kev soj ntsuam kev noj qab haus huv hauv Sweden ntawm cov poj niam hnub nyoog 60 xyoo tau nthuav tawm cov koom haum ntawm cov zis Cd qis (ib puag ncig 0.6ug/L) thiab nce qib N-acetyl- -D-glucosaminidase hauv cov zis, thiab cov teebmeem ntawm GFR [29]. Cov teebmeem ntawm kev raug Cd qis ntawm lub raum tubular muaj nuj nqi kuj tau pom nyob rau hauv kev tshawb fawb tom qab los ntawm Wallin li al. [30]. Kev ua rau muaj kev cuam tshuam ntau ntxiv rau cov neeg mob ntshav qab zib kom tsim cov tubular ua haujlwm tsis zoo thaum raug Cd2 tsawg mus rau nruab nrab tau pom [31]. Kev koom tes ntawm cadmium raug thiab arterial hypertension kuj tau tshaj tawm [32].

Hais txog cov tshuaj lead (Pb), cov pa phem no feem ntau yog nqus tau yooj yim los ntawm cov hnyuv thiab los ntawm lub ntsws thaum raug. Los ntawm kev ncig, Pb2 ntxiv tau muab faib rau hauv cov ntaub so ntswg thiab kab mob sib txawv, suav nrog lub siab thiablub raum, qhov twg nws yuav ua rau oxidative puas hlwb, ia. los ntawm uncoupling txoj hlab pa hauv mitochondria [33]. Cov kev xav sib txawv tau raug xa mus los piav qhia lub raum toxicity ntawm Pb2 ntxiv. Vim muaj qhov sib xws ntawm ionic, Pb2 ntxiv tuaj yeem tswj cov calcium homeostasis. Raws li qhov tshwm sim, Ca2 ntxiv tso tawm los ntawm mitochondria yog txhawb nqa, nrog rau qhov qhib ntawm mitochondrial transitional pores, uas ua rau lub cim ntawm reactive hom thiab oxidative kev nyuaj siab [34]. Ntawm lub raum hlwb, proximal tubulin zoo li tshwj xeeb tshaj yog raug rau Pb2 ntxiv rau kev puas tsuaj, thiab kev tshawb fawb ntawm cov kab lis kev cai ntawm nas proximal tubular hlwb ua raws li qhov kev xav tias Pb2 ntxiv rau nce cytosol Ca2 ntxiv ntawm tus nqi ntawm mitochondrial Ca2 ntxiv [35] . Kev sib kis kab mob sib kis ntawm cov hlau lead raug thiab cov hlab ntsha tawg tau pom [36]. Hauv ib txoj kev tshawb fawb yav tom ntej [37] pom tias kev poob qis hauv lub raum kev ua haujlwm ntawm cov neeg laus thiab cov neeg laus tau tshwm sim los ntawm ob qho tib si ntawm cov khw muag khoom txhuas thiab cov khoom siv lead ua, qhov poob ntawm lub raum ua haujlwm tau tshaj tawm ntawm cov neeg mob ntshav qab zib lossis kub siab ntawm suav nrog. Lwm txoj kev tshawb fawb yav tom ntej ntawm ib pawg neeg uas muaj hnub nyoog ntawm kev suav nrog yuav luag 60 xyoo thiab lub sijhawm rov qab los ntawm 16 xyoo tau qhia tias txawm tias cov hlau lead qis qis tau cuam tshuam nrog lub raum tsis ua haujlwm [38].

Cov hlau hnyav ua rau lub raum ua haujlwm

3. Kev hloov pauv hauv lub raum laus thiab lub luag haujlwm ntawm ib puag ncig cov pa phem

Raws li Denic et al. Lub pathogenesis ntawm glomerulosclerosis yog xav tias yuav koom nrog ntau yam xws li kev hloov pauv hauv cov ntshav khiav thiab nce kev cuam tshuam rau inflammatory cytokines [40]. Qhov tshwm sim ntawm cov lus teb inflammatory hauv cov neeg laus tuaj yeem cuam tshuam txog kev txo qis ntawm sirtuins J41. Cov ntaub ntawv uas twb muaj lawm qhia tau hais tias raug Cd, Hg, thiab Pb tuaj yeem cuam tshuam SIRT1 kev ua haujlwm thiab yog li ua rau cov kev ua haujlwm tsis zoo [42]. Raws li nephrons poob vim kev laus thiab mob, kev hloov pauv hloov pauv tshwm sim hauv cov nephrons ntxiv uas ua rau glomerular hyperfiltration thiab proteinuria [43].

Kev hloov pauv hnub nyoog kuj tshwm sim hauv lub raum tubulin, ia. nrog interstitial o thiab fibrosis [4]. Deposition ntawm collagens, kho los ntawm invading hlwb, yog koom nyob rau hauv pathogenesis ntawm ib tug maj mam tsim fibrosis. Cov qauv kev hloov pauv yog sib piv los ntawm kev hloov pauv hauv tubular muaj nuj nqi, ua rau ia. kom txo tau lub peev xwm los mloog cov zis.

Nws tau kwv yees tias glomerular filtration rate (GFR) txo qis, qhov nruab nrab, kwv yees li 10 feem pua ​​​​ntawm ib xyoo caum ntawm lub neej tom qab muaj hnub nyoog li ntawm 50-60 xyoo [43]. Qhov kev txo qis no tau ua ib feem rau kev txo qis ntawm tag nrho cov haujlwm nephrons [45]. Kev laus kuj tseem cuam tshuam rau lub raum cov ntshav khiav, xav tias muaj kev cuam tshuam txog kev hloov pauv hauv cov zis thiab hloov pauv vascular tsis kam hauv afferent thiab efferent arterioles [46].

Hauv cov neeg mob uas muaj kab mob xws li ntshav qab zib thiab ntshav siab, qhov poob ntawm lub raum ua haujlwm feem ntau yog ntau tshaj li cov neeg uas tsis muaj cov kab mob no [47]. Nws kuj tau pom tseeb tias kev mob raum tsis ua haujlwm, piv txwv li, vim kev tswj tsis tau cov ntshav qab zib mellitus, tshwm sim sai dua hauv cov neeg laus dua piv nrog cov hluas. Ntshav siab, kab mob plawv, ntshav qab zib mellitus, lossis metabolic syndrome nrog insulin tsis kam, uas feem ntau tshwm sim hauv cov neeg laus, suav tias yog qhov tseem ceeb rau kev loj hlob ntawm lub raum tsis ua haujlwm [48]. Hauv Tebchaws Meskas, ib yam li hauv Tebchaws Europe, kwv yees li 65 feem pua ​​​​ntawm cov neeg laus hnub nyoog 60 xyoo tau kuaj pom tias muaj ntshav siab, thiab muaj qhov zoo sib xws rau ntshav qab zib [49]. Yog li, ua ke nrog tsub zuj zuj ntawmcov hlau hnyavthiab lwm yam kev qias neeg ib puag ncig, cov kab mob xws li kub siab thiab ntshav qab zib mellitus tuaj yeem ua rau lub cev muaj hnub nyoog txog kev poob qis hauv lub raum ua haujlwm [10].

Cov hlau hnyavFeem ntau tso rau hauv lub raum tubulin yog li ua rau ntau dua cov concentration ntawmcov hlau hnyavnyob rau hauv tubular hlwb tshaj li nyob rau hauv tas li ntawd ntawm lub cev. Txij li thaumcov hlau hnyavFeem ntau ua rau kev puas tsuaj rau tubular hlwb, ib qho qauv hauv cov hlau hnyav hnyav yog tubular proteinuria. Lub reabsorption thiab concentration ntawm hlau ions nyob rau hauv lub tubular hlwb feem ntau yog ib tug zog-yuav tsum tau txheej txheem, raws li lawv nyob rau hauv feem ntau yog nqa los ntawm amino acid transporters. Feem ntau, cov cim tso zis thaum ntxov rau kev puas tsuaj rau lub raum yog lub raum raug mob molecule (KIM-1)50]. Cov zis 2-microglobulin ( , M) yog siv tsis tu ncua los saib xyuas lub raum thiab xav tias raug mob hauv cov neeg ua haujlwm ua haujlwm raugcov hlau hnyav.

Kev sib xyaw ua ke ntawm ob hom kev nthuav tawm, atherosclerosis, thiabcov hlau hnyav, feem ntau yuav ua rau muaj kev pheej hmoo ntawm kev raug mob. Kev raug mob raum hauv cov tshuaj kho mob feem ntau yog saib xyuas los ntawm cov zis albumin thiab cov zis albumin / creatinine piv, uas feem ntau pom kev raug mob glomerular, txawm tias lawv siv biomarkers rau tubular raug mob yuav muab cov ntaub ntawv tseem ceeb ntxiv.

Txawm hais tias urinary excretion ntawm low-molecular-yuag protein yog ib qho cim ntxov ntawm cadmium-induced lub raum puas, hypercalciuria kuj sawv cev rau ib tug kos npe rau ntawm tubular dysfunction, thiab ua ke nrog kev cuam tshuam ntawm cov vitamin D metabolism tuaj yeem ua rau kev txhim kho pob txha [51] .

Kev cuam tshuam rau inorganic mercury tuaj yeem ua rau hnyav proteinuria nrog hypoproteinemia thiab edema [52]. Niaj hnub no, feem ntau txoj kev ntawm tib neeg raug cov tshuaj mercury yog los ntawm kev noj cov zaub mov, feem ntau ntawm cov ntses kis nrog MeHg. Cov ntses loj loj, xws li swordfish thiab sharks, tej zaum yuav muaj cov MeHg siab thiab sawv cev rau qhov loj ntawm cov mercury raug [53]. Thaum noj, MeHg tau nqus sai sai los ntawm txoj hnyuv, nrog rau qee qhov raug xa mus raulub raum, feem ntau tom qab biotransformation rau daim ntawv inorganic [54].

Tsis ntev los no cov kev tshawb fawb txog kev kis kab mob hauv tib neeg tau qhia tias lub raum lub raum ntawm cov mercury nce ntxiv nrog rau hnub nyoog [55]. Interestingly, kev raug mob rau MeHg tau raug tshaj tawm tias muaj feem cuam tshuam nrog kev loj hlob ntawm hom II ntshav qab zib thiab kub siab [56]. Pom tau tias, raug rau mercury tuaj yeem txhim kho kev mob raum tsis ua haujlwm. Ib txoj kev tshawb fawb ntawm cov neeg nyob ze ntawm lub mine nyob rau sab hnub poob ntawm Tuam Tshoj tau tshaj tawm tias cov tib neeg muaj hnub nyoog tshaj 60 xyoo muaj cov ntshav mercury ntau dua thiab nce cov ntshav creatinine ntau dua piv nrog cov neeg laus hauv tib cheeb tsam [57I. Ua ke, ntau qhov kev tshawb fawb tau pom tias muaj kev cuam tshuam ntev musnephrotoxichlau, xws li mercury, cadmium, thiab txhuas tuaj yeem ua rau lub raum tsis txaus rau cov neeg laus [58,59].

Cistanche tiv thaiv lub raum thiab txhim kho lub raum ua haujlwm

4. Kev sib cuam tshuam ntawm cov hlau hnyav nrog Endogenous Thiols

Hauv cov txheej txheem lom neeg, xws li hauv cov ntshav, mercury ions, thiab qee qhov kuj tseem muaj cadmium thiab cov hlau lead yog khi rau thiol-muaj biomolecules, xws li albumin, MT, glutathione (GSH), thiab cysteine ​​(Cys-SH) [60] ( Daim duab 1). Raws li rau lub raum uptake, kev tshawb fawb tau qhia tias mercuric ions raug coj mus rau hauv cov kab mob sib kis thoob plaws lub luminal ciam teb raws li Cys-S-conjugate [61]. Txij li thaum lub conjugate Cys-S-Hg-S-Cys muaj qhov zoo sib xws nrog cov amino acid cystine (Cys-SS-Cys) (Daim duab 1), nws zoo li tsim nyog tias qhov amino acid-mercuric conjugate siv cov cystine transporter nkag mus rau hauv tubular. hlwb. Ib yam li ntawd, vim yog kev sib tw nrog methionine, Cys-S-conjugates ntawm MeHg kuj tau raug suav tias yog cov substrates rau cov khoom sib txuam amino acid [62]. Nyob rau hauv sib piv, cadmium yog xam tau tias yuav coj mus rau hauv tib lub tubular hlwb raws li complexes uas tsis muaj molecular yuag protein MT, tom qab uas Cd-MT complexes yog pauv mus rau lysosomes thiab degraded [63]. Intracellularly, MT khi ib feem tseem ceeb ntawm mercuric ions nyob rau hauv ib qho complex uas tsis yooj yim thauj tawm ntawm lub hlwb, ua rau intracellular tuav ntawm mercuric ions, ntxiv rau kev tuav ntawm lwm yam hnyav hlau ions [64].

Daim duab 1. Molecular formulas ntawm (a) glutathione, (b) cysteine, thiab (c) cystine

Hnyav hlau ions, tshwj xeeb tshaj yog mercuric ions, kuj muaj ib tug muaj zog affinity rau GSH thiab tej zaum yuav raug khi thiab detoxified los ntawm GSH intracellularly [17]. Physiologically, qhov concentration ntawm GSH nyob rau hauv lub raum tubular hlwb yog hais txog 3 mmol / L, uas ua rau cov peptide no zoo haum rau khi li intracellular hlau ions. Tshaj tawm ntawm cov tsiaj sim mus rau HgC, txo qis rau hauv lub raum theem ntawm intracellular GSH [65], qhia tias GSH yog siv los ua ib qho nyuaj thiab / lossis tiv thaiv tus neeg sawv cev thaum raug. Txawm hais tias kev khi ntawm cov hlau hnyav ions rau intracellular SH-molecules sawv cev rau kev tiv thaiv kev tiv thaiv, tib txoj kev khi kuj tseem tuaj yeem ua rau kev tuav hauv lub cev ntawm lub cev.hlau.

Nyob rau hauv cov kab mob uas tsis tshua muaj tshwm sim, acetylcysteine ​​​​(Daim duab 2) yuav raug siv los ua tus neeg sawv cev tiv thaiv vim nws muaj peev xwm ua kom cov cellular GSH-theem [66], uas thib ob yuav nce cov kev ua haujlwm enzymatic ntawm GPX [67]. Raws li rau chelating thiols 2, 3-dimercaptopropane-1-sulfonic acid (DMPS) thiab 2, 3-dimercaptosuccinic acid (DMSA) (Daim duab 2), cov tshuaj no tau tshwj tseg rau cov mob lom lom [ 68] ib.

Daim duab 2. Cov qauv molecular ntawm (a) DMSA, (b) DMPS thiab (c) acetylcysteine ​​​​.

NYEEM NO PART Ⅱ