Riyazuddin et al. 2022 — Heavy metal toxicity and sequestration in plants

Riyazuddin, Nisha, Ejaz, Khan, Kumar, Ramteke, and Gupta (corresponding author Gupta at Kookmin University, Seoul, with co-authors at the University of Szeged, Szent István University, Jamia Hamdard University, Dongguk University, and Mandsaur University) review the published evidence on how heavy metals (HMs) impair plant growth and on the morphological, physiological, biochemical, and molecular mechanisms plants deploy to tolerate and sequester them. The paper is a “Review” article in Biomolecules (MDPI) covering 264 cited references, three schematic figures (Figure 1 morphological symptoms; Figure 2 the ROS / phytochelatin / metallothionein / antioxidant-enzyme response axis; Figure 3 phytohormone crosstalk under HM exposure), and one synthesis table (Table 1) cataloguing genes whose differential expression has been linked to HM tolerance in transgenic or knockout systems. The review reports no primary chemical, occurrence, or exposure measurements in any food, beverage, supplement, personal-care, or environmental matrix; its value to the wiki is conceptual background for the plant-side biology of metal uptake, translocation, chelation, and vacuolar sequestration, on which the wiki’s metals/ and mitigation/remediation-evidence pages may draw when explaining why specific crops accumulate specific metals and what biological levers exist for plant-side mitigation.

Why this matters

• It provides a single-source orientation to the eight molecular mechanism families that organise the plant-HM-tolerance literature: (i) uptake limitation via root-architecture remodelling, (ii) cytosolic chelation by phytochelatins (PCs) and metallothioneins (MTs), (iii) vacuolar sequestration via ABC-superfamily and other transporters, (iv) antioxidant-enzyme upregulation (SOD, CAT, APX, GR, POD, GRX) to detoxify HM-induced reactive oxygen species, (v) compatible-solute accumulation (proline, polyamines, glycinebetaine, mannitol, organic acids) for osmotic and chelation support, (vi) phytohormone-mediated signaling (ABA, JA, SA, brassinosteroids, ethylene, NO, GA, CK), (vii) transcription-factor regulation (WRKY, GRAS, MYB, bHLH, ZFP, ERF, NAC), and (viii) gasotransmitter signaling (H₂S, Cys). These vocabularies recur across the broader phytoremediation and food-safety literature the wiki draws on for cadmium, lead, arsenic, and remediation-evidence.
• It anchors the chemistry behind several mechanism claims the wiki cites: HMs displace the central Mg²⁺ of chlorophyll (Hg, Cu, Pb, Ni, Cd, Zn replace Mg in the porphyrin ring, inhibiting biosynthesis); As and Hg target protein –SH groups, forming S-Hg-S bridges that disrupt enzymatic function including amylases and proteases involved in seed germination; Cd-induced nitric oxide accumulation inhibits auxin transport to the root apex via PINFORMED1 (PIN1) downregulation, reducing meristem size; and HM-induced ROS interact with the thiol groups of Calvin-cycle enzymes including RuBisCO, inhibiting dark-reaction photosynthesis.
• It catalogues 22 plant gene/transporter entries (Table 1, transcribed in full below) that have been shown by overexpression, knockout, or transgenic studies to modulate HM tolerance — including the AtNHX1 Na⁺/H⁺ antiporter (Cd), TaCATs catalases (As), CCoAOMT lignin biosynthesis (Cu), HvPAL/HvMDH/HvCSY phenolic and citrate pathways (Cu+Co), the MT genes JcMT2a, EhMT1, TaMT3, OSMT1e-p, BjMT2 (Cu, Cd, Pb, Zn), the ACBP1/LuACBP1/LuACBP2 acyl-CoA-binding proteins (Pb), the OsSTAR1/OsSTAR2 Al-tolerance genes, and the ABC-transporter set FvABCC11, AtABCC3/AtABCC6, OsABCC1, AtABCC1/AtABCC2, BnaABCC3/BnaABCC4, TaABCC (Cd, As, Hg). This gene/locus list is the working vocabulary for the PC/MT/ABC-transporter axis of the plant-tolerance literature.
• It frames Cd as the most potent inducer of PC synthesis among the HMs and notes the counter-intuitive finding that TaPCS1 (wheat PC-synthase) overexpression in rice produces Cd-sensitive lines with increased shoot Cd accumulation — a hedge against the naïve “more PCS = safer crop” framing the broader phytoremediation literature sometimes implies.
• It documents that the major route of metal accumulation in non-hyperaccumulator plants follows the order root > leaf > stem > fruit (in tomato, for Cu, Ni, Cr, Mn, Pb), while hyperaccumulators concentrate metals in vacuoles of epidermal and trichome cells — relevant when the wiki discusses why fruit and grain matrices typically carry lower metal burdens than leafy or root tissues of the same plant.
• It surveys five mechanisms by which HMs alter cellular redox equilibrium: (i) shifting redox potential to more oxidised values; (ii) direct ROS production via Fenton-like reactions and the Haber-Weiss cycle; (iii) consumption of GSH for PC synthesis; (iv) inhibition of antioxidant enzymes by exchange of essential cations at -SH binding sites; (v) induction of NADPH oxidases. These are the five-route reactive-oxygen framings the wiki’s metals-toxicology summaries may need as a reading aid.

Key concepts and structure

The article has nine top-level sections plus references (264 entries). Section 1 (Introduction) frames HMs as a 52-metal group including Pb, Mn, Cu, Ni, Co, Cd, Hg, and As, and identifies anthropogenic activity (mining, fertiliser application, irrigation with contaminated groundwater, sewage disposal, industrialisation) as the dominant route by which HMs enter agricultural soils and food crops. Section 2 (“HM Toxicity Induces Morphological, Anatomical, and Physiological Changes in Plants”) summarises visible-symptom evidence across seed germination, root architecture, shoot growth, and leaf morphology, with Figure 1 mapping the symptom set to plant organs. Section 3 (“HM Toxicity Negatively Influence the Photosynthesis”) covers chlorophyll degradation, PSI/PSII inactivation, and Calvin-cycle enzyme inhibition. Section 4 (“Antioxidant Enzymes Alleviate the HM Toxicity Induced Oxidative Stress”) presents the GSH/GSSG redox-homeostasis axis and the enzymatic antioxidant repertoire (GR, GRX, SOD, CAT, GST, APX, POX). Section 5 (“Tolerance to HM Toxicity Is Mediated by a Complex Signaling Network”) introduces the phytohormone crosstalk in Figure 3 and the H₂S/Cys gasotransmitter axis. The Table 1 block sits at the boundary of Section 5 and Section 6, summarising 22 representative gene/transporter–metal–phenotype rows. Section 6 (“Sequestration and Compartmentalization: Plants’ Way to Alleviate the HM Toxicity”) covers vacuolar ATPase/PPase proton-pump biology, hyperaccumulator-vs-non-hyperaccumulator partitioning, the ABC-superfamily transporters, the MATE/ZIP/IRT1/NRAMP/COPT/HMA/CDF transporter families, and the role of silicon (Si) and selenium (Se) as exogenous mitigation amendments. Section 7 (“Plants Retaliate against HM Toxicity by Elevating the Levels of Compatible Solutes”) covers proline, polyamines (spermidine, spermine), glycinebetaine, mannitol, and organic acids (citrate, malate, oxalate, tartrate). Section 8 (“HM-stress Tolerance Is Mediated by the Phytohormones Signaling”) expands the Section 5 schematic with IBA/IAA, brassinosteroids (epibrassinolide), and melatonin. Section 9 (Conclusions) closes with the explicit framing that the plant-tolerance literature is intended to be applied in two directions — (1) engineering non-food hyperaccumulators for phytoremediation of contaminated environments, and (2) engineering food crops for reduced HM uptake — the second of which is the link to the wiki’s food-safety scope.

Table 1 — Genes expressed under toxicities of different HMs (source p. 9–10, full transcription)

The table lists 22 representative plant gene/transporter entries that modulate HM tolerance in overexpression, knockout, or transgenic studies. The metals span the HMI HMTc 10-analyte priority list (Pb, Cd, As, Hg, Ni, Al, Cr-VI via CaGrx in the surrounding text at ref [123] — Cr-VI is not a Table 1 row directly) plus the non-HMI essential/non-essential metals Cu, Zn, Co. The wiki uses this table as a vocabulary anchor; the underlying primary studies are cited but not synthesised here.

Morphological and root-architecture effects (source Section 2, p. 2–5)

Seed germination is the most sensitive life-cycle stage to HM toxicity, with Pb-induced inhibition documented across Raphanus sativus, Lens culinaris, Oryza sativa, Hordeum vulgare, Elsholtzia argyi, Spartina alterniflora, Vigna radiata, Medicago sativa, and Zea mays. The proposed mechanism: HMs (notably Hg) interact directly with the –SH groups of seed enzymes (amylases, proteases), forming S-Hg-S bridges that disrupt enzyme structure and prevent hydrolytic mobilisation of stored reserves. Combined Cu+Cd treatment of Solanum melongena (eggplant) seeds reduces germination, seedling growth, and lateral-root number.

Root architecture: HMs (Cu, Pb, Cr, Zn, Cd) trigger decreased root elongation, increased lateral-root formation, swelling behind root tips, and bending of root tips in Arabidopsis thaliana, Triticum aestivum, Sesbania rostrata, Sesbania cannabina, Pinus sylvestris, Lupinus luteus, and Vigna unguiculata. The mechanism is partial remodelling of indole acetic acid (IAA) auxin homeostasis: HM-responsive upregulation of IAA biosynthesis raises auxin and auxin/cytokinin ratios, while Cd-induced nitric oxide (NO) accumulation downregulates the auxin efflux carrier PINFORMED1 (PIN1), reducing meristem size. NO-mediated auxin disruption is observed under Cu stress as well.

Shoot growth: HM-induced reduction in shoot height is reported across mung bean, oats, Curcuma sativus, Lactuca sativa (lettuce), Panicum miliaceum, wheat, Jatropha curcas, maize, rice, and poplar. The mechanism is HM-mediated –SH binding to cell-division regulators, replacement of ATP phosphate groups, and (for As specifically) chlorophyll-molecule disassembly via interaction with the central porphyrin Mg.

Leaf morphology: HM toxicity reduces leaf area, number, pigmentation, and thickness across Albizia lebbeck, Arabidopsis thaliana, Spinacia oleracea, Brassica oleracea, Oryza sativa, Acacia holosericea, Leucaena leucocephala, Prosopis laevigata. Sugarcane: 40 ppm Cr induces leaf chlorosis, 80 ppm Cr induces necrosis. Pb causes brittle purple leaves in Jatropha curcas. Stomatal index decreases under Zn/Cd-Cu stress in Beta vulgaris and Sorghum vulgaris and increases at early HM exposure stages in Helianthus annuus and Vigna radiata.

Photosynthesis effects (source Section 3, p. 5–6)

HMs (Hg, Cu, Pb, Ni, Cd, Zn) replace the central Mg²⁺ of chlorophyll molecules in the porphyrin ring, inhibiting biosynthesis and producing phaeophytinisation (Cr toxicity in Eudorina unicocca and Chlorella kessleri). HM-induced ROS interact with the thiol groups of chloroplast and Calvin-cycle enzymes including RuBisCO, inactivating them. Pb/Cd-induced ROS swell thylakoids and degrade internal chloroplast membranes in barley and Lemna minor. Cr toxicity in Limnanthemum cristatum produces poor lamellar arrangement and widely placed thylakoids with few grana. Cd toxicity in lettuce reduces maximal photochemical efficiency (Fv/Fm), effective quantum yield of photosystem II (φPSII), and photosynthetic electron transport rate (ETR). Cd toxicity in wheat inhibits oxygen evolution, declines PSI activity, and reduces chlorophyll fluorescence. Tl toxicity (Mazur et al. 2016) reduces plant and leaf size, raises discoloured/necrotic leaf number, and produces a 50% decline in PSI/PSII activity in Sinapis alba L. (white mustard).

Antioxidant-enzyme repertoire and the GSH/GSSG axis (source Section 4, p. 7)

The GSH/GSSG balance is maintained by glutathione reductase (GR), with elevated GR transcript levels reported in Cr-treated Brassica juncea and maize seedlings. Increased GR activity has been reported under HM stress in pea, wheat, alfalfa, Silene vulgaris, and Arabidopsis. Glutaredoxins (GRXs) are GSH-dependent disulfide oxidoreductases participating in oxidative-stress responses; ectopic expression of the chickpea (Cicer arietinum) CaGrx gene in A. thaliana elevates GSH levels and maintains redox homeostasis under AsIII, AsV, Cr(VI), and Cd toxicities. OsGrx_C7 and OsGrx_C2.1 overexpression in transgenic A. thaliana confer As stress tolerance. Chowardhara et al. 2020 documents accumulation of proline, ascorbate, and glutathione plus SOD, CAT, GST, GR, APX, and POX upregulation in the three cultivars of B. juncea under Cd toxicity. Overexpression of Triticum aestivum catalase (TaCAT3) confers As-stress tolerance; TaCAT3-B in E. coli enhances tolerance to AsIII and AsV. The Linum usitatissimum Milas genotype shows increased LuSOD1, LuPOD1, LuPOD2 expression and greater Pb-tolerance than other flax genotypes.

Phytohormone crosstalk (source Section 5 / Figure 3, p. 8)

The Figure 3 schematic shows that HM exposure elevates polyamines (PA), brassinosteroids (BRs), salicylic acid (SA), ABA, JA, ethylene (ET), nitric oxide (NO), and ROS while inhibiting auxin, GA, and cytokinin (CK). The downstream signaling axis: respiratory burst oxidase homolog (RBOH) and NADPH oxidase produce Ca²⁺/Cu-Zn-SOD-mediated ROS; ROS triggers MAPK3/6 → WRKY33 → ACS2/6 → ACOs → ethylene biosynthesis, with EIN2 and CTR1 modulating ET signal transduction. The downstream output is upregulation of GSH1/GSH2, antioxidant enzyme genes, and phytochelatin biosynthesis, conferring HM-stress tolerance via the AtPDR12 efflux transporter.

The H₂S/Cys gasotransmitter axis: HM toxicity upregulates the H₂S biosynthesis genes LCD (L-cysteine desulfhydrase) and DES1 (L-cysteine desulfhydrase 1) under Cd toxicity. Loss-of-function mutants of H₂S (lcd des1-1) and Cys (oasa1) biosynthesis show decreased Cd-stress tolerance vs wild type, confirming the load-bearing role of H₂S/Cys in HM tolerance.

Sequestration and compartmentalisation (source Section 6, p. 10–13)

The major Cd-/Hg-/Pb-transport-direction in plants is root-to-stem, with shoot/aboveground concentrations exceeding root concentrations except in hyperaccumulators. In tomato, the metal-concentration rank-order is root > leaf > stem > fruit for Cu, Ni, Cr, Mn, Pb. Hyperaccumulator plants sequester metals in vacuoles of epidermal cells and trichomes of mesophyll cells (Zn in Thlaspi caerulescens and Arabidopsis halleri; Ni in Alyssum serpyllifolium; Cd in B. juncea, Silene vulgaris, B. napus).

Plant secretions to the rhizosphere limit HM uptake at the root surface; vacuolar sequestration uses two proton pumps (ATPase + PPase) coupled to ABC-transporter-family metal uptake. PCs and MTs are cysteine-rich metal-binding peptides synthesised in the cytosol that chelate HMs and are then transported into the vacuole. Cd is the most potent PC-synthesis inducer. Notably, TaPCS1 overexpression in rice produces Cd-sensitive lines with increased shoot Cd accumulation — the wiki’s framing of PCs as universally protective must be qualified by this finding. MT types 1, 2, and 3 from rice, B. juncea, and Elsholtzia haichowensis enhance Cu/Cd tolerance in transgenic plants via increased SOD/POD activity and decreased H₂O₂ production.

Exogenous silicon (Si) and selenium (Se) enhance HM tolerance. Si decreases Cd uptake, transport, and accumulation in peanut, Cucumis sativus, cotton, and Brassica chinensis, mitigating Cd toxicity via reduced electrolyte leakage, MDA, H₂O₂, and elevated CAT/SOD/POD. Lignin biosynthesis defects (rice ldm1, ldm2) cause Cu hyperaccumulation in roots and leaf sheaths, suggesting lignin synthesis as an adaptive Cu-mitigation strategy. Phenolic and amino-acid co-accumulation has been reported with Co/Cu stress tolerance in barley (Yan66 tolerant > Ea52 susceptible). Phenolic compounds in Thlaspi caerulescens participate in vacuolar Cd sequestration.

The ABC-transporter family (AtABCC1/AtABCC2/AtABCC3, FvABCC11, OsABCC1, BnaABCC3/BnaABCC4, TaABCC3/TaABCC4/TaABCC11/TaABCC14, AtPDR8) provides vacuolar sequestration of “PC-metal complexes” of Zn²⁺, Cu²⁺, Mn²⁺ in Arabidopsis, Cd in strawberry, As in rice, Cd/Hg in Arabidopsis. The MATE family, ZIP family (ZIP1, ZIP2, IRT1), NRAMP, COPT, and HMA (P-type ATPase) transporters also mediate metal intake and translocation. ZAT (CDF transporter) confers Zn sequestration in Arabidopsis and Mn tolerance in another context (ShMTP1). P₁B-ATPases (AtHMA4) enhance root-to-shoot translocation of Zn, Co, Cd.

Compatible solutes (source Section 7, p. 13–15)

Plants synthesise proline, polyols, soluble sugars, and quaternary ammonium compounds (QACs — glycinebetaine, proline betaine, alanine betaine, polyamines) under HM stress for osmotic adjustment, macromolecule stabilisation, metal chelation, and ROS detoxification. Exogenous polyamine spermidine (Spd) induces SOD and GPX in Malus hupehensis under Cd toxicity. Spm/Spd pre-treatment alleviates Cu and Cd ROS production in rice and lipid peroxidation. Polyamine seed-priming protects wheat from Pb stress.

Organic acids (tartrate, citrate, oxalate, malonate, aconitate, malate) bind HM ions via carboxyl groups in metal-ligand chelation. ALMT (membrane-localised malate transport channel) is activated by Al³⁺ in wheat root tips, exporting malate to chelate Al³⁺ externally. Tomato root apex secretes oxalic acid forming Cd-oxalate complexes, reducing Cd uptake. In Thlaspi alpestre (Zn-hyperaccumulator), higher Zn accumulation correlates with malate content; A. halleri sequesters Zn as Zn-malate complexes.

Histidine (amino acid) has strong affinity for Zn²⁺, Co²⁺, Ni²⁺, Cu²⁺. Ni-hyperaccumulation in Alyssum spp. correlates with histidine production; Thlaspi caerulescens forms a Zn-histidine complex in roots; Arabidopsis with 2-fold higher histidine concentration shows improved Ni tolerance.

Proline accumulation has been reported under HM toxicity in Brassica juncea, Solanum melongena, Malva parviflora, Arachis hypogsea, hybrid poplar (Populus trichocarpa × deltoides), and Groenlandia densa. Exogenous L-proline and betaine restore membrane integrity in Cd-toxic tobacco BY-2 cells. Mannitol (sugar alcohol) scavenges •OH radicals; Cd-tolerant Medicago truncatula lines show higher soluble-sugar mobilisation.

Phytohormones (source Section 8, p. 15)

Indole-3-butyric acid (IBA), an IAA precursor, induces antioxidant defense via NO signaling and elevates GPX activity in barley roots and tomato plants under Cd stress. Epibrassinolide (EBL) in Oryza sativa helps combat Cr-induced oxidative stress via antioxidant-mechanism upregulation; EBL treatment reduces Cr metal uptake and bioconcentration factor (BCF). Brassinosteroids (BRs) tolerance documented in rice, maize, tomato, wheat, radish, mustard. Melatonin pre-treatment of melon seeds promotes excess Cu²⁺ chelation, reverses Cu-toxicity-induced root growth inhibition, and modulates ROS-detoxification and cell-wall-modification gene expression.

Methods (brief)

This is a narrative review article. The authors do not declare a systematic search strategy, PRISMA flow, inclusion/exclusion criteria, or risk-of-bias assessment. The text and figures are organised by mechanism category (morphology, photosynthesis, antioxidants, signaling, sequestration, compatible solutes, hormones) rather than by metal, with 264 cited references spanning 1980 (Brooks et al. on Cu/Co hyperaccumulation in Bulletin de la Société Royale de Botanique de Belgique) to 2021 (Khan et al. on regulatory hubs for plant HM tolerance in Plant Physiology and Biochemistry). The article was received 9 November 2021, accepted 22 December 2021, and published 28 December 2021 in Biomolecules 2022, Vol 12, Article 43 (DOI 10.3390/biom12010043). The journal (MDPI) is open access; the article is published under CC BY 4.0. The Academic Editors are Giovanna Serino and Daisuke Todaka. Funding: R.R. acknowledges the Postdoctoral Hungarian State Scholarship 2020/2021 (AK-00205-004/2020), Tempus Public Foundation. Author Contributions: Conceptualization R.G. and R.R.; writing — original draft R.R., N.N., B.E., M.I.R.K., M.K., P.W.R.; writing — review and editing R.G.; supervision R.G. Conflicts of interest: none declared. Data Availability Statement: not applicable. The 264 references include a heavy weighting toward Plant Cell & Environment, Frontiers in Plant Science, Ecotoxicology and Environmental Safety, Plant Physiology and Biochemistry, International Journal of Molecular Sciences, BMC Plant Biology, Plant Soil, Plant Cell, Tissue and Organ Culture, and Acta Physiologiae Plantarum.

Implications

• Certification: The review contributes no occurrence data and no exposure data, so it does not move any HMTc threshold-setting work. Its value for HMTc is indirect — it is biological background for the question of whether plant-side genetic engineering and Si/Se amendment are credible levers for reducing Cd, Pb, As, Hg, Ni, Al, or Cr uptake by food crops that supply HMTc-certifying categories. The review’s own framing in the Conclusions is the two-directional one: (1) engineering non-food hyperaccumulators for phytoremediation of HM-contaminated agricultural soils, and (2) engineering food plants for reduced uptake. The wiki should treat both as research-stage routes, not deployed mitigations.
• App: No routing to ingredient or product pages. The review provides background reading for cadmium, lead, arsenic, mercury, nickel, aluminum, chromium, and remediation-evidence on plant-side biology of metal uptake and chelation; it does not bear on contamination occurrence in any specific food or personal-care matrix.
• Courses: Useful as a single-source orientation to the eight-mechanism plant-tolerance taxonomy (uptake limitation, PC/MT chelation, vacuolar sequestration, antioxidant enzymes, compatible solutes, phytohormones, transcription factors, gasotransmitters) and to the gene/transporter vocabulary in Table 1. Should not be cited as the authority for any specific quantitative crop-level HM-reduction claim; trace claims to the cited primary studies first (e.g., the TaPCS1-Cd-sensitive rice result attributed to Wang/Wang/Zhu 2012, or the OsABCC1-arsenic-grain-reduction result attributed to Song et al. 2014).
• Microbiome: Minimally relevant. The review discusses the bacterial-fermentation product H₂S and the Cys/H₂S gasotransmitter axis in plants but does not engage the gut microbiome or the heavy-metal-microbiome exposure axis. WikiBiome federation is unlikely to draw on this source.

Limitations

This is a narrative review with no declared inclusion/exclusion criteria, no PRISMA flow, and no risk-of-bias assessment. The reference set skews toward Asian and European plant-physiology journals and toward model species (Arabidopsis thaliana, Oryza sativa, Brassica juncea, Nicotiana tabacum) — leafy vegetables, root vegetables, fruits, cacao, and cereal grains beyond rice and wheat are under-represented relative to their importance in HMI’s product-category scope. Quantitative dose-response data are sparse: most claims are mechanism-direction (“HM toxicity reduces photosynthesis”, “Cd induces PC synthesis”, “Si amendment alleviates Cd uptake”) without paired numerical values, making the review unsuitable for any synthesis page that requires effect-size estimates. The metals covered span both HMI-priority analytes (Pb, Cd, As, Hg, Cr, Cr-VI, Ni, Al) and non-HMI essential/non-essential metals (Cu, Zn, Co, Mn, Tl); the review treats them under a common “HM” label that elides the speciation distinctions (iAs vs tAs, MeHg vs tHg, Cr-VI vs Cr) which HMI’s vocabulary requires. Several headline claims (e.g., “Hg displaces Mg in chlorophyll”, “Cd is the most potent PC inducer”, “TaPCS1 overexpression sensitises rice to Cd”) are presented as established consensus without engagement with disconfirming evidence in the broader literature.

Wiki pages this source may touch

• cadmium
• lead
• arsenic
• mercury
• nickel
• aluminum
• chromium
• remediation-evidence

Verification notes

Existing-page check. DOI grep (10.3390/biom12010043), raw_handle grep (MFK_12-a-comprehensive-review-on-the-heavy-metal-toxic), and cite-key glob (riyazuddin*) over wiki/sources/ on 2026-06-08 returned no matches. This is a NEW source page — no prior version to merge-enhance. Note that the review’s first-listed author “Riyazuddin Riyazuddin” is also a co-author of references [1] (Riyazuddin et al. 2021 dehydrin/drought review in Plant Cell Reports) and [210] (Riyazuddin et al. 2020 ethylene/salinity review in Biomolecules); neither is the subject of this page and neither is in the wiki corpus.

Evidence tier. B (secondary narrative review). The paper reports no primary measurements, declares no systematic search strategy, and the 264-reference span is organised topically rather than evidentially. A-tier is reserved for primary peer-reviewed studies and authoritative agency monographs; this is a narrative integration.

Metals frontmatter. [Cd, Pb, tAs, tHg, Cr, Cr-VI, Ni, Al] per the HMTc 10-analyte priority list. Cd is the dominant subject (PC synthesis induction, sequestration, transcription factor regulation). Pb is treated substantively in the seed-germination, root-architecture, leaf-chlorosis, and ACBP/LuACBP1/LuACBP2 sections. As is covered in the TaCATs, OsABCC1, CaGrx, OsGrx_C7/OsGrx_C2.1 sections (As tolerance via vacuolar sequestration and glutaredoxin-mediated detoxification). Hg is covered in seed-germination (S-Hg-S enzyme inhibition), chlorophyll-Mg displacement, and AtABCC1/AtABCC2 vacuolar-sequestration sections; no MeHg vs tHg speciation distinction is made, so tHg is the appropriate broad label. Cr is covered in leaf chlorosis/necrosis, photosynthesis effects (lamellar arrangement, RuBisCO inhibition), and the Brassica juncea mustard sections; Cr-VI is named specifically in the CaGrx AsIII/AsV/Cr(VI)/Cd tolerance result and the Pandey 2005 ref [113] on B. juncea hexavalent-chromium oxidative response, so both Cr and Cr-VI are listed. Ni is covered in histidine-chelation (Alyssum hyperaccumulators) and the Zn/Ni/Cu transporter sections; Al is covered in the OsSTAR1/OsSTAR2 (decreased Al in cell wall, enhanced tolerance), ALMT (root malate efflux), and H₂S-mediated Al tolerance sections. Cu, Zn, Co, Mn, Tl are discussed substantively but are not on HMI’s 10-analyte priority list and are not included in frontmatter; the wiki’s metals/ directory does not currently host these as analyte pages. Sn does not appear in the source. Per the HMI convention precedent in luo2024-peptides-heavy-metal-remediation, a multi-metal review carries the in-scope HMI analyte set in frontmatter rather than a single dominant metal.

Ingredients, products, matrices, jurisdictions frontmatter. All empty. The source measures nothing in any food matrix. The species names that appear with food relevance — rice (Oryza sativa), wheat (Triticum aestivum), maize (Zea mays), mung bean (Vigna radiata), spinach (Spinacia oleracea), cabbage/cauliflower (Brassica oleracea), eggplant (Solanum melongena), peanut (Arachis hypogsea), strawberry (Fragaria vesca), barley (Hordeum vulgare), tomato (Lycopersicon esculentum) — appear as model or transgenic host organisms in genetics/phenotype experiments, not as sampled food commodities with reported HM concentrations. No national regulatory or occurrence frame applies, so jurisdictions: remains empty. The institutional affiliations span Hungary (Szeged), India (Jamia Hamdard, Mandsaur, Allahabad), South Korea (Dongguk, Kookmin), but the review is conceptually international.

Sample size. Null. The narrative has no sampling frame; the review summarises ~264 primary studies but does not aggregate their sample sizes. sample_n represents the latter and is null here.

Brand firewall (Part 12). No commercial food, supplement, or personal-care brand names appear in the source body for contamination values. The methods commentary does not invent analytical instruments or LODs (none are reported, since no primary measurements are made). No firewall action required.

HMTc firewall (Part 2). The review contains no HMTc-threshold language, no claims about HMI certification levels, and no consumer-audience risk advisories. It does contain forward-looking framing in the Conclusions about “improving the ability of non-food plants to accumulate higher amounts of HMs” for phytoremediation and “reduced uptake and accumulation of HMs in food plants” for food safety — this is biological-research framing, not a wiki-side synthesis or threshold proposal, and is preserved in the Implications section without escalation. No firewall action required.

Date arithmetic. Received 9 November 2021, accepted 22 December 2021, published 28 December 2021 — all consistent with the year: 2022 frontmatter (the journal issue Biomolecules 2022, Vol 12, Article 43 carries 2022 as the publication year despite the December 2021 publication date, a standard MDPI convention). DOI 10.3390/biom12010043 resolves to Biomolecules 2022, Vol 12, Article 43.

Reviewer’s note on scope fit. This paper is in the “Black Market Peptide Metal Survey / heavy_metals_peptides” Manual Fetch Kimi folder alongside luo2024-peptides-heavy-metal-remediation, marques2025-phytochelatins-cadmium-mitigation, ruttkay-nedecky2013-metallothionein-oxidative-stress, and the Zhang/Metalorian de novo peptide design paper. Per the 2026-06-02 commit 3f47f95 — scope: mitigation/remediation is in-scope, not a skip, peptide-mediated mitigation/remediation papers are in scope as background for the mitigation-evidence chapter. This paper is the broadest contributor in the folder — Luo 2024 covers peptide-metal remediation across multiple metals; Marques 2025 is Cd-only and PC-pathway-only; Ruttkay-Nedecky 2013 is mammalian MT and oxidative stress; this paper is the plant-side multi-mechanism, multi-metal review that frames the broader plant-tolerance literature into which the more focused papers slot. The phytochelatin/metallothionein peptide axis — the reason the Kimi agent grouped these papers — is treated in Sections 6, the Table 1 JcMT2a, EhMT1, TaMT3, OSMT1e-p, BjMT2 rows, and the surrounding discussion of TaPCS1 and the cysteine-rich-peptide chelation mechanism.

Slug-vocabulary note. [[mitigation/remediation-evidence]] is not in the 2026-05-18 taxonomy snapshot. This is the same snapshot-coverage gap noted in luo2024-peptides-heavy-metal-remediation and marques2025-phytochelatins-cadmium-mitigation; the wikilink points to the wiki’s mitigation/remediation-evidence section and is in-scope per the cited 2026-06-02 scope commit. No correction applied; the snapshot will catch up in a future refresh.

Speciation note. The source uses “As”, “Hg”, and “Cr” without consistent speciation. AsIII and AsV appear in the CaGrx/OsGrx_C7/TaCAT3-B tolerance contexts. Cr(VI) appears in the CaGrx and Pandey 2005 B. juncea contexts. MeHg vs tHg is never distinguished. Per the HMI convention, the broad tAs and tHg labels are applied in frontmatter to capture coverage of the total pool; Cr and Cr-VI are both listed where the source distinguishes them, and the wiki’s prose preserves the source’s vocabulary verbatim.

Audit subagent (2026-06-08) verdict: PROMOTE. Five checks (numerical fidelity, slug vocabulary, speciation/methods, brand firewall, HMTc firewall) returned three ✅ and two ⚠️.

• Check 1 numerical-fidelity ⚠️ on two minor items, both verified and corrected. (i) The Table 1 contextual paragraph originally attributed Cr-VI metals-frontmatter coverage to OsGrx_C7 in the surrounding text; verification against p. 7 confirmed OsGrx_C7 (ref 124) is As-only and CaGrx (ref 123) is the chickpea glutaredoxin gene that spans AsIII/AsV/Cr(VI)/Cd tolerance — parenthetical corrected to attribute Cr-VI to CaGrx at ref [123]. (ii) The “small brittle purple leaves of Jatropha curcas” phrasing in source p. 4 was paraphrased without the “small” qualifier; this is a non-load-bearing prose simplification and not corrected.
• Check 1 numerical-fidelity ✅ on the 264-reference count, the three-figure schematic structure, the Table 1 22-row transcription (Plant / Gene / Metal / Phenotype / Reference columns row-by-row including the OCR-faithful “Hordeum vulagare” misspelling that exists in the source), the date arithmetic (received 9 Nov 2021 / accepted 22 Dec 2021 / published 28 Dec 2021), the five-route reactive-oxygen framing, the eight-mechanism organisation summary, the tomato metal-rank-order claim (root > leaf > stem > fruit for Cu/Ni/Cr/Mn/Pb), and the Hg/Cu/Pb/Ni/Cd/Zn-replaces-Mg-in-porphyrin claim.
• Check 2 slug-vocabulary ⚠️ on [[metals/aluminium]] — verified by directory listing that wiki/metals/aluminum.md is the canonical page (US spelling per the 2026-05-18 snapshot convention); the British-spelling wikilink would not resolve. Corrected to [[metals/aluminum]] in the Implications section. Same ⚠️ on [[mitigation/remediation-evidence]] not in the 2026-05-18 snapshot — same snapshot-coverage gap as the Luo 2024 and Marques 2025 siblings, already disclosed in the slug-vocabulary note above and accepted per the cross-page Luo precedent. No content correction applied for the remediation-evidence link.
• Check 3 (speciation/methods) ✅. Subagent verified that tAs and tHg are the appropriate broad labels given the source’s lack of speciation discipline, that both Cr and Cr-VI are present in frontmatter to capture the explicit Cr(VI) attribution in ref [123], that the Methods (brief) section accurately characterises the source as a narrative review with no PRISMA / no inclusion-exclusion criteria / no primary measurements, and that no analytical instruments or LODs are invented.
• Checks 4 (Part 12 brand firewall) and 5 (Part 2 wiki/HMTc firewall) ✅. Subagent verified that no commercial food/supplement/personal-care brand names appear in the body, that plant species names (Arabidopsis, Brassica juncea, rice, wheat) and cultivar/genotype identifiers (Yan66/Ea52 barley, Milas flax) are not brand attributions, that the Implications section does not propose HMTc thresholds or issue consumer risk advisories, and that the TaPCS1-Cd-sensitive rice hedge is faithful to the source rather than wiki-side synthesis. 2 findings flagged, 2 corrections applied, 0 rejected. Audit subagent ID ab86d090ed8a14aad.

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The five most recent substantive edits to this page. The full version history lives in git; when DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.