Borgmann Aquaponics Hydroponics
Hydroponics · Nutrient Chemistry · Article 1 of 2
Nutrient Interactions in Hydroponics
Antagonism, synergism and molecular mechanisms – based on primary literature (Mulder 1953; Marschner 2012; Mengel & Kirkby 2001).
Nutrient interactions occur at three levels that must be clearly distinguished:
- Transporter competition – Ions with similar ionic radii or the same charge compete for the same membrane transporters in the root plasma membrane (Marschner 2012, Ch. 2).
- Apoplastic precipitation / complexation – Two ions react in the nutrient solution or in the apoplast to form sparingly soluble compounds before they can be taken up (e.g. Fe³⁺ + PO₄³⁻ → FePO₄).
- Rhizosphere pH shift – The uptake of a cation/anion alters the pH of the rhizosphere, which secondarily affects the availability of other elements. NH₄⁺ uptake lowers pH (H⁺ extrusion), NO₃⁻ uptake raises it (OH⁻/HCO₃⁻ release) (Mengel & Kirkby 2001).
Note on reading this table: "Antagonism" means: an excess of nutrient A inhibits the uptake of B. "Synergism" means: an optimal supply of A improves the uptake of B, usually as an indirect consequence of the pH or transporter effect mentioned. The mechanisms are assigned directly to the columns.
Interactions – Table with Mechanisms
| Cause | Antagonism inhibits uptake of | Synergism promotes uptake of | Molecular / Chemical Mechanism |
|---|---|---|---|
| Nitrogen Species | |||
| NH₄⁺ Ammonium |
Ca²⁺ Mg²⁺ K⁺ | H₂PO₄⁻ SO₄²⁻ | NH₄⁺ and K⁺ share the same high-affinity transporters of the HAK/KUP family (Km 0.02–0.05 mM for K⁺ vs. ∼0.3 mM for NH₄⁺); at NH₄⁺ excess, K⁺ uptake is competitively inhibited. Ca²⁺ and Mg²⁺ are displaced by H⁺ extrusion (rhizosphere pH reduction) (Marschner 2012). The NH₄⁺-induced rhizosphere acidification simultaneously improves the solubility of H₂PO₄⁻ and SO₄²⁻ → synergism via pH effect, not via transporters. |
| NO₃⁻ Nitrate |
H₂PO₄⁻ Cl⁻ | Ca²⁺ Mg²⁺ K⁺ Mn²⁺ | NO₃⁻ and H₂PO₄⁻ compete at anion channels of the plasma membrane (NRT/PHT family, Epstein & Bloom 2005). NO₃⁻ uptake causes OH⁻/HCO₃⁻ release → rhizosphere pH rises → improved Ca²⁺, Mg²⁺ and K⁺ availability through improved membrane charge balance (The membrane charge balance describes the state in which the chemical driving force (concentration gradient) and the electrical driving force (potential difference) for an ion are in equilibrium, so that no net ion transport occurs.) (Mengel & Kirkby 2001). Cl⁻ inhibits NO₃⁻ uptake reciprocally (NRT1.1 is Cl⁻-sensitive). |
| Macronutrients – Cations | |||
| Ca²⁺ Calcium |
Mg²⁺ Fe²⁺ Mn²⁺ B | – | Ca²⁺ (ionic radius 1.00 Å) and Mg²⁺ (0.72 Å) compete despite their different radii at the same low-affinity channels (NSCC, non-selective cation channels) as well as at apoplastic exchange sites in the cell wall (Marschner 2012). Ca²⁺ excess increases the apoplastic Ca/Mg ratio, which kinetically disadvantages Mg²⁺ uptake. Fe²⁺ and Mn²⁺ are displaced by Ca²⁺ at IRT1-related transporters. Boron inhibition arises indirectly: Ca²⁺ stabilises the boron-pectin matrix of the cell wall (RG-II–B–ester), which reduces symplastic boron mobility. |
| K⁺ Potassium |
Ca²⁺ Mg²⁺ NH₄⁺ | NO₃⁻ | High K⁺ activity in solution inhibits Ca²⁺ and Mg²⁺ uptake at NSCC channels (charge competition for the electrochemical potential of the membrane). K⁺/NH₄⁺ antagonism: reciprocal to NH₄⁺ entry (see above), as both ions bind to the same HAK/KUP transporter (Mengel & Kirkby 2001). K⁺ is preferentially taken up as a counter-ion for anion transport under NO₃⁻-dominant supply (electrical neutrality, Viets effect). |
| Mg²⁺ Magnesium |
Ca²⁺ K⁺ NH₄⁺ | H₂PO₄⁻ | Mg²⁺ uptake occurs via MGT/MRS2 transporters (Marschner 2012). Ca²⁺ and K⁺ competitively inhibit by occupying the binding site. Mg²⁺ synergises with phosphate because Mg²⁺ is an essential intracellular co-factor for all phosphate-transferring enzymes (ATP-Mg complex); Mg deficiency thus reduces the efficiency of P assimilation, not uptake per se. |
| Macronutrients – Anions | |||
| H₂PO₄⁻ Phosphate |
Fe²⁺/³⁺ Zn²⁺ Cu²⁺ B | Zn²⁺ (only at optimal P; excess reverses the effect) | Primarily apoplastic precipitation: Fe³⁺ + PO₄³⁻ → FePO₄ (Ksp ≈ 10⁻²²); this precipitate forms even in the nutrient solution at an unbalanced Fe/P ratio (Epstein & Bloom 2005). Zn²⁺ is precipitated as Zn₃(PO₄)₂ at P excess (Marschner 2012). Secondarily: P excess suppresses FRO2 ferric reductase activity, which reduces Fe³⁺ → Fe²⁺ (Strategy I plants). At optimal P, Zn uptake is improved because PHT1 transporters also take up Zn under P-deficiency responses (dual-substrate kinetics). |
| SO₄²⁻ Sulphate |
MoO₄²⁻ | Ca²⁺ | SO₄²⁻ and MoO₄²⁻ are both tetrahedral dianions with similar geometry; they compete at sulphate transporters of the SULTR family (SULTR1;2 has demonstrated affinity for MoO₄²⁻, Km values comparable, Marschner 2012). At SO₄²⁻ excess, Mo is practically completely displaced – relevant at pH > 6.0, where Mo availability already increases. Ca²⁺ synergism: SO₄²⁻ only precipitates as CaSO₄ above > 2 g/L (solubility 2.1 g/L at 20°C); below that it improves membrane stability. |
| Micronutrients | |||
| Mn²⁺ Manganese |
Fe²⁺ Zn²⁺ Mg²⁺ B | NO₃⁻ | Mn²⁺ is a primary substrate of IRT1 (Iron-Regulated Transporter 1), which is normally responsible for Fe²⁺ uptake; under Fe deficiency, IRT1 is upregulated, allowing Mn²⁺ accumulation to toxic levels (Marschner 2012). Mn²⁺ reciprocally inhibits Fe²⁺ at IRT1. Zn²⁺ and Mg²⁺ are displaced at overlapping ZIP transporter substrates. B is indirectly inhibited because excess Mn²⁺ triggers oxidative stress that destabilises boron-pectin complexes. |
| Fe²⁺/³⁺ Iron |
Mn²⁺ Zn²⁺ Cu²⁺ | – | Fe²⁺ (after reduction by FRO2) is taken up via IRT1; IRT1 demonstrably also transports Mn²⁺, Zn²⁺, Co²⁺ and Cd²⁺ (Vert et al. 2002, Plant J. 31, primary source). Fe excess competes with these ions at IRT1. Under Fe deficiency, IRT1 and FRO2 are upregulated, favouring Mn²⁺/Zn²⁺ uptake. |
| Zn²⁺ Zinc |
Fe²⁺ Mn²⁺ H₂PO₄⁻ | – | Zn²⁺ reciprocally inhibits Fe and Mn uptake at IRT1/ZIP transporters (see Fe and Mn above). P/Zn antagonism is bidirectional: phosphate excess precipitates Zn²⁺ and suppresses IRT1 expression; Zn excess inhibits PHT1-mediated phosphate uptake (Cakmak & Marschner 1987, J. Plant Physiol.). |
| Cu²⁺ Copper |
Fe²⁺ Zn²⁺ Mn²⁺ | – | Cu²⁺ is taken up via COPT transporters and the ZIP family; at Cu excess, the same transporters for Fe²⁺, Zn²⁺ and Mn²⁺ are blocked. Cu is also a potent inhibitor of FRO2 ferric reductase under oversupply (Mengel & Kirkby 2001). |
| Cl⁻ Chloride |
NO₃⁻ H₂PO₄⁻ | Ca²⁺ | Cl⁻ competitively inhibits NO₃⁻ uptake via NRT1.1 (CHL1); Km ratios documented in Xu et al. (1992, Plant Physiol. 99). H₂PO₄⁻ inhibition is analogous at anion channels. Ca²⁺ synergism: Cl⁻ improves turgor regulation in root cells as an osmolyte, indirectly promoting Ca²⁺ mass flow (transpiration). |
| Na⁺ Sodium |
Ca²⁺ K⁺ Mg²⁺ | – | Na⁺ displaces K⁺ at HKT transporters (High-affinity K⁺ Transporter); at high Na⁺ (elevated EC value), K⁺ uptake is completely suppressed (Rus et al. 2004). Ca²⁺ inhibition: Na⁺ destabilises Ca²⁺ binding sites in the cell wall pectin matrix, reversing the Viets effect and blocking Ca²⁺ uptake (Mengel & Kirkby 2001). This is the primary cause of Ca deficiency symptoms in areas with sodium-rich well water. |
| MoO₄²⁻ Molybdate |
SO₄²⁻ | – | Reciprocal SULTR antagonism (see SO₄²⁻ above). Additionally, Mo is poorly available as MoO₄²⁻ at pH < 5.5 (protonation → HMoO₄⁻); this is the only macronutrient antagonism that resolves with increasing pH (Troug 1946; Marschner 2012). |
| Special Effects – Boron, Viets Effect | |||
| B Boron (optimal supply) |
– | Ca²⁺ K⁺ H₂PO₄⁻ | Boron forms covalent esters with cis-diol groups of the pectin polymer rhamnogalacturonan II (RG-II) in the cell wall. This cross-linking (RG-II–B–RG-II) is a prerequisite for the structural integrity of the primary wall and the selective permeability of the apoplast (O'Neill et al. 2004, Annu. Rev. Plant Biol. 55). B deficiency → cell wall collapse → carbohydrate congestion → blockade of phloem loading with K⁺, Mg²⁺ and H₂PO₄⁻. |
| Ca²⁺ Viets Effect |
Na⁺ Cd²⁺ Mn²⁺ (undesirable cations) | K⁺ inner uptake in general | Ca²⁺ binds to negative charges of pectin galacturonate chains (junction zones) and reduces the apoplastic mobility of competing cations (Viets 1944, Plant Physiol. 19 – primary source). This prevents the leakage of sugars, amino acids and K⁺ from the cell. The effect is strongest at acidic pH (5.5–6.0), as protonation of the carboxyl groups increases Ca²⁺ affinity. |
pH Value and Nutrient Availability
The following representation is based on Troug (1946) as interpreted by Marschner (2012). Bar width corresponds to the available range, the dark green marking indicates the optimal window for hydroponics. The scale is linear from pH 4.0 to pH 8.0. Our dosing systems (from class >= 5-3-1) deliberately oscillate around the pH value to further optimise nutrient uptake. This function is not part of the standard version 5-3-1 and is implemented by us through appropriate programming tailored to your cultivation.
Optimum (Hydroponics) Available (tolerated range)
4.04.55.05.5 6.06.57.07.58.0
Macronutrients
N (NO₃⁻)
P (H₂PO₄⁻)
K⁺
Ca²⁺
Mg²⁺
S (SO₄²⁻)
Micronutrients
Fe²⁺
Mn²⁺
B
Cu²⁺
Zn²⁺
Mo (MoO₄²⁻)
4.04.55.05.5 6.06.57.07.58.0
Source: Troug, E. (1946). Soil reaction influence on availability of plant nutrients. Soil Sci. Soc. Am. Proc. 11:305–308 – reinterpreted for hydroponic systems after Marschner, P. (ed.) (2012). Marschner's Mineral Nutrition of Higher Plants, 3rd ed., Academic Press, London, Fig. 2.4.
Target range for hydroponics: pH 5.5–6.2 is the only range in which all listed elements are simultaneously available – although Fe, Mn, Cu and Zn have their maximum further into the acidic range. A compromise is unavoidable; hence Fe-EDTA or Fe-EDDHA in chelated form (see Article 2) at pH > 6.0 is not a luxury but a necessity.
Primary Sources (peer-reviewed / publicly accessible)
- Mulder, E.G. (1953). Inorganic nitrogen compounds and soil fertility. Plant and Soil 4(4):368–415. DOI: 10.1007/BF01373584
- Viets, F.G. (1944). Calcium and other polyvalent cations as accelerators of ion accumulation by excised barley roots. Plant Physiology 19(3):466–480. DOI: 10.1104/pp.19.3.466
- Troug, E. (1946). Soil reaction influence on availability of plant nutrients. Soil Science Society of America Proceedings 11:305–308.
- Vert, G. et al. (2002). IRT1, an Arabidopsis transporter essential for iron uptake from the soil and for plant growth. The Plant Journal 31(4):529–537. DOI: 10.1046/j.1365-313X.2002.01381.x
- Cakmak, I. & Marschner, H. (1987). Mechanism of phosphorus-induced zinc deficiency in cotton. III. Changes in physiological availability of zinc in plants. Physiologia Plantarum 70(1):13–20. DOI: 10.1111/j.1399-3054.1987.tb01449.x
- O'Neill, M.A. et al. (2004). Rhamnogalacturonan II: structure and function of a borate cross-linked cell wall pectic polysaccharide. Annual Review of Plant Biology 55:109–139. DOI: 10.1146/annurev.arplant.55.031903.141750
- Marschner, P. (ed.) (2012). Marschner's Mineral Nutrition of Higher Plants, 3rd ed. Academic Press, London. ISBN 978-0-12-384905-2
- Mengel, K. & Kirkby, E.A. (2001). Principles of Plant Nutrition, 5th ed. Kluwer Academic Publishers, Dordrecht. ISBN 978-0-7923-7150-2
- Epstein, E. & Bloom, A.J. (2005). Mineral Nutrition of Plants: Principles and Perspectives, 2nd ed. Sinauer Associates, Sunderland MA. ISBN 978-0-87893-172-9
Add Comment