Metal-binding protein
Metallothionein
Also searched as Metallothionein.
You want it high: it is the only defense the body builds for itself, and it binds cadmium and mercury tighter than almost anything else.
In depth
Metallothionein — a small cysteine-rich protein the body makes to grab heavy metals and hold them where they cannot react.
What drives it
Zinc status increases it.
Zinc binds the transcription factor MTF-1, which drives metal-response-element-dependent metallothionein transcription. doi 10.3390/life13010067
Copper status increases it.
Copper likewise induces metallothionein transcription through MTF-1 and the metal-response element. doi 10.3390/ani9060353
What it drives
It increases Heavy metal burden.
The body's own trap - and it is A TRAP. Confirmed across USA, Swedish and Japanese sources in two languages: MT lowers metal toxicity but raises body burden. Verbatim, doi 10.1093/toxsci/55.1.223 (Klaassen group, MT-null knockout): wild-type hepatic Cd reached '400 ug/g liver' while 'in MT I/II-null mice, hepatic Cd concentrations were about 10 ug/g liver' - 40-fold lower without MT - yet liver injury was worse in the null. Liu & Klaassen: 'the elimination of Cd was much faster in MT-null mice than in control mice'. Nordberg (PMC8945717, independent group): 'These observations support a role of MT in tissue retention and transport of cadmium to the kidney'. Japan Food Safety Commission: Cd binds hepatic MT and accumulates as Cd-MT; Cd-MT is filtered at the glomerulus, reabsorbed in the proximal tubule and accumulates in the renal cortex, with only a very small amount excreted in urine. Tokushima Bunri Univ: when MT is deficient the tissue concentration of zinc and cadmium falls, so MT functions to retain metals in tissue. Why detoxification studies do not answer this: two often-cited papers (PMC262672, PMC5634692) measure detoxification and 'concentration to a physiological or nontoxic level', a toxicity endpoint, not body burden. Different endpoints. Cd-dominant; not generalized to Pb/Hg/As. Counter-evidence: one Nrf2-KO chronic study reports lowered MT with subsequent Cd accumulation, but Nrf2 knockout is confounded across many genes; the direct MT-knockout designs govern. doi 10.1093/toxsci/55.1.223 · PMC8945717
It increases Zinc status.
Metallothionein is the principal intracellular zinc reservoir, donating zinc to apo-metalloproteins on thiol oxidation. PMID 10092590 · PMC10210066
It increases Copper status.
Metallothionein is the major intracellular copper-binding protein in hepatic copper handling. PMC2920313
It reduces Oxidative stress.
Its cysteine thiol cluster scavenges hydroxyl radical and superoxide directly. doi 10.3390/antiox12030640
It increases Cell survival.
Metallothionein induction is cytoprotective, raising cell survival under metal and oxidant stress. doi 10.1590/S0004-282X2011000100020
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.