dorsal/arxiv
View SchemaBistable equilibrium points of mercury body burden
| Authors | Houman Owhadi, Areen Boulos |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0606024 |
| URL | https://arxiv.org/abs/q-bio/0606024 |
Abstract
In the last century mercury levels in the global environment have tripled as a result of increased pollution from industrial, occupational, medicinal and domestic uses \cite{BaMe03}. Glutathione is known to be the main agent responsible for the excretion of mercury (we refer to \cite{Thim05}, \cite{ZalBar99} and \cite{Lyn02}). It has also been shown that mercury inhibits glutathione synthetase (an enzyme acting in the synthesization of Glutathione), therefore leading to decreased glutathione levels (we refer to \cite{Thim05}, \cite{GeGe05}, \cite{GeGe06} and \cite{RDeth04}). Mercury also interferes with the production of heme in the porphyrin pathway \cite{WoMaEc93}. Heme is needed for biological energy production and ability to detox organic toxins via the P450 enzymes \cite{Boy06}. The purpose of this paper is to show that body's response to mercury exposure is hysteretic, i.e. when this feedback of mercury on its main detoxifying agents is strong enough then mercury body burden has two points of equilibrium: one with normal abilities to detoxify and low levels of mercury and one with inhibited abilities to detoxify and high levels of mercury. Furthermore, a small increase of body's mercury burden may not be sufficient to trigger observable neurotoxic effects but it may be sufficient to act as a switch leading to an accumulation of mercury in the body through environmental exposure until its toxicity becomes manifest.
{
"annotation_id": "c7a0c2af-4d3a-42b5-a861-ecddfd40837f",
"date_created": "2026-03-02T18:01:35.339000Z",
"date_modified": "2026-03-02T18:01:35.339000Z",
"file_hash": "0ec8eb2461772f89889b00339582b7018c45edc2ac3d3e5d07bb67a4719e8699",
"private": false,
"record": {
"abstract": "In the last century mercury levels in the global environment have tripled as\na result of increased pollution from industrial, occupational, medicinal and\ndomestic uses \\cite{BaMe03}. Glutathione is known to be the main agent\nresponsible for the excretion of mercury (we refer to \\cite{Thim05},\n\\cite{ZalBar99} and \\cite{Lyn02}). It has also been shown that mercury inhibits\nglutathione synthetase (an enzyme acting in the synthesization of Glutathione),\ntherefore leading to decreased glutathione levels\n (we refer to \\cite{Thim05}, \\cite{GeGe05}, \\cite{GeGe06} and \\cite{RDeth04}).\nMercury also interferes with the production of heme in the porphyrin pathway\n\\cite{WoMaEc93}. Heme is needed for biological energy production and ability to\ndetox organic toxins via the P450 enzymes \\cite{Boy06}. The purpose of this\npaper is to show that body\u0027s response to mercury exposure is hysteretic, i.e.\nwhen this feedback of mercury on its main detoxifying agents is strong enough\nthen mercury body burden has two points of equilibrium: one with normal\nabilities to detoxify and low levels of mercury and one with inhibited\nabilities to detoxify and high levels of mercury. Furthermore, a small increase\nof body\u0027s mercury burden may not be sufficient to trigger observable neurotoxic\neffects but it may be sufficient to act as a switch leading to an accumulation\nof mercury in the body through environmental exposure until its toxicity\nbecomes manifest.",
"arxiv_id": "q-bio/0606024",
"authors": [
"Houman Owhadi",
"Areen Boulos"
],
"categories": [
"q-bio.OT"
],
"title": "Bistable equilibrium points of mercury body burden",
"url": "https://arxiv.org/abs/q-bio/0606024"
},
"schema_id": "dorsal/arxiv",
"source": {
"execution_id": "06518d80-4b5f-45da-a87e-a0f5dea20d61",
"id": "arXiv Dataset IDs",
"type": "Model",
"variant": "snapshot-2026-03-01",
"version": "0.1.0"
},
"user_id": 1000002
}