Intoxication à l'arsenic

Résumé

L’intoxication à l’arsenic est un empoisonnement provoqué par l’arsenic. On le dit aigu (en cas de forte dose) ou chronique (exposition longue à de faibles doses). La principale source d'intoxication chronique dans le monde semble être l'eau de forage qui dans plusieurs pays ou régions est naturellement chargée en arsenic. Selon une étude publiée en 2007, plus de 137 millions de personnes, vivant dans plus de 70 pays sont probablement affectées par une intoxication chronique à l'arsenic à partir de l'eau de boisson. Ce métalloïde est un poison qui peut conduire à la mort par inhibition allostérique des enzymes indispensables au métabolisme, induisant une défaillance multiple des organes. Il inhibe principalement les enzymes exigeant la présence d'acide lipoïque comme cofacteur, tels que la pyruvate déshydrogénase et l'alpha-cetoglutarate déshydrogénase. Pour cette raison, les substrats produits avant l’étape de la déshydrogénase comme le pyruvate et le lactate s'accumulent. Il af

Source officielle

https://fr.wikipedia.org/wiki/Intoxication_%C3%A0_l'arsenic

À propos de ce résultat

Cette page est générée automatiquement et peut contenir des informations qui ne sont pas correctes, complètes, à jour ou pertinentes par rapport à votre recherche. Il en va de même pour toutes les autres pages de ce site. Veillez à vérifier les informations auprès des sources officielles de l'EPFL.

Publications associées (2)

Publications associées

Chargement

Personnes associées

Chargement

Unités associées

Chargement

Concepts associés (11)

Concepts associés

Chargement

Cours associés (3)

Cours associés

Chargement

Séances de cours associées (4)

Séances de cours associées

Chargement

A luminescent bacterial biosensor was used to quantify bioavailable arsenic in artificial groundwater. Its light production above the background emission was proportional to the arsenite concentration in the toxicologically relevant range of 0 to 0.5 mu M. Effects of the inorganic solutes phosphate, Fe(II) and silicate on the biosensor signal were studied. Phosphate at a concentration of 0.25 g L-1 phosphate slightly stimulated the light emission, but much less than toxicologically relevant concentrations of the much stronger inducer arsenite. No effect of phosphate was oberved in the presence of arsenite. Freshly prepared sodium silicate solution at a concentration of 10 g L-1 Si reduced the arsenite-induced light production by roughly 37%, which can be explained by transient polymerization leading to sequestration of some arsenic. After three days of incubation, silicate did not have this effect anymore, probably because depolymerization occurred. In the presence of 0.4 g L-1 Fe(II), the arsenite-induced light emission was reduced by up to 90%, probably due to iron oxidation followed by arsenite adsorption on the less soluble Fe(III) possibly along with some oxidation to the stronger adsorbing As(V). Addition of 100 mu M EDTA was capable of releasing all arsenic from the precipitate and to transform it into the biologically measurable, dissolved state. The biosensor also proved valuable for monitoring the effectiveness of an arsenic removal procedure based on water filtration through a mixture of sand and iron granules.

Springer Verlag2005

Chargement

Tunable reporter signal production in feedback-uncoupled arsenic bioreporters

Vassily Hatzimanikatis, Jan Roelof van der Meer

Escherichia coli-based bioreporters for arsenic detection are typically based on the natural feedback loop that controls ars operon transcription. Feedback loops are known to show a wide range linear response to the detriment of the overall amplification of the incoming signal. While being a favourable feature in controlling arsenic detoxification for the cell, a feedback loop is not necessarily the most optimal for obtaining highest sensitivity and response in a designed cellular reporter for arsenic detection. Here we systematically explore the effects of uncoupling the topology of arsenic sensing circuitry on the developed reporter signal as a function of arsenite concentration input. A model was developed to describe relative ArsR and GFP levels in feedback and uncoupled circuitry, which was used to explore new ArsR-based synthetic circuits. The expression of arsR was then placed under the control of a series of constitutive promoters, which differed in promoter strength, and which could be further modulated by TetR repression. Expression of the reporter gene was maintained under the ArsRcontrolled Pars promoter. ArsR expression in the systems was measured by using ArsR-mCherry fusion proteins. We find that stronger constitutive ArsR production decreases arsenite-dependent EGFP output from Pars and vice versa. This leads to a tunable series of arsenite-dependent EGFP outputs in a variety of systematically characterized circuitries. The higher expression levels and sensitivities of the response curves in the uncoupled circuits may be useful for improving field-test assays using arsenic bioreporters.

Wiley-Blackwell2013

Chargement