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Molecules 2010, 15(12), 8890-8903; doi:10.3390/molecules15128890

Thiol Signalling Network with an Eye to Diabetes

Department of Internal Medicine, University of Pisa, Pisa, Italy
Author to whom correspondence should be addressed.
Received: 24 October 2010 / Revised: 29 November 2010 / Accepted: 6 December 2010 / Published: 6 December 2010
(This article belongs to the Special Issue Antioxidants)
Download PDF [139 KB, 18 June 2014; original version 18 June 2014]


Redox regulatory system controls normal cellular functions. Controlled changes in redox couples potential serve as components for signal transduction, similarly to the phosphorylation cascade. Cellular redox biology requires both compartimentalisation and communication of redox systems: the thermodynamic disequilibrium of the major redox switches allows rapid and sensitive responses to perturbations in redox environments. The many oxidation states of sulphur are found in numerous sulphur species with distinct functional groups (thiols, disulphides, polysulphides, sulphenic, sulphinic and sulphonic acids, etc.), which participate in a complicated network of sulphur-based redox events. Human diseases such as diabetes mellitus and its cardiovascular complications have been associated with increased production of reactive oxygen species and perturbations of thiol redox homeostasis. The review surveys literature related to some etiopathogenic aspects and therapeutic perspectives. The dual toxic-protective property of sulphydryl-donor molecules in experimental settings proposes the general problem of designing antioxidants for therapeutic use.
Keywords: oxidation-reduction; sulphydryl compounds; N-acetylcysteine; diabetes mellitus; arterial hypertension oxidation-reduction; sulphydryl compounds; N-acetylcysteine; diabetes mellitus; arterial hypertension
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Matteucci, E.; Giampietro, O. Thiol Signalling Network with an Eye to Diabetes. Molecules 2010, 15, 8890-8903.

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