• Molecules and Cells
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• v.39 no.1
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• pp.6-19
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• 2016

Redox signalling comprises the biology of molecular signal transduction mediated by reactive oxygen (or nitrogen) species. By specific and reversible oxidation of redoxsensitive cysteines, many biological processes sense and respond to signals from the intracellular redox environment. Redox signals are therefore important regulators of cellular homeostasis. Recently, it has become apparent that the cellular redox state oscillates in vivo and in vitro, with a period of about one day (circadian). Circadian timekeeping allows cells and organisms to adapt their biology to resonate with the 24-hour cycle of day/night. The importance of this innate biological timekeeping is illustrated by the association of clock disruption with the early onset of several diseases (e.g. type II diabetes, stroke and several forms of cancer). Circadian regulation of cellular redox balance suggests potentially two distinct roles for redox signalling in relation to the cellular clock: one where it is regulated by the clock, and one where it regulates the clock. Here, we introduce the concepts of redox signalling and cellular timekeeping, and then critically appraise the evidence for the reciprocal regulation between cellular redox state and the circadian clock. We conclude there is a substantial body of evidence supporting circadian regulation of cellular redox state, but that it would be premature to conclude that the converse is also true. We therefore propose some approaches that might yield more insight into redox control of cellular timekeeping.

• Molecules and Cells
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• v.39 no.1
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• pp.40-45
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• 2016

Peroxiredoxins are highly conserved and abundant peroxidases. Although the thioredoxin peroxidase activity of peroxiredoxin (Prx) is important to maintain low levels of endogenous hydrogen peroxide, Prx have also been shown to promote hydrogen peroxide-mediated signalling. Mitogen activated protein kinase (MAPK) signalling pathways mediate cellular responses to a variety of stimuli, including reactive oxygen species (ROS). Here we review the evidence that Prx can act as both sensors and barriers to the activation of MAPK and discuss the underlying mechanisms involved, focusing in particular on the relationship with thioredoxin.

• Environmental Analysis Health and Toxicology
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• v.20 no.1
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• pp.87-95
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• 2005

Cadmium is well known as a toxic metal and has insulin mimicking effects in rat adipose tissue. This study was undertaken to investigate the effect of CdCl₂ on glucose transport and its mechanism in 3T3 - L1 adipocytes. CdCl₂ exhibits respectively 2.2 and 2.8 fold increases in the 2-deoxyglucose uptake when exposed to 10 and 25 μM of CdCl₂ for 12 hr. To investigate the stimulating mechanism of glucose transport induced by CdCl₂. Wortmannin and PD98059 were used respectively as PI3K inhibitor and MAPK inhibitor, which did not affect 2-DOG uptake. This results suggest that induced 2-deoxy-(l-3H)-D-glucose (2-DOG) uptake by CdCl₂ may not be concerned with the insulin signalling pathway. Whereas nifedipine, a calcium channel blocker inhibited the 2- DOG uptake stimulated by CdCl₂. In addition, we also measured the increased production of Reactive oxygen substances (ROS) and glutathione (GSH) level in 3T3-L1 adipocytes to investigate correlation between the glucose uptake and increased production of ROS with H2DCFDA. CdCl₂ increased production of ROS. Induced 2-DOG uptake and increased production of ROS by CdCl₂ were decreased by N-acetylcystein (NAC). And L-buthionine sulfoximine (BSO) a potent inhibitor of γ-GCS, decreased of 2-DOG uptake. Also NAC and BSO changed the cellular GSH level, but GSH/GSSG ratio remained unchanged at 10, 25 μM of CdCl₂.