scholarly journals Role of intracellular second messengers and reactive oxygen species in the pathophysiology of V. cholera O139 treated rabbit ileum

Author(s):  
Sushumna Gorowara ◽  
Sunita Sapru ◽  
Nirmal Kumar Ganguly
2004 ◽  
Vol 287 (2) ◽  
pp. C246-C256 ◽  
Author(s):  
Henry Jay Forman ◽  
Jon M. Fukuto ◽  
Martine Torres

Except for the role of NO in the activation of guanylate cyclase, which is well established, the involvement of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in signal transduction remains controversial, despite a large body of evidence suggestive of their participation in a variety of signaling pathways. Several problems have limited their acceptance as signaling molecules, with the major one being the difficulty in identifying the specific targets for each pathway and the chemical reactions supporting reversible oxidation of these signaling components, consistent with a second messenger role for ROS and RNS. Nevertheless, it has become clear that cysteine residues in the thiolate (i.e., ionized) form that are found in some proteins can be specific targets for reaction with H2O2 and RNS. This review focuses on the chemistry of the reversible oxidation of those thiolates, with a particular emphasis on the critical thiolate found in protein tyrosine phosphatases as an example.


2004 ◽  
Vol 32 (6) ◽  
pp. 1015-1017 ◽  
Author(s):  
C. Jacob ◽  
J.R. Lancaster ◽  
G.I. Giles

Intense interest has been generated by the discovery that reactive oxygen species can function as intracellular second messengers. Reactive oxygen species have been implicated in diverse cellular processes, including growth factor signal transduction, gene expression and apoptosis. Additionally, there is evidence for proteins that are regulated by redox environment through the reversible oxidation of their cysteine residues. However, the direct reaction of reactive oxygen species with cysteine at physiological concentrations is generally a slow process, suggesting that intermediates are required to convey efficiently the oxidative stimulus. Here, we discuss the evidence that DSOs (disulphide-S-oxides) are formed from glutathione under oxidizing conditions and specifically modulate the redox status of thiols, indicating the existence of specialized cellular oxidative pathways. DSO inactivated glyceraldehyde 3-phosphate and alcohol dehydrogenases and released zinc from metallothionein and a zinc finger domain. In contrast, equivalent concentrations of H2O2 showed minimal effect. The antioxidants ascorbate, NADH, trolox and melatonin were unable to quench DSO-induced oxidation. These findings support the paradigm of oxidative signal transduction and provide a general pathway whereby reactive oxygen species can convert thiols into disulphides.


2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.


2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.


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