In times of stress all living organisms, from bacteria to humans, alter their steady-state rates of energy production. The importance of the metabolic pathways by which this adaptation occurs cannot be overstated. The consequence of an inadequate energy supply is catastrophic to the individual, ultimately affected so many vital processes that death is inevitable. This laboratory has observed sufficient experimental evidence to put forth a scheme that can explain the modulation of energy production in mitochondria. The sulfurtransferase activity of he mitochondrial enzyme rhodanese is central to the scheme. It is proposed that rhodanese, which in turn is regulated by phosphorylation-dephosphorylation, controls the rate of electron transport and thus ATP production by the reversible sulfuration-desulfuration or iron-sulfur (FeS) clusters of the respiratory chain. Hence, by controlling the rate of electron transport rhodanese controls the rate of energy (ATP) production.
The specific aim of this project is to gain insight into the molecular mechanisms by which the phospho- and dephospho-forms of rhodanese interact with FeS proteins. It is intended that the kinetics of FeS cluster assembly and disassembly, catalyzed by rhodanese, will be studied. It is further intended that a novel free radical mechanism which is designed to explain the interaction of rhodanese with FeS centers will be tested by electron paramagnetic resonance (EPR) techniques.?
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|Shan, Guo-Qiang; Yu, Ao; Zhao, Chuan-Fang et al. (2015) A combined experimental and computational investigation on the unusual molecular mechanism of the Lossen rearrangement reaction activated by carcinogenic halogenated quinones. J Org Chem 80:180-9|
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|Sheng, Zhi-Guo; Huang, Wei; Liu, Yu-Xiang et al. (2013) Ofloxacin induces apoptosis via ?1 integrin-EGFR-Rac1-Nox2 pathway in microencapsulated chondrocytes. Toxicol Appl Pharmacol 267:74-87|
|Sheng, Zhi-Guo; Huang, Wei; Liu, Yu-Xiang et al. (2013) Bisphenol A at a low concentration boosts mouse spermatogonial cell proliferation by inducing the G protein-coupled receptor 30 expression. Toxicol Appl Pharmacol 267:88-94|
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