Tyrosine

Publication Title: 
Free Radical Biology & Medicine

Steroid hormones exhibit diverse biological activities. Despite intensive studies on steroid function at the genomic level, their nongenomic actions remain an enigma. In this study, we investigated the role of reactive oxygen species (ROS) in androgen-stimulated prostate cancer (PCa) cell proliferation. In androgen-treated PCa cells, increased cell growth and ROS production correlated with elevated p66Shc protein, an authentic oxidase. This growth stimulation was blocked by antioxidants.

Author(s): 
Veeramani, Suresh
Chou, Yu-Wei
Lin, Frank C.
Muniyan, Sakthivel
Lin, Fen-Fen
Kumar, Satyendra
Xie, Yan
Lele, Subodh M.
Tu, Yaping
Lin, Ming-Fong
Publication Title: 
Canadian Anaesthetists' Society Journal
Author(s): 
Lee, P. K.
Cho, M. H.
Dobkin, A. B.
Publication Title: 
Activitas Nervosa Superior

The present study conducted on twelve normal healthy male subjects showed decrease in blood urea, increase in creatinine and tyrosine after one minute of Kapalabhati, a fast-breathing technique of Hatha Yoga (120 respiratory strokes (min.). From biochemical point of view the practice of Kapalabhati seems to promote decarboxylation and oxidation mechanisms due to which quieting of respiratory centres is achieved, which is also the prerequisite for the practice of Pranayama, another important technique of Yoga.

Author(s): 
Desai, B. P.
Gharote, M. L.
Publication Title: 
Canadian Journal of Physiology and Pharmacology

Ayurveda is an Indian system of medicine. Despite clinical efficacy, lack of scientific validation has limited the effective use of Ayurvedic drugs. Cardoguard is an Ayurvedic antihypertensive drug formulated by Nagarjuna Herbal Concentrates Ltd., Kerala, India. Left ventricular hypertrophy (LVH) is a modifiable risk factor, and regression of LVH reduces the propensity for adverse cardiovascular events. This study was taken up with the objective of evaluating the efficacy of Cardoguard in the prevention of cardiac remodeling.

Author(s): 
Sankar, Vandana
Nair, Renuka R.
Harikrishnan, Vijayakumar S.
Fernandez, Adelaide C.
Kumar, Cherumanal S. Krishna
Madhavachandran, Viswanathamenon
Publication Title: 
Circulation

BACKGROUND: In addition to being a risk marker for cardiovascular disease, much recent data suggest that C-reactive protein (CRP) promotes atherogenesis. Decreased endothelial NO and prostacyclin (PGI2) contribute to a proatherogenic and prothrombotic state. We have shown that CRP decreases endothelial NO synthase expression and bioactivity in human aortic endothelial cells (HAECs). PGI2 is a potent vasodilator and inhibitor of platelet aggregation. Hence, the aim of this study was to examine the effect of CRP on PGI2 release from HAECs and human coronary artery endothelial cells (HCAECs).

Author(s): 
Venugopal, Senthil Kumar
Devaraj, Sridevi
Jialal, Ishwarlal
Publication Title: 
American Journal of Physiology. Heart and Circulatory Physiology

The antiatherogenic effects of soy isoflavone consumption have been demonstrated in a variety of studies. However, the mechanisms involved remain poorly defined. Adhesion of monocytes to vascular endothelial cells is a key step within the inflammatory cascade that leads to atherogenesis. Many factors, including the physical forces associated with blood flow, regulate this process.

Author(s): 
Chacko, Balu K.
Chandler, Robert T.
Mundhekar, Ameya
Khoo, Nicholas
Pruitt, Heather M.
Kucik, Dennis F.
Parks, Dale A.
Kevil, Christopher G.
Barnes, Stephen
Patel, Rakesh P.
Publication Title: 
Journal of Cellular Biochemistry

Endothelin-1 (ET-1) disrupts insulin-regulated glucose transporter GLUT4 trafficking. Since the negative consequence of chronic ET-1 exposure appears to be independent of signal disturbance along the insulin receptor substrate-1/phosphatidylinositol (PI) 3-kinase (PI3K)/Akt-2 pathway of insulin action, we tested if ET-1 altered GLUT4 regulation engaged by osmotic shock, a PI3K-independent stimulus that mimics insulin action. Regulation of GLUT4 by hyperosmotic stress was impaired by ET-1.

Author(s): 
Strawbridge, Andrew B.
Elmendorf, Jeffrey S.
Publication Title: 
The Journal of Biological Chemistry

Although peroxynitrite stimulates apoptosis in many cell types, whether peroxynitrite acts directly as an oxidant or the induction of apoptosis is because of the radicals derived from peroxynitrite decomposition remains unknown. Before undergoing apoptosis because of trophic factor deprivation, primary motor neuron cultures become immunoreactive for nitrotyrosine. We show here using tyrosine-containing peptides that free radical processes mediated by peroxynitrite decomposition products were required for triggering apoptosis in primary motor neurons and in PC12 cells cultures.

Author(s): 
Ye, Yaozu
Quijano, Celia
Robinson, Kristine M.
Ricart, Karina C.
Strayer, Amy L.
Sahawneh, Mary Anne
Shacka, John J.
Kirk, Marion
Barnes, Stephen
Accavitti-Loper, Mary Ann
Radi, Rafael
Beckman, Joseph S.
Estévez, Alvaro G.
Publication Title: 
Atherosclerosis

Chlorotyrosine is an oxidative product of hypochlorous acid and l-tyrosine, and is considered as a biomarker for oxidative stress and cardiovascular disease. However, it is not clear whether chlorotyrosine could directly contribute to vascular pathogenesis. In this study, we investigated the effect and potential mechanisms of chlorotyrosine on human aortic smooth muscle cell (AoSMC) migration. With Boyden chamber and wound healing assays, chlorotyrosine significantly increased AoSMC migration in a concentration- and time-dependent manner.

Author(s): 
Mu, Hong
Wang, Xinwen
Lin, Peter H.
Yao, Qizhi
Chen, Changyi
Publication Title: 
Neuroscience

Parkinson's disease is a common progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. Mitochondrial dysfunction has been strongly implicated in the pathogenesis of Parkinson's disease. Thus, therapeutic approaches that improve mitochondrial function may prove to be beneficial.

Author(s): 
Liang, H. L.
Whelan, H. T.
Eells, J. T.
Wong-Riley, M. T. T.

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