C. Pleural plaques
Pleural plaques is a medical condition as a result of exposure to asbestos that lead to accumulated plagues within the pleural cavity(a). Many diseases such as pneumonia, breast cancer, and heart failure can affect the pleural space.,therefore, it is often a secondary effect of another disease process.
5. Antioxidants to prevent pleural effusion
In the study to evaluate the Oxidative stress of thirty-six consecutive patients with clinically stable moderate to very severe COPD (30 men; mean±S.D.=66.6±7.8yr) randomized to receive 3mg melatonin (N=18) or placebo for 3 months found that dyspnea was improved by melatonin (P=0.01), despite no significant changes in lung function or exercise capacity(33).
According to the study bythe John Hunter Hospital, Newcastle, Antioxidants provide protection against the damaging effects of oxidative stress and thus may be useful in the management of inflammatory airways disease. Resveratrol, a polyphenol that demonstrates both antioxidative and anti-inflammatory functions, has been shown to improve outcomes in a variety of diseases(34).
c. Vitamin C
Although many epidemiological studies indicate protective effect of vitamin C against a variety of human malignancies its mechanism(s) of action is questionable, the presented results show that the part of its effect may be accomplished by mononuclear cells, as necessary participants in body defence. Namely, in a long-term in vitro assay we tested vitamin C influence on random migration ability of malignant pleural effusion mononuclears (PEM) obtained from breast cancer patients. Vitamin C in a dose- (50-500 micrograms) and time-dependent (4-44 h) manner inhibited PEM motility, suggesting that immobilization of cells in situ may contribute to its beneficial effect in human cancers, according to the Institute of Physiology, Medical Faculty, Belgrade(35)
According to the study by Hôpital Cochin, Paris, in the study to assess the vNO generation in the course of two acute, non immune, inflammatory reactions (pleurisy induced by rat isologous serum and carrageenan) by means of nitrite measurement in pleural exudate from 0.5 to 24 h, indicated that NO release varied time-dependently, similarly for the two inflammatory reactions. A first, but transient, peak was reached in 30 min while a second peak, more sustained, began at the fourth hour and was maximum at the tenth. Kinetic evolution of NO release was consistent with activation, in a first step, of a constitutive NO synthase probably from endothelial origin (inhibited by 2-Methyl-2-Thiopseudourea sulfate but not by dexamethasone) and with activation, in a second wave, of inducible NOS from endothelial and exudative cells. NO release was potentiated by administration per os of L-Arginine and seems to be involved in the evolution of acute inflammatory reactions and oxygen metabolite production(36).
e. Other antioxidants
According to the study by the University of Rochester Medical Center, antioxidant and/or anti-inflammatory agents such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine and N-acystelyn), dietary polyphenol (curcumin-diferuloylmethane, a principal component of turmeric), resveratrol (a flavanoid found in red wine), green tea (theophylline and epigallocatechin-3- gallate), ergothioneine (xanthine and peroxynitrite inhibitor), quercetin, erdosteine and carbocysteine lysine salt, have been reported to control NF-kappaB activation, regulation of glutathione biosynthesis genes, chromatin remodeling and hence inflammatory gene expression. Specific spin traps such as alpha-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), manganese (III) meso-tetrakis (N,N’-diethyl-1,3-imidazolium-2-yl) porphyrin (AEOL 10150 and AEOL 10113), and a SOD mimetic M40419 have also been reported to inhibit cigarette smoke-induced inflammatory responses in vivo(37).
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