Metal scavangers

BAL was developed during the Second World War as an antidote for arsenic-containing chemical weapons. DMPS (2,3-dimercaptopropane-l-sulfonate) and DMSA (2,3-dimercaptosucci-nic acid) are similarly effective. D-Penicillinamine— also a metal scavanger—is recommended on account of fewer side effects. The donation is employed 12-48 hr after BAL therapy. Besides As elimination predominant precautions are control of water and electrolyte loss (4,11,39,51, 52,91,96,119,120,123,124]. 

Sodium hypochlorite solution is strongly alkaline (pH = 11.55) and the free caustic present in the solution acts as a stabiliser. Soda-ash scavanges free hydrochloric acid forming a non-volatile salt and maintain its alkalinity. Stability of sodium hypochlorite solution is also improved by storing it in a dark room below 30°C and free from contaminations of any heavy metal salts. The decomposition of sodium hypochlorite can be represented by the following reactions ... 

It was argued [1256] that provided the tropolones did not act simply as metal ion scavangers (as in the case, for example, with ethylene diamine tetra-cetic acid [1258]), since chelation with metal ions undoubtedly underlies the antifungal properties [1259, 1260] of the thujaplicins and their congeners, then they should be able to compete with the catecholamines for the active enzymic site. The results showed that some of the tropolones, including the two thujaplicins, did in fact act in this way. Presumably the inhibition [1261] of dopamine jS-hydroxylase by y-thujaplicin occurs by a similar mechanism. 

An elucidation of the mechanisms of brain iron homeostasis, as outlined in figure 1, will help our understanding of AD especially since iron binds to Ap-peptide and enhances beta-amyloid toxicity [35-38]. Excess iron accumulation is a consistent observation in the AD brain. As discussed above, patients with hemochromatosis are at risk developing AD at an earlier age [2]. Brain autopsy samples from AD patients have elevated levels of ferritin iron, particularly in the neurons of the basal ganglia [39] and most amyloid plaques contain iron and ferritin-rich cells [40]. Clinically there is a reported decrease in the rate of decline in AD patients who were treated with the intramuscular iron chelator, desferrioxamine [41]. Iron enhances cleavage of the Ap-peptide domain of APP by the metalloprotease alpha secretase [42, 43]. Part of the protective effect of the major cleavage product of APP, APP(s), may derive from its capacity to scavange metals to diminish metal-catalyzed oxidative stress to neuronal cells [44]. APP is, itself, a metalloprotein [4]. 

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