The effect of high or low levels of trace metals in human tissues has been studied widely. There have been detectable significant variations in the concentrations of trace metals in normal and cancerous tissues suggesting that these variations could be a causative factor to various cancers. Even though essential trace metals play an important role such as stabilizers, enzyme cofactors, elements of structure, and essential elements for normal hormonal functions, their imbalanced toxic effects contribute to the rate of the reactive oxygen species (ROS) and formation of complexities in the body cells which may lead to DNA damage. The induction of oxidative-induced DNA damage by ROS may lead to isolated base lesions or single-strand breaks, complex lesions like double-strand breaks, and some oxidative generated clustered DNA lesions (OCDLs) which are linked to cell apoptosis and mutagenesis. The difference in published works on the level of variations of trace metals in different cancer tissues can be attributed to the accuracy of the analytical techniques, sample preparation methods, and inability of taking uniform samples from the affected tissues. This paper reviews comparative trace elemental concentrations of cancerous and noncancerous tissues using PIXE that has been reported in the published literature. 1. Introduction Studies have shown that the imbalance in the composition of trace metals which are generally recognized to be essential to normal human homeostasis besides accumulation of potentially toxic and nonessential trace metals may cause disease. The significance of the essential trace metals is indisputable due to their positive roles when in specific concentration ranges while on the other hand displaying toxic effects in relatively high or low concentration levels. Physiochemical properties of trace metals govern their uptake, intracellular distribution, and the binding of the metal compounds in biological systems. In spite of diverse physiochemical properties of metals compounds, there are three main predominant mechanisms related to metal genotoxicity. The first is the interference with cellular redox regulation and production of oxidative stress which does cause oxidative DNA damage or trigger signaling cascades that may lead to stimulation of malignant growth [1]. Second is the ability to inhibit the major DNA repairs mechanisms which may result in genomic instability and accumulation of critical mutations. And third is the deregulation of cell proliferation by induction of signaling pathways or ability to inactivate the growth controls
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