No abstract

Mercury exhibits cytotoxic and mutagenic properties as a result of its effect on tubulin. This toxicity mechanism is related to the production of free radicals that can cause DNA damage. Methylmercury (MeHg) is one of the most toxic of the mercury compounds. It accumulates in the aquatic food chain, eventually reaching the human diet. Several studies have demonstrated that prolactin (PRL) may be differently affected by inorganic and organic mercury based on interference with various neurotransmitters involved in the regulation of PRL secretion. This study evaluated the cytoprotective effect of PRL on human lymphocytes exposed to MeHg in vitro, including observation of the kinetics of HL-60 cells (an acute myeloid leukemia lineage) treated with MeHg and PRL at different concentrations, with both treatments with the individual compounds and combined treatments. All treatments with MeHg produced a significant increase in the frequency of chromatid gaps, however, no significant difference was observed in the chromosomal breaks with any treatment. A dose-dependent increase in the mitotic index was observed for treatments with PRL, which also acts as a co-mitogenic factor, regulating proliferation by modulating the expression of genes that are essential for cell cycle progression and cytoskeleton organization. These properties contribute to the protective action of PRL against the cytotoxic and mutagenic effects of MeHg.

Human populations are frequently exposed to several mutagenic agents that have the potential to damage the DNA, and this, in many cases, may result in the formation of chromosomal aberrations (CAs). CAs are recognized as an important biomarker of human exposure, being a very important tool for environmental biomonitoring. Although there are several types, little is known about the mechanisms involved in the processing of induced lesions in DNA and how these could result in CAs. Thus, cytogenetics and molecular cytogenetics are tools of great importance for identifying these agents, the conditions that can exercise their mutagenic potential, and their action mechanism. This chapter discusses the history of CA formation and some cytogenetic protocols that may be used to perform the chromosomal aberration test in in vivo and in vitro studies.