**1. Introduction**

DNA is constantly damaged by both endogenous and exogenous sources, and genotoxicity can be considered as an imbalance between DNA damage and DNA repair mechanisms. Mainte‐ nance of DNA integrity is essential for proper cellular and organismal function, and the capacity to withstand genotoxic challenge is important to avoid long-term genetic instability and population vulnerability. Unrepaired DNA damage can lead to mutations, cellular senes‐

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

cence, apoptosis, progression of cancer, and the process of aging [1]. Mutation is a broad term covering a whole range of changes to the informational molecule, DNA packaged into chro‐ mosomes, of an organism from gene changes to modifications of the number and/or structure of chromosomes. Mutagenicity in normal cells is one of the most serious problems due to the possibility of inducing secondary malignancies and abnormal reproductive outcomes such as Down, Klinefelter, and Turner syndromes [2]. Such changes can be assessed directly by measuring the interaction of agents with DNA or more indirectly through the assessment of DNA repair or the production of gene mutations or chromosome alterations.

Genotoxicity covers a broader spectrum of endpoints than mutagenicity. For example, unscheduled DNA synthesis, sister chromatid exchanges, and DNA strand breaks are the measures of genotoxicity, not mutagenicity, because they are not themselves transmissible from cell to cell or generation to generation. Mutagenicity on the other hand refers to the production of transmissible genetic alterations. Although all cells of an organism contain the same DNA, somatic cells in different organs and tissues of the adult body become specialized to perform defined functions so that only some parts of the genome are expressed. A common feature of mutations in cancer-causing genes, such as those controlling cell division and proliferation, is that this results in genes being expressed in the wrong tissue at the wrong time. The effect of a mutation will depend upon the position of the mutation within the DNA and the location and activity of the particular gene in which the mutation has been induced. Mutations in the many genes that have been implicated in the multistage events leading to cancer can be produced by a variety of mechanisms and interactions and modifications of the genetic material [2, 3].

With the recent focus on environmental problems, increasing awareness of the harmful effects of industrial and agricultural pollution has created a demand for progressively more sophis‐ ticated pollutant and toxicity detection methods. In recent years, there has been a growing concern about the increasing number of environmental pollutants that may disrupt normal endocrine function in exposed humans and animals. Endocrine disrupting compounds comprise a large group of synthetic chemicals that mimic the actions of natural hormones, act as antagonist, or block their synthesis, release, or metabolism. The xenoestrogen bisphenols have received much attention due to their high production volume and widespread human exposure. Recent research in various animal models has shown the genotoxic activity of bisphenols using *in vivo* and *in vitro* assays. Nevertheless, notable differences have been reported, leading to opposite conclusions, which may well have been caused by differences in the screening test, the organisms used, and the exposure conditions assayed [4].

Many important agricultural products, especially those rich in carbohydrates, are attractive colonization sites for fungi. Some toxic secondary metabolites of fungal growth are identified as mycotoxins and may be found to contaminate agricultural products [5]. Mycotoxins are virtually ubiquitous at some concentration in the average human diet. Mycotoxins are able to resist decomposition or being broken down by mammalian digestion, even by ruminant livestock, allowing these compounds to persist in meat and even dairy products [6]. This gives rise to certain partially metabolized mycotoxins, such as aflatoxin M1, which are present in milk from cows or humans that consumed feed or food contaminated by aflatoxins. Even temperature treatments, such as cooking and freezing, do not inactivate some mycotoxins. This section broadly discusses the genotoxic properties of the environmental genotoxicants bisphenols and aflatoxins, which are prominent environmental contaminates, and is believed to be genotoxic agents that contributes to the high incidence of genotoxicity and carcinogenicity among populations.
