**1. Introduction**

In toxicology, the term "toxicant" defines a noxious substance that induces a series of delete‐ rious effects on organs, tissues and biological functions and processes in living organisms. Another term used to describe a toxicant is "poison" [1]. The list of toxicants regardless their origin, of natural sources or ensued from human activities, is quite long.

Some of the main detrimental responses that a toxicant is able to generate at cellular level include: production of reactive oxygen species (ROS) and free radicals. These "basic" processes could be associated with carcinogenesis, immunotoxicity, teratogenesis and genotoxicity. The toxic mechanism of action in such cases is initiated by a terminal toxicant and a target molecule and might involve different types of reactions, including: covalent or non-covalent bonds, hydrogen subtraction, electron transfer, and enzymatic reactions.

The cascade of processes that occur at cellular level and involve ROS is initiated by events like ischemia and lipid peroxidation, which are noticed after the first exposure to reactive metab‐ olites and are considered primary events. As secondary events were described important processes as follows: changes in structure and permeability of membranes, mitochondrial dysfunctions, cytoskeletal and DNA changes, lysosomal destabilization, intervention in apoptosis/necrosis and endoplasmic reticulum destruction. The final step of the cascade is associated with severe pathological destruction on organs level.

In the past decade, the toxicity of heavy metals and their risks on human health has been a subject of high interest, an argument in this regard being the impressive number of publica‐ tions available (over 2000 articles according to PubMed database). Heavy metals are inorganic elements, natural components of earth's crust, and are labeled as the oldest toxins known by humans [2]. It has been demonstrated that heavy metals induce toxicity at different levels in

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human body, including: gastrointestinal system, central and peripheral nervous systems, cardiovascular, renal and hematopoietic systems [2]. As regards the toxic mechanism of action of heavy metals, it has been stated that generation of reactive oxygen species represents one of the main mechanisms involved in heavy metals induced-toxicity. It is believed that gener‐ ation of reactive oxygen species is responsible for the hepatotoxicity, neurotoxicity and nephrotoxicity associated to heavy metals [2, 3].

Free radicals and reactive oxygen species generated by toxicants were described to hold key roles in lipid peroxidation, DNA damage, oxidation of sulfhydryl groups of proteins, depletion of protein, and alteration of calcium homeostasis [2, 4].

Reactive oxygen species (ROS) are oxygen-free radicals that contain one or more unpaired electrons, formed during oxidative metabolism and were characterized as exceedingly active compounds which act by inducing oxidative changes of cellular proteins, lipids and polynu‐ cleotides [5-7].

Under normal conditions, ROS play essential functions in cellular homeostasis, as signal molecules in several signaling pathways involved in cell differentiation, organogenesis, stress response and wound healing, and as redox regulators [6]. Oxidative stress represents a status characterized by excessive cellular levels of ROS as a result of an imbalance in the redox homeostasis explained by increased production of ROS or declined antioxidant capacity [2, 6, 7]. A considerable number of studies endorse the fact that oxidative stress is linked to a plethora of pathologies including cardiovascular diseases, atherosclerosis, diabetes, chronic inflamma‐ tory processes, neurodegenerative disorders, and mostly to cancer [6-8].

This chapter summarizes an update of available data regarding ROS in physiological and pathophysiological conditions, the roles of ROS in cancer and heavy metals induced toxicity via ROS generation.
