**Abstract**

The free radicals are reactive molecules with electron-rich groups produced during metabolic reactions occurring in the cells. These free radicals are collectively known as reactive oxygen species (ROS) and reactive nitrogen species (RNS). Lipid peroxidation products and protein carbonyls species are under the group of ROS, and nitric oxide and peroxynitrites are under the group of RNS. The malondialdehyde that reacts with LDL-C indirectly induced the risk of atherosclerosis. The protein carbonyls acts as marker of protein oxidation and exerts damage to proteins. The nitric oxide plays an important role in DNA damage, inflammation, proliferation of cancer cells, and dysfunction of apoptosis. The peroxynitrites could induce the process of lipid peroxidation, DNA damage, and may exert chronic damage to all biomolecules. The aim of the present study is that the free radicals may react with biomolecules of the cells and play an important role in the development of chronic disease conditions in the humans.

**Keywords:** reactive oxygen species, reactive nitrogen species, oxidative stress, pathological conditions

#### **1. Introduction**

Free radical is a molecule with an unpaired electron and capable of high reactivity [1, 2]. Free radicals are found to be involved in alteration of redox system, induced DNA damage, activation of procarcinogens, these all markers of induction of cancer [3]. Some of the radicals are the superoxide (O<sup>−</sup><sup>2</sup> ), hydroxyl (OH∙), alkoxy radical (RO∙), and nitric oxide (NO), and nonradical species are hydrogen peroxide (H2O2), singlet oxygen (1 O2), and peroxynitrites (ONOO▬), which play an important role in the development and progression of different pathological conditions [4]. NO-induced dose-responsive DNA strand breakage and deaminations of cytosine to uracil and 5-methylcytosine to thymine account for the mutagenicity of nitric oxide toward bacteria and mammalian cells [5]. Antioxidants are proved that reduce the actions of reactive oxygen and nitrogen species, which are capable of damaging cells and tissues [6]. The proteins contain nitrotyrosine residues accumulate in cells which disrupts multiple regulatory pathways [7].

Nitroxidative stress maker species are actively engaged in the chronic disease complications, and their toxicity is reduced by antioxidants which have protective effects [8]. The enzymes of NADPH oxidases, xanthine oxidase, uncoupled nitric oxide synthase, and mitochondria act as markers of reactive oxygen species production in all metabolic cells [9]. Free radicals thus adversely alter lipids, proteins, and DNA and trigger a number of human diseases [10]. Peroxynitrites are the leading molecule of reactive nitrogen species by enhancing the process of lipid peroxidation, DNA

#### **Figure 1.**

*Impact of free radicals on biomolecules present in cells leads to formation of adducts, markers of various diseases [19].*

damage, and protein oxidation and act as molecular target for drug development for cardiovascular, inflammatory, and neurodegenerative diseases [11]. In the cells, the interaction of excess superoxides with excess nitric oxide results in the generation of peroxynitrite which specify the chronic disease conditions of stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders [12]. The reduced glutathione, glutathione disulfide, and glutathionylated proteins act as markers of redox imbalance are directly proportional to oxidative stress [13].

The ROS requires oxygen for its formation and play an important role in human health and disease [14]. The development of increased ROS production with the simultaneous dysfunction of mitochondria has been exhibited in the pathogenesis of disorders [15]. Every cell especially vascular cells are involved in the higher production of free radicals implicated in the pathogenesis of ischemic heart disease, atherosclerosis, cardiac arrhythmia, hypertension, and diabetes [16]. The scavenging role of hydrogen peroxide is performed by catalase and decreases catalase activity results in aggregation of hydrogen peroxide leads to formation of oxidative distress [17]. The aerobic metabolic reactions are faced to greater a concentration of oxygen generates and is increased oxidation it leads inflammation, mitochondrial dysfunction, and chronic kidney diseases [18]. The purpose of the present review is to investigate the role of free radicals in various physiological and pathological diseases like neurodisorders, cancer, renal, cardiovascular, and immunological dysfunctions (**Figure 1**).

#### **2. Oxidation and cancer**

The reactive oxygen and nitrogen species (RONS) are synthesized in greater concentration by reducing antioxidant defense, and formation of redox imbalance leads to oxidative damage to the DNA and proteins in the oral squamous cell carcinoma [20]. In animals, ROS may influence cell proliferation and cell death through the activation of several signaling pathways in the development of carcinogenesis [21]. The higher level of ROS is directly proportional to the suppression of antioxidant enzymes and significant role of oxidative-induced injury in the breast cancer [22]. The prolonged exposure and intake of tobacco is strongly associated with decreased status of antioxidant enzymes, increased oxidative stress markers with the pathogenesis of oral cancer [23]. The strong correlations of ROS and RNS with lowered antioxidants are found in oral precancer and cancer [2] (**Figures 2**–**3**).

**371**

**Figure 2.**

**Figure 3.**

**2.1 Free radical cause nitric oxide**

*The functions of free radicals on biomolecules and its consequences [24].*

The nitric oxide (NO) has dual role in health and disease and depends on its concentration. Nitric oxide is the active marker of the development of cancer by induction of angiogenesis, blood vessel formation during physiological and pathological processes [25]. NO may modulate tumor DNA repair mechanisms by upregulating p53, poly (ADP-ribose) polymerase, and DNA-dependent protein kinase (DNA-PK). The role of NO in cancer will have profound therapeutic implications for the diagnosis and treatment of disease [26]. Alterations in the NO metabolism and to increase protein nitration may contribute to the mutagenic processes and promote lung carcinogenesis [27]. NO promotes intravasation and angiogenesis to enhance cancer cell growth and increase the properties of cancer cells [28].

*Reactive oxygen species are involved in the development of various pathological disorders [38].*

*Diseases Related to Types of Free Radicals DOI: http://dx.doi.org/10.5772/intechopen.82879*

### *Diseases Related to Types of Free Radicals DOI: http://dx.doi.org/10.5772/intechopen.82879*

*Antioxidants*

**Figure 1.**

*diseases [19].*

damage, and protein oxidation and act as molecular target for drug development for cardiovascular, inflammatory, and neurodegenerative diseases [11]. In the cells, the interaction of excess superoxides with excess nitric oxide results in the generation of peroxynitrite which specify the chronic disease conditions of stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders [12]. The reduced glutathione, glutathione disulfide, and glutathionylated proteins act as markers of redox imbal-

*Impact of free radicals on biomolecules present in cells leads to formation of adducts, markers of various* 

The ROS requires oxygen for its formation and play an important role in human health and disease [14]. The development of increased ROS production with the simultaneous dysfunction of mitochondria has been exhibited in the pathogenesis of disorders [15]. Every cell especially vascular cells are involved in the higher production of free radicals implicated in the pathogenesis of ischemic heart disease, atherosclerosis, cardiac arrhythmia, hypertension, and diabetes [16]. The scavenging role of hydrogen peroxide is performed by catalase and decreases catalase activity results in aggregation of hydrogen peroxide leads to formation of oxidative distress [17]. The aerobic metabolic reactions are faced to greater a concentration of oxygen generates and is increased oxidation it leads inflammation, mitochondrial dysfunction, and chronic kidney diseases [18]. The purpose of the present review is to investigate the role of free radicals in various physiological and pathological diseases like neurodisorders, cancer, renal, cardiovascular, and immunological dysfunctions (**Figure 1**).

The reactive oxygen and nitrogen species (RONS) are synthesized in greater concentration by reducing antioxidant defense, and formation of redox imbalance leads to oxidative damage to the DNA and proteins in the oral squamous cell carcinoma [20]. In animals, ROS may influence cell proliferation and cell death through the activation of several signaling pathways in the development of carcinogenesis [21]. The higher level of ROS is directly proportional to the suppression of antioxidant enzymes and significant role of oxidative-induced injury in the breast cancer [22]. The prolonged exposure and intake of tobacco is strongly associated with decreased status of antioxidant enzymes, increased oxidative stress markers with the pathogenesis of oral cancer [23]. The strong correlations of ROS and RNS with lowered antioxidants are found in oral precancer and cancer [2] (**Figures 2**–**3**).

ance are directly proportional to oxidative stress [13].

**370**

**2. Oxidation and cancer**

**Figure 2.** *The functions of free radicals on biomolecules and its consequences [24].*

**Figure 3.** *Reactive oxygen species are involved in the development of various pathological disorders [38].*
