3.2. The biological application of Ag NPs/CS-Starch bio-nanocomposite
A living cell is a collection of microscopic components with specific functions and functions. The plasma membrane surrounds the cell contents and is in contact with the external environment. The selective permeability of the membrane maintains the stability of the cell with the help of various transport mechanisms [15-18]. Small-sized nanoparticles easily pass through the membrane and due to their special surface properties, they interact with important cellular components such as mitochondria, lysosomes, and nuclei. The continuity of the structure and maintenance of the function of cells is often determined by biological macromolecules such as carbohydrates, lipids, and proteins. The structure of biomolecules changes under the influence of interaction with various types of nanoparticles [19,20].
Molecular oxygen dissolved in biological fluids is transformed into singlet oxygen under the influence of light energy required for biological transfer reactions. Superoxide radical is formed by a reduction reaction of oxygen molecule. This reaction can be done as a result of the redox cycle, or enzymatically with the catalysis of NADPH oxidase, and also as a byproduct of enzymatic reactions with Xanthine oxidase and a byproduct of the electron transport chain in mitochondria [20-23]. By upregulating the xanthine oxidase and NADPH oxidase enzymes, nanomaterials increase the production of superoxide radicals in some cells such as macrophages and neutrophils and trigger inflammatory reactions. The superoxide anion is suddenly converted to hydrogen peroxide (H2O2) by the catalysis of the superoxide dismutase enzyme and with the help of copper, manganese or zinc as a cofactor. The dissolution of nanomaterials based on iron or copper catalyzes the formation of active oxygen species and through the Fenton reaction leads to the production of hydroxyl (OH) and peroxyl (OOH) free radicals [24,25]. For example, TiO2nanoparticles used in sunscreens produce singlet oxygen and superoxide under the influence of light rays. An increase in the level of ROS leads to inflammatory responses such as an increase in cells with polymorphous nuclei and disturbances in the phagocytosis process of macrophages in some model animals such as rodents [21-25]. Oxidative stress is caused by the predominance of free radicals on antioxidants and is one of the main mechanisms of toxicity of most metal nanoparticles such as gold, zinc oxide, and silver. Oxidative stress by regulating redox-sensitive transcription factors, activates some kinase enzymes and intermediate proteins of inflammatory reactions and causes tissue damage such as damage to the cell membrane, genetic material and biological macromolecules [18-22]. At very high levels, disruption of the signaling pathways inside the cell leads to apoptosis and cell necrosis. Reactive oxygen species disrupt the function of the central nervous system by peroxidizing the unsaturated fatty acids of neuronal cells. Clogging of blood vessels, blood pressure and re-narrowing of arteries after angioplasty due to ROS cause disorders of the cardiovascular system. Mitochondria are one of the ROS production main sources through the electron transport respiratory chain [19-21]. Several clinical syndromes such as stroke, Duchenne muscular dystrophy, cardiac conduction defects due to ROS oxidative attack and mitochondrial DNA double-strand break occur. By producing reactive oxygen species in cancer cells, nanoparticles create changes in the chemical structure of histones or other proteins that are effective in shaping the structure of DNA [23-25]. Unfolding of the helical structure of DNA disrupts gene expression and malfunction of regulation of cellular function of cancer cells. In addition to ROS toxicity, some nanoparticles use other effective mechanisms for cell damage by releasing metal ions, accumulating in some cellular components, and interacting with nuclear components. In general, the cell damage mechanisms by nanoparticles include (1) membranes physical damage (2) Structural changes in the cell skeleton components (3) Disturbance in oxidative and transcription damage (4) Mitochondria damage (5) Dysfunction of lysosome (6) ROS production (7) Membrane proteins dysfunction (8) Mediators and inflammatory factors synthesis [19-25].
Herein, the antioxidant potential of Ag NPs/CS-Starch nanocomposite was assessed by DPPH radical scavenging capacity and the results is expressed in terms of percentage inhibition. This is displayed in Fig. 7. The data output at different sample concentrations were compared to BHT as the reference compound. In the corresponding analysis, the IC50 of Ag NPs/CS-Starch nanocomposite and BHT against DPPH free radicals were 314 and 125 µg/mL, respectively.