Nanotechnology has become a research hotspot to explore functional nanodevices and design materials compatible with nanoscale topography. Recently, titanium dioxide nanotube arrays (TNA) have garnered considerable interest as biomedical implant materials and nanomedicine applications (such as nanotherapeutics, nanodiagnostics and nanobiosensors). In bio-implants studies, the properties of TNA nanostructures could modulate diverse cellular processes, such as cell adhesion, migration, proliferation, and differentiation. Furthermore, this unique structure of TNA provides larger surface area and energy to regulate positive cellular interactions toward the mechanosensitivity activities. As for an advanced medical application, the TNA—biomolecular interactions knowledge are critical for further characterization of nanomaterial particularly in nanotherapeutic manipulation. Knowledge of these aspects will create opportunities for better understanding which may help researchers to develop better nanomaterial products to be used in medicine and health-line services.
Part of the book: Titanium Dioxide
TiO2 nanotube arrays (TNA) have attracted scientific interest due to the combination of functional material properties with controllable nanostructure. Superior properties of TNA, including vectorial pathway of e− transport, minimized e− recombination, and high specific surface area render them as the most promising candidate for environment remediation, energy conversion and biocompatibility applications. The superior properties and efficacy of the TNA in various applications influenced by structural characteristics such as pore size, length and wall thickness. Therefore in this chapter the effect of various electrochemical parameters such as applied voltage, anodization time, electrolyte composition on the formation of controlled dimension of TNA in aqueous and organic electrolytes are reviewed.
Part of the book: Titanium Dioxide
Redox homeostasis is attained by the cautious regulation of both reactive oxygen species (ROS) formation and removal from the body system. A shift in ROS balance promotes oxidative injury and tumour development by inflicting damage to DNA and inducing inconsistencies in the genome. The sources of endogenous ROS in a cell include mETC, NOX, LOX, cytochrome P450 and XO. The exogenous risk factors of ROS are pollutants, chemicals/drugs, radiation and heavy metals. Oxidative phosphorylation in the mitochondria produces ROS with unpaired electrons. Superoxide anion is the major ROS produced in the human mitochondria. Bulk of the ROS generation in the mitochondria occurs at the electron transport chain as derivatives of respiration. Cancer cells sustain ROS production by suppressing the antioxidant-generation system. Balance between ROS production and subsequent detoxification is regulated by scavenging enzymes and antioxidant agents. Failure in sirtuin-3 (SIRT3), ATM and p53 activities elevates the intracellular levels of ROS. PKCα induces the expression of NOX (DUOX) during cancer development and the consequent increase in ROS production. The PI3K/AKT signalling pathway activates NOX with consequent ROS production and subsequent induction of instability in the genome, leading to cancer. In conclusion, the interruption of the redox pathways that regulate ROS and its redox signalling activities affects cell physiology and can ultimately result in abnormal signalling, uncontrolled oxidative impairment and tumorigenesis.
Part of the book: Homeostasis