**Part 3**

**New Techniques and Findings in Bioenergetics Research** 

234 Bioenergetics

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*Abu Dhabi* 

*United Arab Emirates* 

**Phosphorescence Oxygen Analyzer as** 

Fatma Al-Jasmi, Ahmed R. Al Suwaidi, Mariam Al-Shamsi,

*United Arab Emirates University, Faculty of Medicine and Health Sciences* 

The "*phosphorescence oxygen analyzer*" and its use to monitor O2 consumption by cells and tissues are discussed in this chapter (Lo et al., 1996; Souid et al., 2003). This analytical tool assesses bioenergetics in cells undergoing apoptosis (e.g., the mitochondrial cell death pathway), in cells exposed to toxins (e.g., loss of viability) and in cells with a genetically altered energy metabolism (e.g., mitochondrial disorders) (Tacka et al., 2004a-b; Tao et al., 2007; Tao et al., 2008a). This method is applicable to suspended (e.g., Jurkat and HL-60 cells) and adherent (TU183 human oral cancer cells) cells and to fresh tissues from humans (e.g., lymphocytes, spermatozoa and tumors) and animals (e.g., liver, spleen, heart, pancreas and kidney) (Badawy et al., 2009a-b; Whyte et al., 2010; Al Shamsi et al., 2010; Al-Salam et al., 2011; Al Samri et al., 2011). The analyzer allows investigating anticancer compounds (single agents or combinations) for dosing, order of administration and exposure (Jones et al., 2009; Tao et al., 2008b; Souid et al., 2006; Goodisman et al., 2006; Tao et al., 2006a-b; Tack et al. 2004b). It can also be used to monitor reactions consuming or producing O2 (Tao et al.,

The term "*cellular bioenergetics*" describes the biochemical processes involved in energy metabolism (energy conversion or transformation), while the term "*cellular respiration*" describes delivery of O2 to the mitochondria, the breakdown of reduced metabolic fuels with passage of electrons to O2, and the resulting synthesis of ATP. Impaired respiration thus implies any abnormality involving cellular bioenergetics, including glycolysis. The term "*apoptosis*" describes cellular mechanisms responsible for initiating and executing cell death. The initiation step requires a leakage of cytochrome c from the mitochondrial intermembrane to the cytosol. In the cytosol, cytochrome c binds to the apoptotic protease activating factor-1 (Apaf-1), triggering the caspase cascade (a series of cysteine, aspartatespecific proteases). Caspase activation executes mitochondrial dysfunction (Nicholson et al., 1997). This mitochondrial perturbation involves opening the permeability transition pores (accelerating oxidations in the mitochondrial respiratory chain) and collapsing the

**1. Introduction** 

2008b; Tao et al., 2009).

**2. Relevant biological processes** 

Farida Marzouqi, Aysha Al Mansouri, Sami Shaban,

Harvey S. Penefsky and Abdul-Kader Souid

**a Measuring Tool for Cellular Bioenergetics** 
