Superoxide is biologically toxic and is deployed by the immune system to kill invading microorganisms. In phagocytes, superoxide is produced in large quantities by the enzyme NADPH oxidase for use in oxygen-dependent killing mechanisms of invading pathogens.

The pro-apoptotic proteins in the BCL-2 family, including Bax and Bak, normally act on the mitochondrial membrane to promote permeabilization and release of cytochrome C and ROS, that are important signals in the apoptosis cascade. Growing evidence suggests that activated BAX and/or Bak form an oligomeric pore, MAC in the mitochondrial outer membrane. This results in the release of cytochrome c and other pro-apoptotic factors from the mitochondria, often referred to as mitochondrial outer membrane permeabilization, leading to activation of caspases.

The cycle consumes acetate (in the form of acetyl-CoA) and water, reduces NAD+ to NADH, and produces carbon dioxide as a waste by-product. The NADH generated by the citric acid cycle is fed into the oxidative phosphorylation (electron transport) pathway. At the end of each cycle, the four-carbon oxaloacetate has been regenerated, and the cycle continues. The net result of these two closely linked pathways is the oxidation of nutrients to produce usable chemical energy in the form of ATP. Acetyl-CoA, is the starting point for the citric acid cycle and in eukaryotic cells, the citric acid cycle occurs in the matrix of the mitochondrion. Though the Krebs cycle does not directly require oxygen, it can only take place when oxygen is present because it relies on by-products and is therefore an aerobic process.

Neutrophil and macrophage phagocytosis stimulates various cellular processes including the respiratory burst whereby increased cellular oxygen uptake results in the production of the potent oxidant bactericidal agents, hypochlorous acid and hydroxyl radical.

The cell membrane consists primarily of a thin layer of amphipathic phospholipids that spontaneously arrange with the hydrophobic tail regions on the inside and the hydrophilic head regions outside. Membranes typically have a large content of proteins, around 50% of membrane volume.

P53 has many mechanisms of anticancer function and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. In its anti-cancer role, p53 works through several mechanisms:It can activate DNA repair proteins when DNA has sustained damage. Thus, it may be an important factor in aging.It can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognitionIt can initiate apoptosis (i.e., programmed cell death) if DNA damage proves to be irreparable.It is essential for the senescence response to short telomeres.

First messengers may not physically cross the phospholipid bilayer to initiate changes within the cell directly. This functional limitation necessitates the cell to devise signal transduction mechanisms to transduce first messenger into second messengers, so that the extracellular signal may be propagated intracellularly. Second messengers are intracellular signalling molecules released by the cell to trigger physiological changes such as proliferation, differentiation, migration, survival, and apoptosis. Secondary messengers are therefore one of the initiating components of intracellular signal transduction cascades.

Cellular theories of aging propose that human aging is the result of cellular aging, whereby an increasing proportion of cells reach senescence, a terminal stage at which cells will cease to divide. This will limit the body’s ability to regenerate and to respond to injury or stress. Telomeres are bits of DNA on the ends of chromosomes that protect chromosomes from sticking to each other or tangling, which could cause DNA to abnormally function. As cells replicate, telomeres shorten at the end of chromosomes, and this process correlates to senescence or cellular aging.

Other theories include:

1. The Free Radical Theory: Implicates the gradual accumulation of oxidative cellular damage as a fundamental driver of cellular aging. This theory has evolved over time to emphasize the role of free radical induced mitochondrial DNA (mtDNA) mutations and the accumulation of mtDNA deletions. Given the proximity of mtDNA to the electron transport chain, a primary producer of free radicals, it postulates that the mutations would promote mitochondrial dysfunction and concomitantly increase free radical production in a positive feedback loop. It is known that diet, lifestyle, drugs (e.g. tobacco and alcohol) and radiation etc., are all accelerators of free radical production within the body.
2. Error theory: based on the idea that errors can occur in the transcription of the synthesis of DNA. These errors are perpetuated and eventually lead to systems that do not function at the optimum level. The organism’s aging and death are attributable to these events (Sonneborn, 1979).
3. The Cross-Linking Theory: also referred to as the Glycosylation Theory of Aging. In this theory it is the binding of glucose (simple sugars) to protein, (a process that occurs under the presence of oxygen) that causes various problems. Once this binding has occurred the protein becomes impaired and is unable to perform as efficiently. Living a longer life is going to lead to the increased possibility of oxygen meeting glucose and protein and known cross-linking disorders include senile cataract and the appearance of tough, leathery and yellow skin.
4. The Neuroendocrine Theory First proposed by Professor Vladimir Dilman and Ward Dean MD, this theory elaborates on wear and tear by focusing on the neuroendocrine system. This system is a complicated network of biochemicals that govern the release of hormones which are altered by the walnut sized gland called the hypothalamus located in the brain. The hypothalamus controls various chain-reactions to instruct other organs and glands to release their hormones etc. The hypothalamus also responds to the body hormone levels as a guide to the overall hormonal activity. But as we grow older the hypothalamus loses it precision regulatory ability and the receptors which uptake individual hormones become less sensitive to them. Accordingly, as we age the secretion of many hormones declines and their effectiveness (compared unit to unit) is also reduced due to the receptors down-grading
5. The Membrane Theory of Aging: According to this theory it is the age-related changes of the cell’s ability to transfer chemicals, heat and electrical processes that impair it. As we grow older the cell membrane becomes less lipid (less watery and more solid). This impedes its efficiency to conduct normal function and in particular there is a toxic accumulation
6. The Decline Theory: The mitochondria are the power producing organelles found in every cell of every organ. Their primary job is to create Adenosine Triphosphate (ATP) and they do so in the various energy cycles that involve nutrients such as Acetyl-L-Carnitine, CoQ10 (Idebenone), NADH and some B vitamins etc. Enhancement and protection of the mitochondria is an essential part of preventing and slowing aging. Enhancement can be achieved with the above mention nutrients, as well as ATP supplements themselves.

Integrins are transmembrane receptors that facilitate cell-extracellular matrix (ECM) adhesion. Upon ligand binding, integrins activate signal transduction pathways that mediate cellular signals such as regulation of the cell cycle, organization of the intracellular cytoskeleton, and movement of new receptors to the cell membrane. Integrins are obligate heterodimers, meaning that they have two subunits: α (alpha) and β (beta). Integrins play an important role in cell signalling by modulating the cell signalling pathways of transmembrane protein kinases such as receptor tyrosine kinases (RTK).

Dynamic instability refers to the coexistence of assembly and disassembly at the ends of a microtubule. The microtubule can dynamically switch between growing and shrinking phases in this region. Although both assembly and disassembly occur at both ends they occur preferentially at the (+) end.