Na+/K+ pump or sodium–potassium pump is an enzyme found in the plasma membrane. This pumping is active (i.e. it uses energy from ATP) and is important for cell physiology. Its simple function is to pump 3 sodium ions out for every 2 potassium ions taken in and since they both have equal ionic charges, this creates a electrochemical gradient between a cell and its exterior.

Steroidogenesis is a multi-step process that occurs in two organelles, the endoplasmic reticulum (ER) and the mitochondrion. The Golgi apparatus is a major collection and dispatch station of protein products received from the endoplasmic reticulum (ER). Proteins synthesized in the ER are packaged into vesicles, which then fuse with the Golgi apparatus. The majority of proteins synthesized in the rough ER undergo glycosylation which occurs in the Golgi apparatus. Glycosylation mainly refers in particular to the enzymatic process that attaches glycans to proteins, lipids, or other organic molecules. These cargo proteins are modified and destined for secretion via exocytosis or for use in the cell. The Golgi apparatus is also involved in lipid transport and lysosome formation.

At the plasma membrane, some keratins interact with desmosomes (cell-cell adhesion) and hemidesmosomes (cell-matrix adhesion) via adapter proteins.

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.

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.

Carbamoyl phosphate is converted to citrulline by ornithine transcarbamoylase.

Apoptosis is a programmed form of cell death involving the degradation of cellular constituents by a group of cysteine proteases called caspases. The caspases can be activated through either the intrinsic (mitochondrial mediated) or extrinsic (death receptor mediated) apoptotic pathways.

The intrinsic apoptotic pathway, also known as the mitochondrial pathway, is primarily initiated within the mitochondria. This pathway is activated in response to various internal stimuli, such as DNA damage, oxidative stress, and other cellular stresses.

When the intrinsic pathway is triggered, several events occur in the mitochondria:

1. Release of cytochrome c: Cytochrome c is released from the mitochondrial intermembrane space into the cytoplasm.
2. Formation of the apoptosome: Cytochrome c in the cytoplasm binds to apoptotic protease activating factor-1 (Apaf-1) and procaspase-9, forming a complex known as the apoptosome.
3. Activation of caspase-9: The apoptosome activates caspase-9, an initiator caspase.
4. Caspase cascade: Activated caspase-9 then activates executioner caspases, such as caspase-3, leading to the execution phase of apoptosis, which results in the orderly dismantling of the cell.

The mitochondria play a crucial role in this pathway by regulating the release of pro-apoptotic factors that are essential for the activation of downstream apoptotic processes.

Cyclic AMP works by activating protein kinase A (PKA, or cAMP-dependent protein kinase). Protein kinase A can also phosphorylate specific proteins that bind to promoter regions of DNA, causing increases in transcription.

As superoxide is toxic, nearly all organisms living in the presence of oxygen contain isoforms of the superoxide-scavenging enzyme superoxide dismutase, or SOD. SOD is an extremely efficient enzyme; it catalyses the neutralization of superoxide nearly as quickly as the two can diffuse together spontaneously in solution.